Sample records for sleep sleep deprivation

  1. Sleep Deprivation.

    PubMed

    Abrams, Robert M

    2015-09-01

    Sleep deprivation occurs when inadequate sleep leads to decreased performance, inadequate alertness, and deterioration in health. It is incompletely understood why humans need sleep, although some theories include energy conservation, restoration, and information processing. Sleep deprivation has many deleterious health effects. Residency programs have enacted strict work restrictions because of medically related errors due to sleep deprivation. Because obstetrics is an unpredictable specialty with long irregular hours, enacting a hospitalist program enhances patient safety, decreases malpractice risk, and improves the physician's quality of life by allowing obstetricians to get sufficient rest. Copyright © 2015 Elsevier Inc. All rights reserved.

  2. Genetic Dissociation of Daily Sleep and Sleep Following Thermogenetic Sleep Deprivation in Drosophila.

    PubMed

    Dubowy, Christine; Moravcevic, Katarina; Yue, Zhifeng; Wan, Joy Y; Van Dongen, Hans P A; Sehgal, Amita

    2016-05-01

    Sleep rebound-the increase in sleep that follows sleep deprivation-is a hallmark of homeostatic sleep regulation that is conserved across the animal kingdom. However, both the mechanisms that underlie sleep rebound and its relationship to habitual daily sleep remain unclear. To address this, we developed an efficient thermogenetic method of inducing sleep deprivation in Drosophila that produces a substantial rebound, and applied the newly developed method to assess sleep rebound in a screen of 1,741 mutated lines. We used data generated by this screen to identify lines with reduced sleep rebound following thermogenetic sleep deprivation, and to probe the relationship between habitual sleep amount and sleep following thermogenetic sleep deprivation in Drosophila. To develop a thermogenetic method of sleep deprivation suitable for screening, we thermogenetically stimulated different populations of wake-promoting neurons labeled by Gal4 drivers. Sleep rebound following thermogenetically-induced wakefulness varies across the different sets of wake-promoting neurons that were stimulated, from very little to quite substantial. Thermogenetic activation of neurons marked by the c584-Gal4 driver produces both strong sleep loss and a substantial rebound that is more consistent within genotypes than rebound following mechanical or caffeine-induced sleep deprivation. We therefore used this driver to induce sleep deprivation in a screen of 1,741 mutagenized lines generated by the Drosophila Gene Disruption Project. Flies were subjected to 9 h of sleep deprivation during the dark period and released from sleep deprivation 3 h before lights-on. Recovery was measured over the 15 h following sleep deprivation. Following identification of lines with reduced sleep rebound, we characterized baseline sleep and sleep depth before and after sleep deprivation for these hits. We identified two lines that consistently exhibit a blunted increase in the duration and depth of sleep after

  3. Genetic Dissociation of Daily Sleep and Sleep Following Thermogenetic Sleep Deprivation in Drosophila

    PubMed Central

    Dubowy, Christine; Moravcevic, Katarina; Yue, Zhifeng; Wan, Joy Y.; Van Dongen, Hans P.A.; Sehgal, Amita

    2016-01-01

    Study Objectives: Sleep rebound—the increase in sleep that follows sleep deprivation—is a hallmark of homeostatic sleep regulation that is conserved across the animal kingdom. However, both the mechanisms that underlie sleep rebound and its relationship to habitual daily sleep remain unclear. To address this, we developed an efficient thermogenetic method of inducing sleep deprivation in Drosophila that produces a substantial rebound, and applied the newly developed method to assess sleep rebound in a screen of 1,741 mutated lines. We used data generated by this screen to identify lines with reduced sleep rebound following thermogenetic sleep deprivation, and to probe the relationship between habitual sleep amount and sleep following thermogenetic sleep deprivation in Drosophila. Methods: To develop a thermogenetic method of sleep deprivation suitable for screening, we thermogenetically stimulated different populations of wake-promoting neurons labeled by Gal4 drivers. Sleep rebound following thermogenetically-induced wakefulness varies across the different sets of wake-promoting neurons that were stimulated, from very little to quite substantial. Thermogenetic activation of neurons marked by the c584-Gal4 driver produces both strong sleep loss and a substantial rebound that is more consistent within genotypes than rebound following mechanical or caffeine-induced sleep deprivation. We therefore used this driver to induce sleep deprivation in a screen of 1,741 mutagenized lines generated by the Drosophila Gene Disruption Project. Flies were subjected to 9 h of sleep deprivation during the dark period and released from sleep deprivation 3 h before lights-on. Recovery was measured over the 15 h following sleep deprivation. Following identification of lines with reduced sleep rebound, we characterized baseline sleep and sleep depth before and after sleep deprivation for these hits. Results: We identified two lines that consistently exhibit a blunted increase in the

  4. Vascular Compliance Limits during Sleep Deprivation and Recovery Sleep

    PubMed Central

    Phillips, Derrick J.; Schei, Jennifer L.; Rector, David M.

    2013-01-01

    Study Objectives: Our previous studies showed that evoked hemodynamic responses are smaller during wake compared to sleep; suggesting neural activity is associated with vascular expansion and decreased compliance. We explored whether prolonged activity during sleep deprivation may exacerbate vascular expansion and blunt hemodynamic responses. Design: Evoked auditory responses were generated with periodic 65dB speaker clicks over a 72-h period and measured with cortical electrodes. Evoked hemodynamic responses were measured simultaneously with optical techniques using three light-emitting diodes, and a photodiode. Setting: Animals were housed in separate 30×30×80cm enclosures, tethered to a commutator system and maintained on a 12-h light/dark cycle. Food and water were available ad libitum. Patients or Participants: Seven adult female Sprague-Dawley rats. Interventions: Following a 24-h baseline recording, sleep deprivation was initiated for 0 to 10 h by gentle handling, followed by a 24-h recovery sleep recording. Evoked electrical and hemodynamic responses were measured before, during, and after sleep deprivation. Measurements and Results: Following deprivation, evoked hemodynamic amplitudes were blunted. Steady-state oxyhemoglobin concentration increased during deprivation and remained high during the initial recovery period before returning to baseline levels after approximately 9-h. Conclusions: Sleep deprivation resulted in blood vessel expansion and decreased compliance while lower basal neural activity during recovery sleep may allow blood vessel compliance to recover. Chronic sleep restriction or sleep deprivation could push the vasculature to critical levels, limiting blood delivery, and leading to metabolic deficits with the potential for neural trauma. Citation: Phillips DJ; Schei JL; Rector DM. Vascular compliance limits during sleep deprivation and recovery sleep. SLEEP 2013;36(10):1459-1470. PMID:24082305

  5. Can sleep deprivation studies explain why human adults sleep?

    PubMed

    Brown, Lee K

    2012-11-01

    This review will concentrate on the consequences of sleep deprivation in adult humans. These findings form a paradigm that serves to demonstrate many of the critical functions of the sleep states. The drive to obtain food, water, and sleep constitutes important vegetative appetites throughout the animal kingdom. Unlike nutrition and hydration, the reasons for sleep have largely remained speculative. When adult humans are nonspecifically sleep-deprived, systemic effects may include defects in cognition, vigilance, emotional stability, risk-taking, and, possibly, moral reasoning. Appetite (for foodstuffs) increases and glucose intolerance may ensue. Procedural, declarative, and emotional memory are affected. Widespread alterations of immune function and inflammatory regulators can be observed, and functional MRI reveals profound changes in regional cerebral activity related to attention and memory. Selective deprivation of rapid eye movement (REM) sleep, on the contrary, appears to be more activating and to have lesser effects on immunity and inflammation. The findings support a critical need for sleep due to the widespread effects on the adult human that result from nonselective sleep deprivation. The effects of selective REM deprivation appear to be different and possibly less profound, and the functions of this sleep state remain enigmatic.

  6. Vascular compliance limits during sleep deprivation and recovery sleep.

    PubMed

    Phillips, Derrick J; Schei, Jennifer L; Rector, David M

    2013-10-01

    Our previous studies showed that evoked hemodynamic responses are smaller during wake compared to sleep; suggesting neural activity is associated with vascular expansion and decreased compliance. We explored whether prolonged activity during sleep deprivation may exacerbate vascular expansion and blunt hemodynamic responses. Evoked auditory responses were generated with periodic 65 dB speaker clicks over a 72-h period and measured with cortical electrodes. Evoked hemodynamic responses were measured simultaneously with optical techniques using three light-emitting diodes, and a photodiode. Animals were housed in separate 30×30×80 cm enclosures, tethered to a commutator system and maintained on a 12-h light/dark cycle. Food and water were available ad libitum. Seven adult female Sprague-Dawley rats. Following a 24-h baseline recording, sleep deprivation was initiated for 0 to 10 h by gentle handling, followed by a 24-h recovery sleep recording. Evoked electrical and hemodynamic responses were measured before, during, and after sleep deprivation. Following deprivation, evoked hemodynamic amplitudes were blunted. Steady-state oxyhemoglobin concentration increased during deprivation and remained high during the initial recovery period before returning to baseline levels after approximately 9-h. Sleep deprivation resulted in blood vessel expansion and decreased compliance while lower basal neural activity during recovery sleep may allow blood vessel compliance to recover. Chronic sleep restriction or sleep deprivation could push the vasculature to critical levels, limiting blood delivery, and leading to metabolic deficits with the potential for neural trauma.

  7. [Sleep deprivation in somnambulism. Effect of arousal, deep sleep and sleep stage changes].

    PubMed

    Mayer, G; Neissner, V; Schwarzmayr, P; Meier-Ewert, K

    1998-06-01

    Diagnosis of parasomnias in the sleep laboratory is difficult since the nocturnal behavior reported by the patients often does not show up in the laboratory. To test the efficacy of sleep deprivation as a tool to provoke somnambulism we investigated ten patients (three women and seven men, mean age 27 +/- 3.4) with somnambulism. Their standard polysomnographies and videomonitored nocturnal behavior was compared to that of sex- and age-matched controls and to polysomnography and behavior after sleep deprivation. Patients with parasomnias and controls did not show significant differences in sleep parameters with the exception of longer arousal duration in controls, which was nonsignificant. In magnetic resonance tomography, patients with parasomnias did not reveal abnormality of the brain that might explain release of nocturnal behavior. Sleep deprivation led to significantly reduced number of arousals, reduced arousal index, significantly prolonged arousal duration and more stage shifts from all sleep stages (nonsignificant). Complex behavior during sleep increased under sleep deprivation, whereas sleepwalking did not increase. The majority of complex behavior during sleep is triggered by stage shifts and not by arousal in the sense of the arousal definition of the American Sleep Disorder Society. Complex behavior in sleep is stereotypical and nonviolent. Its complexity seems to depend on the duration and intensity of arousals. Sleep deprivation can be recommended as an efficacious method of increasing complex behavior in sleep, which is a preliminary stage of sleepwalking. Concerning the underlying pathology it seems to be important to register the quality and duration of stimuli that trigger arousals instead of focusing the number of arousals alone.

  8. Sleep Deprivation and Neurobehavioral Dynamics

    PubMed Central

    Basner, Mathias; Rao, Hengyi; Goel, Namni; Dinges, David F.

    2013-01-01

    Lifestyles involving sleep deprivation are common, despite mounting evidence that both acute total sleep deprivation and chronically restricted sleep degrade neurobehavioral functions associated with arousal, attention, memory and state stability. Current research suggests dynamic differences in the way the central nervous system responds to acute versus chronic sleep restriction, which is reflected in new models of sleep-wake regulation. Chronic sleep restriction likely induces long-term neuromodulatory changes in brain physiology that could explain why recovery from it may require more time than from acute sleep loss. High intraclass correlations in neurobehavioral responses to sleep loss suggest that these trait-like differences are phenotypic and may include genetic components. Sleep deprivation induces changes in brain metabolism and neural activation that involve distributed networks and connectivity. PMID:23523374

  9. Effects of different sleep deprivation protocols on sleep perception in healthy volunteers.

    PubMed

    Goulart, Leonardo I; Pinto, Luciano R; Perlis, Michael L; Martins, Raquel; Caboclo, Luis Otavio; Tufik, Sergio; Andersen, Monica L

    2014-10-01

    To investigate whether different protocols of sleep deprivation modify sleep perception. The effects of total sleep deprivation (TD) and selective rapid eye movement (REM) sleep deprivation (RD) on sleep perception were analyzed in normal volunteers. Thirty-one healthy males with normal sleep were randomized to one of three conditions: (i) normal uninterrupted sleep; (ii) four nights of RD; or (iii) two nights of TD. Morning perception of total sleep time was evaluated for each condition. Sleep perception was estimated using total sleep time (in hours) as perceived by the volunteer divided by the total sleep time (in hours) measured by polysomnography (PSG). The final value of this calculation was defined as the perception index (PI). There were no significant differences among the three groups of volunteers in the total sleep time measured by PSG or in the perception of total sleep time at baseline condition. Volunteers submitted to RD exhibited lower sleep PI scores as compared with controls during the sleep deprivation period (P <0.05). Both RD and TD groups showed PI similar to controls during the recovery period. Selective REM sleep deprivation reduced the ability of healthy young volunteers to perceive their total sleep time when compared with time measured by PSG. The data reinforce the influence of sleep deprivation on sleep perception. Copyright © 2014 Elsevier B.V. All rights reserved.

  10. Sleep deprivation suppresses aggression in Drosophila

    PubMed Central

    Kayser, Matthew S; Mainwaring, Benjamin; Yue, Zhifeng; Sehgal, Amita

    2015-01-01

    Sleep disturbances negatively impact numerous functions and have been linked to aggression and violence. However, a clear effect of sleep deprivation on aggressive behaviors remains unclear. We find that acute sleep deprivation profoundly suppresses aggressive behaviors in the fruit fly, while other social behaviors are unaffected. This suppression is recovered following post-deprivation sleep rebound, and occurs regardless of the approach to achieve sleep loss. Genetic and pharmacologic approaches suggest octopamine signaling transmits changes in aggression upon sleep deprivation, and reduced aggression places sleep-deprived flies at a competitive disadvantage for obtaining a reproductive partner. These findings demonstrate an interaction between two phylogenetically conserved behaviors, and suggest that previous sleep experiences strongly modulate aggression with consequences for reproductive fitness. DOI: http://dx.doi.org/10.7554/eLife.07643.001 PMID:26216041

  11. Are You Sleep Deprived?

    MedlinePlus

    ... of this page please turn JavaScript on. Feature: Sleep Disorders Are You Sleep Deprived? Past Issues / Summer 2015 Table of Contents ... even if you think you've had enough sleep? You might have a sleep disorder. There are ...

  12. Benefits of Sleep Extension on Sustained Attention and Sleep Pressure Before and During Total Sleep Deprivation and Recovery

    PubMed Central

    Arnal, Pierrick J.; Sauvet, Fabien; Leger, Damien; van Beers, Pascal; Bayon, Virginie; Bougard, Clément; Rabat, Arnaud; Millet, Guillaume Y.; Chennaoui, Mounir

    2015-01-01

    Objectives: To investigate the effects of 6 nights of sleep extension on sustained attention and sleep pressure before and during total sleep deprivation and after a subsequent recovery sleep. Design: Subjects participated in two experimental conditions (randomized cross-over design): extended sleep (EXT, 9.8 ± 0.1 h (mean ± SE) time in bed) and habitual sleep (HAB, 8.2 ± 0.1 h time in bed). In each condition, subjects performed two consecutive phases: (1) 6 nights of either EXT or HAB (2) three days in-laboratory: baseline, total sleep deprivation and after 10 h of recovery sleep. Setting: Residential sleep extension and sleep performance laboratory (continuous polysomnographic recording). Participants: 14 healthy men (age range: 26–37 years). Interventions: EXT vs. HAB sleep durations prior to total sleep deprivation. Measurements and Results: Total sleep time and duration of all sleep stages during the 6 nights were significantly higher in EXT than HAB. EXT improved psychomotor vigilance task performance (PVT, both fewer lapses and faster speed) and reduced sleep pressure as evidenced by longer multiple sleep latencies (MSLT) at baseline compared to HAB. EXT limited PVT lapses and the number of involuntary microsleeps during total sleep deprivation. Differences in PVT lapses and speed and MSLT at baseline were maintained after one night of recovery sleep. Conclusion: Six nights of extended sleep improve sustained attention and reduce sleep pressure. Sleep extension also protects against psychomotor vigilance task lapses and microsleep degradation during total sleep deprivation. These beneficial effects persist after one night of recovery sleep. Citation: Arnal PJ, Sauvet F, Leger D, van Beers P, Bayon V, Bougard C, Rabat A, Millet GY, Chennaoui M. Benefits of sleep extension on sustained attention and sleep pressure before and during total sleep deprivation and recovery. SLEEP 2015;38(12):1935–1943. PMID:26194565

  13. Benefits of Sleep Extension on Sustained Attention and Sleep Pressure Before and During Total Sleep Deprivation and Recovery.

    PubMed

    Arnal, Pierrick J; Sauvet, Fabien; Leger, Damien; van Beers, Pascal; Bayon, Virginie; Bougard, Clément; Rabat, Arnaud; Millet, Guillaume Y; Chennaoui, Mounir

    2015-12-01

    To investigate the effects of 6 nights of sleep extension on sustained attention and sleep pressure before and during total sleep deprivation and after a subsequent recovery sleep. Subjects participated in two experimental conditions (randomized cross-over design): extended sleep (EXT, 9.8 ± 0.1 h (mean ± SE) time in bed) and habitual sleep (HAB, 8.2 ± 0.1 h time in bed). In each condition, subjects performed two consecutive phases: (1) 6 nights of either EXT or HAB (2) three days in-laboratory: baseline, total sleep deprivation and after 10 h of recovery sleep. Residential sleep extension and sleep performance laboratory (continuous polysomnographic recording). 14 healthy men (age range: 26-37 years). EXT vs. HAB sleep durations prior to total sleep deprivation. Total sleep time and duration of all sleep stages during the 6 nights were significantly higher in EXT than HAB. EXT improved psychomotor vigilance task performance (PVT, both fewer lapses and faster speed) and reduced sleep pressure as evidenced by longer multiple sleep latencies (MSLT) at baseline compared to HAB. EXT limited PVT lapses and the number of involuntary microsleeps during total sleep deprivation. Differences in PVT lapses and speed and MSLT at baseline were maintained after one night of recovery sleep. Six nights of extended sleep improve sustained attention and reduce sleep pressure. Sleep extension also protects against psychomotor vigilance task lapses and microsleep degradation during total sleep deprivation. These beneficial effects persist after one night of recovery sleep. © 2015 Associated Professional Sleep Societies, LLC.

  14. Stress-free automatic sleep deprivation using air puffs

    PubMed Central

    Gross, Brooks A.; Vanderheyden, William M.; Urpa, Lea M.; Davis, Devon E.; Fitzpatrick, Christopher J.; Prabhu, Kaustubh; Poe, Gina R.

    2015-01-01

    Background Sleep deprivation via gentle handling is time-consuming and personnel-intensive. New Method We present here an automated sleep deprivation system via air puffs. Implanted EMG and EEG electrodes were used to assess sleep/waking states in six male Sprague-Dawley rats. Blood samples were collected from an implanted intravenous catheter every 4 hours during the 12-hour light cycle on baseline, 8 hours of sleep deprivation via air puffs, and 8 hours of sleep deprivation by gentle handling days. Results The automated system was capable of scoring sleep and waking states as accurately as our offline version (~90% for sleep) and with sufficient speed to trigger a feedback response within an acceptable amount of time (1.76 s). Manual state scoring confirmed normal sleep on the baseline day and sleep deprivation on the two manipulation days (68% decrease in non-REM, 63% decrease in REM, and 74% increase in waking). No significant differences in levels of ACTH and corticosterone (stress hormones indicative of HPA axis activity) were found at any time point between baseline sleep and sleep deprivation via air puffs. Comparison with Existing Method There were no significant differences in ACTH or corticosterone concentrations between sleep deprivation by air puffs and gentle handling over the 8-hour period. Conclusions Our system accurately detects sleep and delivers air puffs to acutely deprive rats of sleep with sufficient temporal resolution during the critical 4-5 h post learning sleep-dependent memory consolidation period. The system is stress-free and a viable alternative to existing sleep deprivation techniques. PMID:26014662

  15. Stress-free automatic sleep deprivation using air puffs.

    PubMed

    Gross, Brooks A; Vanderheyden, William M; Urpa, Lea M; Davis, Devon E; Fitzpatrick, Christopher J; Prabhu, Kaustubh; Poe, Gina R

    2015-08-15

    Sleep deprivation via gentle handling is time-consuming and personnel-intensive. We present here an automated sleep deprivation system via air puffs. Implanted EMG and EEG electrodes were used to assess sleep/waking states in six male Sprague-Dawley rats. Blood samples were collected from an implanted intravenous catheter every 4h during the 12-h light cycle on baseline, 8h of sleep deprivation via air puffs, and 8h of sleep deprivation by gentle handling days. The automated system was capable of scoring sleep and waking states as accurately as our offline version (∼90% for sleep) and with sufficient speed to trigger a feedback response within an acceptable amount of time (1.76s). Manual state scoring confirmed normal sleep on the baseline day and sleep deprivation on the two manipulation days (68% decrease in non-REM, 63% decrease in REM, and 74% increase in waking). No significant differences in levels of ACTH and corticosterone (stress hormones indicative of HPA axis activity) were found at any time point between baseline sleep and sleep deprivation via air puffs. There were no significant differences in ACTH or corticosterone concentrations between sleep deprivation by air puffs and gentle handling over the 8-h period. Our system accurately detects sleep and delivers air puffs to acutely deprive rats of sleep with sufficient temporal resolution during the critical 4-5h post learning sleep-dependent memory consolidation period. The system is stress-free and a viable alternative to existing sleep deprivation techniques. Copyright © 2015 Elsevier B.V. All rights reserved.

  16. Sleep deprived and sweating it out: the effects of total sleep deprivation on skin conductance reactivity to psychosocial stress.

    PubMed

    Liu, Jean C J; Verhulst, Silvan; Massar, Stijn A A; Chee, Michael W L

    2015-01-01

    We examined how sleep deprivation alters physiological responses to psychosocial stress by evaluating changes in skin conductance. Between-subjects design with one group allocated to 24 h of total sleep deprivation and the other to rested wakefulness. The study took place in a research laboratory. Participants were 40 healthy young adults recruited from a university. Sleep deprivation and feedback. Electrodermal activity was monitored while participants completed a difficult perceptual task with false feedback. All participants showed increased skin conductance levels following stress. However, compared to well-rested participants, sleep deprived participants showed higher skin conductance reactivity with increasing stress levels. Our results suggest that sleep deprivation augments allostatic responses to increasing psychosocial stress. Consequentially, we propose sleep loss as a risk factor that can influence the pathogenic effects of stress. © 2014 Associated Professional Sleep Societies, LLC.

  17. Effects of sleep deprivation on cognition.

    PubMed

    Killgore, William D S

    2010-01-01

    Sleep deprivation is commonplace in modern society, but its far-reaching effects on cognitive performance are only beginning to be understood from a scientific perspective. While there is broad consensus that insufficient sleep leads to a general slowing of response speed and increased variability in performance, particularly for simple measures of alertness, attention and vigilance, there is much less agreement about the effects of sleep deprivation on many higher level cognitive capacities, including perception, memory and executive functions. Central to this debate has been the question of whether sleep deprivation affects nearly all cognitive capacities in a global manner through degraded alertness and attention, or whether sleep loss specifically impairs some aspects of cognition more than others. Neuroimaging evidence has implicated the prefrontal cortex as a brain region that may be particularly susceptible to the effects of sleep loss, but perplexingly, executive function tasks that putatively measure prefrontal functioning have yielded inconsistent findings within the context of sleep deprivation. Whereas many convergent and rule-based reasoning, decision making and planning tasks are relatively unaffected by sleep loss, more creative, divergent and innovative aspects of cognition do appear to be degraded by lack of sleep. Emerging evidence suggests that some aspects of higher level cognitive capacities remain degraded by sleep deprivation despite restoration of alertness and vigilance with stimulant countermeasures, suggesting that sleep loss may affect specific cognitive systems above and beyond the effects produced by global cognitive declines or impaired attentional processes. Finally, the role of emotion as a critical facet of cognition has received increasing attention in recent years and mounting evidence suggests that sleep deprivation may particularly affect cognitive systems that rely on emotional data. Thus, the extent to which sleep deprivation

  18. The Impact of Sleep Deprivation on the Brain

    PubMed

    Trošt Bobić, Tatjana; Šečić, Ana; Zavoreo, Iris; Matijević, Valentina; Filipović, Branimir; Kolak, Željka; Bašić Kes, Vanja; Ciliga, Dubravka; Sajković, Dubravka

    2016-09-01

    Each sleep phase is characterized by specific chemical, cellular and anatomic events of vital importance for normal neural functioning. Different forms of sleep deprivation may lead to a decline of cognitive functions in individuals. Studies in this field make a distinction between total sleep deprivation, chronic sleep restriction, and the situation of sleep disruption. Investigations covering the acute effects of sleep deprivation on the brain show that the discovered behavioral deficits in most cases regenerate after two nights of complete sleep. However, some studies done on mice emphasize the possible chronic effects of long-term sleep deprivation or chronic restriction on the occurrence of neurodegenerative diseases such as Alzheimer’s disease and dementia. In order to better understand the acute and chronic effects of sleep loss, the mechanisms of neural adaptation in the situations of insufficient sleep need to be further investigated. Future integrative research on the impact of sleep deprivation on neural functioning measured through the macro level of cognitive functions and the micro molecular and cell level could contribute to more accurate conclusions about the basic cellular mechanisms responsible for the detected behavioral deficits occurring due to sleep deprivation.

  19. REM Sleep Phase Preference in the Crepuscular Octodon degus Assessed by Selective REM Sleep Deprivation

    PubMed Central

    Ocampo-Garcés, Adrián; Hernández, Felipe; Palacios, Adrian G.

    2013-01-01

    Study Objectives: To determine rapid eye movement (REM) sleep phase preference in a crepuscular mammal (Octodon degus) by challenging the specific REM sleep homeostatic response during the diurnal and nocturnal anticrepuscular rest phases. Design: We have investigated REM sleep rebound, recovery, and documented REM sleep propensity measures during and after diurnal and nocturnal selective REM sleep deprivations. Subjects: Nine male wild-captured O. degus prepared for polysomnographic recordings Interventions: Animals were recorded during four consecutive baseline and two separate diurnal or nocturnal deprivation days, under a 12:12 light-dark schedule. Three-h selective REM sleep deprivations were performed, starting at midday (zeitgeber time 6) or midnight (zeitgeber time 18). Measurements and Results: Diurnal and nocturnal REM sleep deprivations provoked equivalent amounts of REM sleep debt, but a consistent REM sleep rebound was found only after nocturnal deprivation. The nocturnal rebound was characterized by a complete recovery of REM sleep associated with an augment in REM/total sleep time ratio and enhancement in REM sleep episode consolidation. Conclusions: Our results support the notion that the circadian system actively promotes REM sleep. We propose that the sleep-wake cycle of O. degus is modulated by a chorus of circadian oscillators with a bimodal crepuscular modulation of arousal and a unimodal promotion of nocturnal REM sleep. Citation: Ocampo-Garcés A; Hernández F; Palacios AG. REM sleep phase preference in the crepuscular Octodon degus assessed by selective REM sleep deprivation. SLEEP 2013;36(8):1247-1256. PMID:23904685

  20. Neurocognitive Consequences of Sleep Deprivation

    PubMed Central

    Goel, Namni; Rao, Hengyi; Durmer, Jeffrey S.; Dinges, David F.

    2012-01-01

    Sleep deprivation is associated with considerable social, financial, and health-related costs, in large measure because it produces impaired cognitive performance due to increasing sleep propensity and instability of waking neurobehavioral functions. Cognitive functions particularly affected by sleep loss include psychomotor and cognitive speed, vigilant and executive attention, working memory, and higher cognitive abilities. Chronic sleep-restriction experiments—which model the kind of sleep loss experienced by many individuals with sleep fragmentation and premature sleep curtailment due to disorders and lifestyle—demonstrate that cognitive deficits accumulate to severe levels over time without full awareness by the affected individual. Functional neuroimaging has revealed that frequent and progressively longer cognitive lapses, which are a hallmark of sleep deprivation, involve distributed changes in brain regions including frontal and parietal control areas, secondary sensory processing areas, and thalamic areas. There are robust differences among individuals in the degree of their cognitive vulnerability to sleep loss that may involve differences in prefrontal and parietal cortices, and that may have a basis in genes regulating sleep homeostasis and circadian rhythms. Thus, cognitive deficits believed to be a function of the severity of clinical sleep disturbance may be a product of genetic alleles associated with differential cognitive vulnerability to sleep loss. PMID:19742409

  1. Cellular consequences of sleep deprivation in the brain.

    PubMed

    Cirelli, Chiara

    2006-10-01

    Several recent studies have used transcriptomics approaches to characterize the molecular correlates of sleep, waking, and sleep deprivation. This analysis may help in understanding the benefits that sleep brings to the brain at the cellular level. The studies are still limited in number and focus on a few brain regions, but some consistent findings are emerging. Sleep, spontaneous wakefulness, short-term, and long-term sleep deprivation are each associated with the upregulation of hundreds of genes in the cerebral cortex and other brain areas. In fruit flies as well as in mammals, three categories of genes are consistently upregulated during waking and short-term sleep deprivation relative to sleep. They include genes involved in energy metabolism, synaptic potentiation, and the response to cellular stress. In the rat cerebral cortex, transcriptional changes associated with prolonged sleep loss differ significantly from those observed during short-term sleep deprivation. However, it is too early to draw firm conclusions relative to the molecular consequences of sleep deprivation, and more extensive studies using DNA and protein arrays are needed in different species and in different brain regions.

  2. The role of sleep and sleep deprivation in consolidating fear memories.

    PubMed

    Menz, M M; Rihm, J S; Salari, N; Born, J; Kalisch, R; Pape, H C; Marshall, L; Büchel, C

    2013-07-15

    Sleep, in particular REM sleep, has been shown to improve the consolidation of emotional memories. Here, we investigated the role of sleep and sleep deprivation on the consolidation of fear memories and underlying neuronal mechanisms. We employed a Pavlovian fear conditioning paradigm either followed by a night of polysomnographically monitored sleep, or wakefulness in forty healthy participants. Recall of learned fear was better after sleep, as indicated by stronger explicitly perceived anxiety and autonomous nervous responses. These effects were positively correlated with the preceding time spent in REM sleep and paralleled by activation of the basolateral amygdala. These findings suggest REM sleep-associated consolidation of fear memory in the human amygdala. In view of the critical participation of fear learning mechanisms in the etiology of anxiety and post-traumatic stress disorder, deprivation of REM sleep after exposure to distressing events is an interesting target for further investigation. Copyright © 2013 Elsevier Inc. All rights reserved.

  3. Polysomnographic diagnosis of sleepwalking: effects of sleep deprivation.

    PubMed

    Zadra, Antonio; Pilon, Mathieu; Montplaisir, Jacques

    2008-04-01

    Somnambulism affects up to 4% of adults and constitutes one of the leading causes of sleep-related violence and self-injury. Diagnosing somnambulism with objective instruments is often difficult because episodes rarely occur in the laboratory. Because sleep deprivation can precipitate sleepwalking, we aimed to determine the effects of 25 hours of sleep deprivation on the frequency and complexity of somnambulistic episodes recorded in the laboratory. Thirty consecutive sleepwalkers were evaluated prospectively by video-polysomnography for one baseline night and during recovery sleep after 25 hours of sleep deprivation. Ten sleepwalkers with a concomitant sleep disturbance were investigated with the same protocol. Sleepwalkers experienced a significant increase in the mean frequency of somnambulistic episodes during postdeprivation recovery sleep. Postsleep deprivation also resulted in a significantly greater proportion of patients experiencing more complex forms of somnambulism. Sleep deprivation was similarly effective in 9 of the 10 patients presenting with a comorbid sleep disturbance. Combining data from all 40 patients shows that whereas 32 episodes were recorded from 20 sleepwalkers (50%) at baseline, recovery sleep resulted in 92 episodes being recorded from 36 patients (90%). The findings support the view that sleepwalkers suffer from a dysfunction of the mechanisms responsible for sustaining stable slow-wave sleep and suggest that these patients are particularly vulnerable to increased homeostatic sleep pressure. Strong evidence is provided that 25 hours of sleep deprivation can be a valuable tool that facilitates the polysomnographically based diagnosis of somnambulism in predisposed patients.

  4. Beauty sleep: experimental study on the perceived health and attractiveness of sleep deprived people.

    PubMed

    Axelsson, John; Sundelin, Tina; Ingre, Michael; Van Someren, Eus J W; Olsson, Andreas; Lekander, Mats

    2010-12-14

    To investigate whether sleep deprived people are perceived as less healthy, less attractive, and more tired than after a normal night's sleep. Experimental study. Sleep laboratory in Stockholm, Sweden. 23 healthy, sleep deprived adults (age 18-31) who were photographed and 65 untrained observers (age 18-61) who rated the photographs. Participants were photographed after a normal night's sleep (eight hours) and after sleep deprivation (31 hours of wakefulness after a night of reduced sleep). The photographs were presented in a randomised order and rated by untrained observers. Difference in observer ratings of perceived health, attractiveness, and tiredness between sleep deprived and well rested participants using a visual analogue scale (100 mm). Sleep deprived people were rated as less healthy (visual analogue scale scores, mean 63 (SE 2) v 68 (SE 2), P<0.001), more tired (53 (SE 3) v 44 (SE 3), P<0.001), and less attractive (38 (SE 2) v 40 (SE 2), P<0.001) than after a normal night's sleep. The decrease in rated health was associated with ratings of increased tiredness and decreased attractiveness. Our findings show that sleep deprived people appear less healthy, less attractive, and more tired compared with when they are well rested. This suggests that humans are sensitive to sleep related facial cues, with potential implications for social and clinical judgments and behaviour. Studies are warranted for understanding how these effects may affect clinical decision making and can add knowledge with direct implications in a medical context.

  5. Diurnal rhythms in the human urine metabolome during sleep and total sleep deprivation.

    PubMed

    Giskeødegård, Guro F; Davies, Sarah K; Revell, Victoria L; Keun, Hector; Skene, Debra J

    2015-10-09

    Understanding how metabolite levels change over the 24 hour day is of crucial importance for clinical and epidemiological studies. Additionally, the association between sleep deprivation and metabolic disorders such as diabetes and obesity requires investigation into the links between sleep and metabolism. Here, we characterise time-of-day variation and the effects of sleep deprivation on urinary metabolite profiles. Healthy male participants (n = 15) completed an in-laboratory study comprising one 24 h sleep/wake cycle prior to 24 h of continual wakefulness under highly controlled environmental conditions. Urine samples were collected over set 2-8 h intervals and analysed by (1)H NMR spectroscopy. Significant changes were observed with respect to both time of day and sleep deprivation. Of 32 identified metabolites, 7 (22%) exhibited cosine rhythmicity over at least one 24 h period; 5 exhibiting a cosine rhythm on both days. Eight metabolites significantly increased during sleep deprivation compared with sleep (taurine, formate, citrate, 3-indoxyl sulfate, carnitine, 3-hydroxyisobutyrate, TMAO and acetate) and 8 significantly decreased (dimethylamine, 4-DTA, creatinine, ascorbate, 2-hydroxyisobutyrate, allantoin, 4-DEA, 4-hydroxyphenylacetate). These data indicate that sampling time, the presence or absence of sleep and the response to sleep deprivation are highly relevant when identifying biomarkers in urinary metabolic profiling studies.

  6. Occurrence of epileptiform discharges and sleep during EEG recordings in children after melatonin intake versus sleep-deprivation.

    PubMed

    Gustafsson, Greta; Broström, Anders; Ulander, Martin; Vrethem, Magnus; Svanborg, Eva

    2015-08-01

    To determine if melatonin is equally efficient as partial sleep deprivation in inducing sleep without interfering with epileptiform discharges in EEG recordings in children 1-16 years old. We retrospectively analysed 129 EEGs recorded after melatonin intake and 113 EEGs recorded after partial sleep deprivation. Comparisons were made concerning occurrence of epileptiform discharges, the number of children who fell asleep and the technical quality of EEG recordings. Comparison between different age groups was also made. No significant differences were found regarding occurrence of epileptiform discharges (33% after melatonin intake, 36% after sleep deprivation), or proportion of unsuccessful EEGs (8% and 10%, respectively). Melatonin and sleep deprivation were equally efficient in inducing sleep (70% in both groups). Significantly more children aged 1-4 years obtained sleep after melatonin intake in comparison to sleep deprivation (82% vs. 58%, p⩽0.01), and in comparison to older children with melatonin induced sleep (58-67%, p⩽0.05). Sleep deprived children 9-12 years old had higher percentage of epileptiform discharges (62%, p⩽0.05) compared to younger sleep deprived children. Melatonin is equally efficient as partial sleep deprivation to induce sleep and does not affect the occurrence of epileptiform discharges in the EEG recording. Sleep deprivation could still be preferable in older children as melatonin probably has less sleep inducing effect. Melatonin induced sleep have advantages, especially in younger children as they fall asleep easier than after sleep deprivation. The procedure is easier for the parents than keeping a young child awake for half the night. Copyright © 2014 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

  7. Sleep Deprivation Disrupts Recall of Conditioned Fear Extinction.

    PubMed

    Straus, Laura D; Acheson, Dean T; Risbrough, Victoria B; Drummond, Sean P A

    2017-03-01

    Learned fear is crucial in the development and maintenance of posttraumatic stress disorder (PTSD) and other anxiety disorders, and extinction of learned fear is necessary for response to exposure-based treatments. In humans, research suggests disrupted sleep impairs consolidation of extinction, though no studies have examined this experimentally using total sleep deprivation. Seventy-one healthy controls underwent a paradigm to acquire conditioned fear to a visual cue. Twenty-four hours after fear conditioning, participants underwent extinction learning. Twenty-four hours after extinction learning, participants underwent extinction recall. Participants were randomized to three groups: 1) well-rested throughout testing ("normal sleep"; n = 21); 2) 36 hours total sleep deprivation before extinction learning ("pre-extinction deprivation"; n = 25); or 3) 36 hours total sleep deprivation after extinction learning and before extinction recall ("post-extinction deprivation"; n = 25). The groups were compared on blink EMG reactivity to the condition stimulus during extinction learning and recall. There were no differences among the three groups during extinction learning. During extinction recall, the pre-extinction deprivation group demonstrated significantly less extinction recall than the normal sleep group. There was no significant difference between the normal sleep and post-extinction deprivation group during extinction recall. Results indicated sleep deprivation prior to extinction training significantly disrupts extinction recall. These findings suggest that (1) sleep deprivation in the immediate aftermath of trauma could be a potential contributor to PTSD development and maintenance via interference with natural extinction processes and (2) management of sleep symptoms should be considered during extinction-based therapy.

  8. Sleep deprivation affects reactivity to positive but not negative stimuli.

    PubMed

    Pilcher, June J; Callan, Christina; Posey, J Laura

    2015-12-01

    The current study examined the effects of partial and total sleep deprivation on emotional reactivity. Twenty-eight partially sleep-deprived participants and 31 totally sleep-deprived participants rated their valence and arousal responses to positive and negative pictures across four testing sessions during the day following partial sleep deprivation or during the night under total sleep deprivation. The results suggest that valence and arousal ratings decreased under both sleep deprivation conditions. In addition, partial and total sleep deprivation had a greater negative effect on positive events than negative events. These results suggest that sleep-deprived persons are more likely to respond less to positive events than negative events. One explanation for the current findings is that negative events could elicit more attentive behavior and thus stable responding under sleep deprivation conditions. As such, sleep deprivation could impact reactivity to emotional stimuli through automated attentional and self-regulatory processes. Copyright © 2015 Elsevier Inc. All rights reserved.

  9. A new model to study sleep deprivation-induced seizure.

    PubMed

    Lucey, Brendan P; Leahy, Averi; Rosas, Regine; Shaw, Paul J

    2015-05-01

    A relationship between sleep and seizures is well-described in both humans and rodent animal models; however, the mechanism underlying this relationship is unknown. Using Drosophila melanogaster mutants with seizure phenotypes, we demonstrate that seizure activity can be modified by sleep deprivation. Seizure activity was evaluated in an adult bang-sensitive seizure mutant, stress sensitive B (sesB(9ed4)), and in an adult temperature sensitive seizure mutant seizure (sei(ts1)) under baseline and following 12 h of sleep deprivation. The long-term effect of sleep deprivation on young, immature sesB(9ed4) flies was also assessed. Laboratory. Drosophila melanogaster. Sleep deprivation. Sleep deprivation increased seizure susceptibility in adult sesB(9ed4)/+ and sei(ts1) mutant flies. Sleep deprivation also increased seizure susceptibility when sesB was disrupted using RNAi. The effect of sleep deprivation on seizure activity was reduced when sesB(9ed4)/+ flies were given the anti-seizure drug, valproic acid. In contrast to adult flies, sleep deprivation during early fly development resulted in chronic seizure susceptibility when sesB(9ed4)/+ became adults. These findings show that Drosophila is a model organism for investigating the relationship between sleep and seizure activity. © 2015 Associated Professional Sleep Societies, LLC.

  10. A New Model to Study Sleep Deprivation-Induced Seizure

    PubMed Central

    Lucey, Brendan P.; Leahy, Averi; Rosas, Regine; Shaw, Paul J.

    2015-01-01

    Background and Study Objectives: A relationship between sleep and seizures is well-described in both humans and rodent animal models; however, the mechanism underlying this relationship is unknown. Using Drosophila melanogaster mutants with seizure phenotypes, we demonstrate that seizure activity can be modified by sleep deprivation. Design: Seizure activity was evaluated in an adult bang-sensitive seizure mutant, stress sensitive B (sesB9ed4), and in an adult temperature sensitive seizure mutant seizure (seits1) under baseline and following 12 h of sleep deprivation. The long-term effect of sleep deprivation on young, immature sesB9ed4 flies was also assessed. Setting: Laboratory. Participants: Drosophila melanogaster. Interventions: Sleep deprivation. Measurements and Results: Sleep deprivation increased seizure susceptibility in adult sesB9ed4/+ and seits1 mutant flies. Sleep deprivation also increased seizure susceptibility when sesB was disrupted using RNAi. The effect of sleep deprivation on seizure activity was reduced when sesB9ed4/+ flies were given the anti-seizure drug, valproic acid. In contrast to adult flies, sleep deprivation during early fly development resulted in chronic seizure susceptibility when sesB9ed4/+ became adults. Conclusions: These findings show that Drosophila is a model organism for investigating the relationship between sleep and seizure activity. Citation: Lucey BP, Leahy A, Rosas R, Shaw PJ. A new model to study sleep deprivation-induced seizure. SLEEP 2015;38(5):777–785. PMID:25515102

  11. Sleep Deprivation and Time-Based Prospective Memory.

    PubMed

    Esposito, Maria José; Occhionero, Miranda; Cicogna, PierCarla

    2015-11-01

    To evaluate the effect of sleep deprivation on time-based prospective memory performance, that is, realizing delayed intentions at an appropriate time in the future (e.g., to take a medicine in 30 minutes). Between-subjects experimental design. The experimental group underwent 24 h of total sleep deprivation, and the control group had a regular sleep-wake cycle. Participants were tested at 08:00. Laboratory. Fifty healthy young adults (mean age 22 ± 2.1, 31 female). 24 h of total sleep deprivation. Participants were monitored by wrist actigraphy for 3 days before the experimental session. The following cognitive tasks were administered: one time-based prospective memory task and 3 reasoning tasks as ongoing activity. Objective and subjective vigilance was assessed by the psychomotor vigilance task and a visual analog scale, respectively. To measure the time-based prospective memory task we assessed compliance and clock checking behavior (time monitoring). Sleep deprivation negatively affected time-based prospective memory compliance (P < 0.001), objective vigilance (mean RT: P < 0.001; slowest 10% RT: P < 0.001; lapses: P < 0.005), and subjective vigilance (P < 0.0001). Performance on reasoning tasks and time monitoring behavior did not differ between groups. The results highlight the potential dangerous effects of total sleep deprivation on human behavior, particularly the ability to perform an intended action after a few minutes. Sleep deprivation strongly compromises time-based prospective memory compliance but does not affect time check frequency. Sleep deprivation may impair the mechanism that allows the integration of information related to time monitoring with the prospective intention. © 2015 Associated Professional Sleep Societies, LLC.

  12. Slow wave and REM sleep deprivation effects on explicit and implicit memory during sleep.

    PubMed

    Casey, Sarah J; Solomons, Luke C; Steier, Joerg; Kabra, Neeraj; Burnside, Anna; Pengo, Martino F; Moxham, John; Goldstein, Laura H; Kopelman, Michael D

    2016-11-01

    It has been debated whether different stages in the human sleep cycle preferentially mediate the consolidation of explicit and implicit memories, or whether all of the stages in succession are necessary for optimal consolidation. Here we investigated whether the selective deprivation of slow wave sleep (SWS) or rapid eye movement (REM) sleep over an entire night would have a specific effect on consolidation in explicit and implicit memory tasks. Participants completed a set of explicit and implicit memory tasks at night, prior to sleep. They had 1 control night of undisturbed sleep and 2 experimental nights, during which either SWS or REM sleep was selectively deprived across the entire night (sleep conditions counterbalanced across participants). Polysomnography recordings quantified precisely the amount of SWS and REM sleep that occurred during each of the sleep conditions, and spindle counts were recorded. In the morning, participants completed the experimental tasks in the same sequence as the night before. SWS deprivation disrupted the consolidation of explicit memories for visuospatial information (ηp2 = .23), and both SWS (ηp2 = .53) and REM sleep (ηp2 = .52) deprivation adversely affected explicit verbal recall. Neither SWS nor REM sleep deprivation affected aspects of short-term or working memory, and did not affect measures of verbal implicit memory. Spindle counts did not correlate significantly with memory performance. These findings demonstrate the importance of measuring the sleep cycles throughout the entire night, and the contribution of both SWS and REM sleep to memory consolidation. (PsycINFO Database Record (c) 2016 APA, all rights reserved).

  13. Impact of partial sleep deprivation on immune markers.

    PubMed

    Wilder-Smith, A; Mustafa, F B; Earnest, A; Gen, L; Macary, P A

    2013-10-01

    Sleep quality is considered to be an important predictor of immunity. Lack of sleep therefore may reduce immunity, thereby increasing the susceptibility to respiratory pathogens. A previous study showed that reduced sleep duration was associated with an increased likelihood of the common cold. It is important to understand the role of sleep in altering immune responses to understand how sleep deprivation leads to an increased susceptibility to the common cold or other respiratory infections. We sought to examine the impact of partial sleep deprivation on various immune markers. Fifty-two healthy volunteers were partially sleep deprived for one night. We took blood samples before the sleep deprivation, immediately after, and 4 and 7 days after sleep deprivation. We measured various immune markers and used a generalized estimating equation (GEE) to examine the differences in the repeated measures. CD4, CD8, CD14, and CD16 all showed significant time-dependent changes, but CD3 did not. The most striking time-dependent change was observed for the mitogen proliferation assay and for HLA-DR. There was a significant decrease in the mitogen proliferation values and HLA-DR immediately after the sleep deprivation experiment, which started to rise again on day 4 and normalized by day 7. The transiently impaired mitogen proliferation, the decreased HLA-DR, the upregulated CD14, and the variations in CD4 and CD8 that we observed in temporal relationship with partial sleep deprivation could be one possible explanation for the increased susceptibility to respiratory infections reported after reduced sleep duration. Copyright © 2013 Elsevier B.V. All rights reserved.

  14. Augmented Reality as a Countermeasure for Sleep Deprivation.

    PubMed

    Baumeister, James; Dorrlan, Jillian; Banks, Siobhan; Chatburn, Alex; Smith, Ross T; Carskadon, Mary A; Lushington, Kurt; Thomas, Bruce H

    2016-04-01

    Sleep deprivation is known to have serious deleterious effects on executive functioning and job performance. Augmented reality has an ability to place pertinent information at the fore, guiding visual focus and reducing instructional complexity. This paper presents a study to explore how spatial augmented reality instructions impact procedural task performance on sleep deprived users. The user study was conducted to examine performance on a procedural task at six time points over the course of a night of total sleep deprivation. Tasks were provided either by spatial augmented reality-based projections or on an adjacent monitor. The results indicate that participant errors significantly increased with the monitor condition when sleep deprived. The augmented reality condition exhibited a positive influence with participant errors and completion time having no significant increase when sleep deprived. The results of our study show that spatial augmented reality is an effective sleep deprivation countermeasure under laboratory conditions.

  15. Sleep Deprivation and the Epigenome.

    PubMed

    Gaine, Marie E; Chatterjee, Snehajyoti; Abel, Ted

    2018-01-01

    Sleep deprivation disrupts the lives of millions of people every day and has a profound impact on the molecular biology of the brain. These effects begin as changes within a neuron, at the DNA and RNA level, and result in alterations in neuronal plasticity and dysregulation of many cognitive functions including learning and memory. The epigenome plays a critical role in regulating gene expression in the context of memory storage. In this review article, we begin by describing the effects of epigenetic alterations on the regulation of gene expression, focusing on the most common epigenetic mechanisms: (i) DNA methylation; (ii) histone modifications; and (iii) non-coding RNAs. We then discuss evidence suggesting that sleep loss impacts the epigenome and that these epigenetic alterations might mediate the changes in cognition seen following disruption of sleep. The link between sleep and the epigenome is only beginning to be elucidated, but clear evidence exists that epigenetic alterations occur following sleep deprivation. In the future, these changes to the epigenome could be utilized as biomarkers of sleep loss or as therapeutic targets for sleep-related disorders.

  16. Sleep deprivation increases formation of false memory.

    PubMed

    Lo, June C; Chong, Pearlynne L H; Ganesan, Shankari; Leong, Ruth L F; Chee, Michael W L

    2016-12-01

    Retrieving false information can have serious consequences. Sleep is important for memory, but voluntary sleep curtailment is becoming more rampant. Here, the misinformation paradigm was used to investigate false memory formation after 1 night of total sleep deprivation in healthy young adults (N = 58, mean age ± SD = 22.10 ± 1.60 years; 29 males), and 7 nights of partial sleep deprivation (5 h sleep opportunity) in these young adults and healthy adolescents (N = 54, mean age ± SD = 16.67 ± 1.03 years; 25 males). In both age groups, sleep-deprived individuals were more likely than well-rested persons to incorporate misleading post-event information into their responses during memory retrieval (P < 0.050). These findings reiterate the importance of adequate sleep in optimal cognitive functioning, reveal the vulnerability of adolescents' memory during sleep curtailment, and suggest the need to assess eyewitnesses' sleep history after encountering misleading information. © 2016 The Authors. Journal of Sleep Research published by John Wiley & Sons Ltd on behalf of European Sleep Research Society.

  17. Impact of Acute Sleep Deprivation on Sarcasm Detection.

    PubMed

    Deliens, Gaétane; Stercq, Fanny; Mary, Alison; Slama, Hichem; Cleeremans, Axel; Peigneux, Philippe; Kissine, Mikhail

    2015-01-01

    There is growing evidence that sleep plays a pivotal role on health, cognition and emotional regulation. However, the interplay between sleep and social cognition remains an uncharted research area. In particular, little is known about the impact of sleep deprivation on sarcasm detection, an ability which, once altered, may hamper everyday social interactions. The aim of this study is to determine whether sleep-deprived participants are as able as sleep-rested participants to adopt another perspective in gauging sarcastic statements. At 9am, after a whole night of sleep (n = 15) or a sleep deprivation night (n = 15), participants had to read the description of an event happening to a group of friends. An ambiguous voicemail message left by one of the friends on another's phone was then presented, and participants had to decide whether the recipient would perceive the message as sincere or as sarcastic. Messages were uttered with a neutral intonation and were either: (1) sarcastic from both the participant's and the addressee's perspectives (i.e. both had access to the relevant background knowledge to gauge the message as sarcastic), (2) sarcastic from the participant's but not from the addressee's perspective (i.e. the addressee lacked context knowledge to detect sarcasm) or (3) sincere. A fourth category consisted in messages sarcastic from both the participant's and from the addressee's perspective, uttered with a sarcastic tone. Although sleep-deprived participants were as accurate as sleep-rested participants in interpreting the voice message, they were also slower. Blunted reaction time was not fully explained by generalized cognitive slowing after sleep deprivation; rather, it could reflect a compensatory mechanism supporting normative accuracy level in sarcasm understanding. Introducing prosodic cues compensated for increased processing difficulties in sarcasm detection after sleep deprivation. Our findings support the hypothesis that sleep deprivation might

  18. Sleep Extension Improves Neurocognitive Functions in Chronically Sleep-Deprived Obese Individuals

    PubMed Central

    Lucassen, Eliane A.; Piaggi, Paolo; Dsurney, John; de Jonge, Lilian; Zhao, Xiong-ce; Mattingly, Megan S.; Ramer, Angela; Gershengorn, Janet; Csako, Gyorgy; Cizza, Giovanni

    2014-01-01

    Background Sleep deprivation and obesity, are associated with neurocognitive impairments. Effects of sleep deprivation and obesity on cognition are unknown, and the cognitive long-term effects of improvement of sleep have not been prospectively assessed in short sleeping, obese individuals. Objective To characterize neurocognitive functions and assess its reversibility. Design Prospective cohort study. Setting Tertiary Referral Research Clinical Center. Patients A cohort of 121 short-sleeping (<6.5 h/night) obese (BMI 30–55 kg/m2) men and pre-menopausal women. Intervention Sleep extension (468±88 days) with life-style modifications. Measurements Neurocognitive functions, sleep quality and sleep duration. Results At baseline, 44% of the individuals had an impaired global deficit score (t-score 0–39). Impaired global deficit score was associated with worse subjective sleep quality (p = 0.02), and lower urinary dopamine levels (p = 0.001). Memory was impaired in 33%; attention in 35%; motor skills in 42%; and executive function in 51% of individuals. At the final evaluation (N = 74), subjective sleep quality improved by 24% (p<0.001), self-reported sleep duration increased by 11% by questionnaires (p<0.001) and by 4% by diaries (p = 0.04), and daytime sleepiness tended to improve (p = 0.10). Global cognitive function and attention improved by 7% and 10%, respectively (both p = 0.001), and memory and executive functions tended to improve (p = 0.07 and p = 0.06). Serum cortisol increased by 17% (p = 0.02). In a multivariate mixed model, subjective sleep quality and sleep efficiency, urinary free cortisol and dopamine and plasma total ghrelin accounted for 1/5 of the variability in global cognitive function. Limitations Drop-out rate. Conclusions Chronically sleep-deprived obese individuals exhibit substantial neurocognitive deficits that are partially reversible upon improvement of sleep in a non-pharmacological way. These

  19. Effects of Sleep Deprivation on Brain Bioenergetics, Sleep, and Cognitive Performance in Cocaine-Dependent Individuals

    PubMed Central

    Trksak, George H.; Bracken, Bethany K.; Jensen, J. Eric; Plante, David T.; Penetar, David M.; Tartarini, Wendy L.; Maywalt, Melissa A.; Dorsey, Cynthia M.; Renshaw, Perry F.; Lukas, Scott E.

    2013-01-01

    In cocaine-dependent individuals, sleep is disturbed during cocaine use and abstinence, highlighting the importance of examining the behavioral and homeostatic response to acute sleep loss in these individuals. The current study was designed to identify a differential effect of sleep deprivation on brain bioenergetics, cognitive performance, and sleep between cocaine-dependent and healthy control participants. 14 healthy control and 8 cocaine-dependent participants experienced consecutive nights of baseline, total sleep deprivation, and recovery sleep in the research laboratory. Participants underwent [31]P magnetic resonance spectroscopy (MRS) brain imaging, polysomnography, Continuous Performance Task, and Digit Symbol Substitution Task. Following recovery sleep, [31]P MRS scans revealed that cocaine-dependent participants exhibited elevated global brain β-NTP (direct measure of adenosine triphosphate), α-NTP, and total NTP levels compared to those of healthy controls. Cocaine-dependent participants performed worse on the Continuous Performance Task and Digit Symbol Substitution Task at baseline compared to healthy control participants, but sleep deprivation did not worsen cognitive performance in either group. Enhancements of brain ATP levels in cocaine dependent participants following recovery sleep may reflect a greater impact of sleep deprivation on sleep homeostasis, which may highlight the importance of monitoring sleep during abstinence and the potential influence of sleep loss in drug relapse. PMID:24250276

  20. Cues of Fatigue: Effects of Sleep Deprivation on Facial Appearance

    PubMed Central

    Sundelin, Tina; Lekander, Mats; Kecklund, Göran; Van Someren, Eus J. W.; Olsson, Andreas; Axelsson, John

    2013-01-01

    Study Objective: To investigate the facial cues by which one recognizes that someone is sleep deprived versus not sleep deprived. Design: Experimental laboratory study. Setting: Karolinska Institutet, Stockholm, Sweden. Participants: Forty observers (20 women, mean age 25 ± 5 y) rated 20 facial photographs with respect to fatigue, 10 facial cues, and sadness. The stimulus material consisted of 10 individuals (five women) photographed at 14:30 after normal sleep and after 31 h of sleep deprivation following a night with 5 h of sleep. Measurements: Ratings of fatigue, fatigue-related cues, and sadness in facial photographs. Results: The faces of sleep deprived individuals were perceived as having more hanging eyelids, redder eyes, more swollen eyes, darker circles under the eyes, paler skin, more wrinkles/fine lines, and more droopy corners of the mouth (effects ranging from b = +3 ± 1 to b = +15 ± 1 mm on 100-mm visual analog scales, P < 0.01). The ratings of fatigue were related to glazed eyes and to all the cues affected by sleep deprivation (P < 0.01). Ratings of rash/eczema or tense lips were not significantly affected by sleep deprivation, nor associated with judgements of fatigue. In addition, sleep-deprived individuals looked sadder than after normal sleep, and sadness was related to looking fatigued (P < 0.01). Conclusions: The results show that sleep deprivation affects features relating to the eyes, mouth, and skin, and that these features function as cues of sleep loss to other people. Because these facial regions are important in the communication between humans, facial cues of sleep deprivation and fatigue may carry social consequences for the sleep deprived individual in everyday life. Citation: Sundelin T; Lekander M; Kecklund G; Van Someren EJW; Olsson A; Axelsson J. Cues of fatigue: effects of sleep deprivation on facial appearance. SLEEP 2013;36(9):1355-1360. PMID:23997369

  1. Sleep Deprivation in Pigeons and Rats Using Motion Detection

    PubMed Central

    Newman, Sarah M.; Paletz, Elliott M.; Obermeyer, William H.; Benca, Ruth M.

    2009-01-01

    Study Objectives: Forced sleep deprivation results in substantial behavioral and physiologic effects in mammals. The disk-over-water (DOW) method produces a syndrome characterized by increased energy expenditure and a robust preferentially rapid-eye-movement sleep rebound upon recovery or eventual death after several weeks of sleep deprivation. The DOW has been used successfully only in rats. This paper presents a method to enforce long-term controlled sleep deprivation across species and to compare its effects in rats and pigeons. Design and Intervention: A conveyor was substituted for the DOW disk. Behavior rather than electroencephalography was used to trigger arousal stimuli, as in gentle-handling deprivation. Rats and pigeons were deprived using this apparatus, and the were compared with each other and with published reports. Measurements and Results: The physiologic consequences and recovery sleep in rats were like those published for DOW rats. Magnitude of sleep loss and recovery patterns in pigeons were similar to those seen in rats, but expected symptoms of the sleep deprivation syndrome were absent in pigeons. The use of a motion trigger allowed us to measure and, thus, to assess the quality and impact of the procedure. Conclusion: Prolonged and controlled sleep deprivation can be enforced using automated motion detection and a conveyor-over-water system. Pigeons and rats, deprived of sleep to the same extent, showed similar patterns of recovery sleep, but pigeons did not exhibit the hyperphagia, weight loss, and debilitation seen in rats. Citation: Newman SM; Paletz EM; Obermeyer WH; Benca RM. Sleep Deprivation In Pigeons And Rats Using Motion Detection. SLEEP 2009;32(10):1299-1312. PMID:19848359

  2. Acute Sleep Deprivation Enhances Post-Infection Sleep and Promotes Survival during Bacterial Infection in Drosophila

    PubMed Central

    Kuo, Tzu-Hsing; Williams, Julie A.

    2014-01-01

    Study Objectives: Sleep is known to increase as an acute response to infection. However, the function of this behavioral response in host defense is not well understood. To address this problem, we evaluated the effect of acute sleep deprivation on post-infection sleep and immune function in Drosophila. Setting: Laboratory. Participants: Drosophila melanogaster. Methods and Results: Flies were subjected to sleep deprivation before (early DEP) or after (late DEP) bacterial infection. Relative to a non-deprived control, flies subjected to early DEP had enhanced sleep after infection as well as increased bacterial clearance and survival outcome. Flies subjected to late DEP experienced enhanced sleep following the deprivation period, and showed a modest improvement in survival outcome. Continuous DEP (early and late DEP) throughout infection also enhanced sleep later during infection and improved survival. However, improved survival in flies subjected to late or continuous DEP did not occur until after flies had experienced sleep. During infection, both early and late DEP enhanced NFκB transcriptional activity as measured by a luciferase reporter (κB-luc) in living flies. Early DEP also increased NFκB activity prior to infection. Flies that were deficient in expression of either the Relish or Dif NFκB transcription factors showed normal responses to early DEP. However, the effect of early DEP on post-infection sleep and survival was abolished in double mutants, which indicates that Relish and Dif have redundant roles in this process. Conclusions: Acute sleep deprivation elevated NFκB-dependent activity, increased post-infection sleep, and improved survival during bacterial infection. Citation: Kuo TH, Williams JA. Acute sleep deprivation enhances post-infection sleep and promotes survival during bacterial infection in Drosophila. SLEEP 2014;37(5):859-869. PMID:24790264

  3. Meta-Analysis of the Antidepressant Effects of Acute Sleep Deprivation.

    PubMed

    Boland, Elaine M; Rao, Hengyi; Dinges, David F; Smith, Rachel V; Goel, Namni; Detre, John A; Basner, Mathias; Sheline, Yvette I; Thase, Michael E; Gehrman, Philip R

    To provide a quantitative meta-analysis of the antidepressant effects of sleep deprivation to complement qualitative reviews addressing response rates. English-language studies from 1974 to 2016 using the keywords sleep deprivation and depression searched through PubMed and PsycINFO databases. A total of 66 independent studies met criteria for inclusion: conducted experimental sleep deprivation, reported the percentage of the sample that responded to sleep deprivation, provided a priori definition of antidepressant response, and did not seamlessly combine sleep deprivation with other therapies (eg, chronotherapeutics, repetitive transcranial magnetic stimulation). Data extracted included percentage of responders, type of sample (eg, bipolar, unipolar), type of sleep deprivation (eg, total, partial), demographics, medication use, type of outcome measure used, and definition of response (eg, 30% reduction in depression ratings). Data were analyzed with meta-analysis of proportions and a Poisson mixed-effects regression model. The overall response rate to sleep deprivation was 45% among studies that utilized a randomized control group and 50% among studies that did not. The response to sleep deprivation was not affected significantly by the type of sleep deprivation performed, the nature of the clinical sample, medication status, the definition of response used, or age and gender of the sample. These findings support a significant effect of sleep deprivation and suggest the need for future studies on the phenotypic nature of the antidepressant response to sleep deprivation, on the neurobiological mechanisms of action, and on moderators of the sleep deprivation treatment response in depression. © Copyright 2017 Physicians Postgraduate Press, Inc.

  4. Unsupervised Online Classifier in Sleep Scoring for Sleep Deprivation Studies

    PubMed Central

    Libourel, Paul-Antoine; Corneyllie, Alexandra; Luppi, Pierre-Hervé; Chouvet, Guy; Gervasoni, Damien

    2015-01-01

    Study Objective: This study was designed to evaluate an unsupervised adaptive algorithm for real-time detection of sleep and wake states in rodents. Design: We designed a Bayesian classifier that automatically extracts electroencephalogram (EEG) and electromyogram (EMG) features and categorizes non-overlapping 5-s epochs into one of the three major sleep and wake states without any human supervision. This sleep-scoring algorithm is coupled online with a new device to perform selective paradoxical sleep deprivation (PSD). Settings: Controlled laboratory settings for chronic polygraphic sleep recordings and selective PSD. Participants: Ten adult Sprague-Dawley rats instrumented for chronic polysomnographic recordings Measurements: The performance of the algorithm is evaluated by comparison with the score obtained by a human expert reader. Online detection of PS is then validated with a PSD protocol with duration of 72 hours. Results: Our algorithm gave a high concordance with human scoring with an average κ coefficient > 70%. Notably, the specificity to detect PS reached 92%. Selective PSD using real-time detection of PS strongly reduced PS amounts, leaving only brief PS bouts necessary for the detection of PS in EEG and EMG signals (4.7 ± 0.7% over 72 h, versus 8.9 ± 0.5% in baseline), and was followed by a significant PS rebound (23.3 ± 3.3% over 150 minutes). Conclusions: Our fully unsupervised data-driven algorithm overcomes some limitations of the other automated methods such as the selection of representative descriptors or threshold settings. When used online and coupled with our sleep deprivation device, it represents a better option for selective PSD than other methods like the tedious gentle handling or the platform method. Citation: Libourel PA, Corneyllie A, Luppi PH, Chouvet G, Gervasoni D. Unsupervised online classifier in sleep scoring for sleep deprivation studies. SLEEP 2015;38(5):815–828. PMID:25325478

  5. Cues of fatigue: effects of sleep deprivation on facial appearance.

    PubMed

    Sundelin, Tina; Lekander, Mats; Kecklund, Göran; Van Someren, Eus J W; Olsson, Andreas; Axelsson, John

    2013-09-01

    To investigate the facial cues by which one recognizes that someone is sleep deprived versus not sleep deprived. Experimental laboratory study. Karolinska Institutet, Stockholm, Sweden. Forty observers (20 women, mean age 25 ± 5 y) rated 20 facial photographs with respect to fatigue, 10 facial cues, and sadness. The stimulus material consisted of 10 individuals (five women) photographed at 14:30 after normal sleep and after 31 h of sleep deprivation following a night with 5 h of sleep. Ratings of fatigue, fatigue-related cues, and sadness in facial photographs. The faces of sleep deprived individuals were perceived as having more hanging eyelids, redder eyes, more swollen eyes, darker circles under the eyes, paler skin, more wrinkles/fine lines, and more droopy corners of the mouth (effects ranging from b = +3 ± 1 to b = +15 ± 1 mm on 100-mm visual analog scales, P < 0.01). The ratings of fatigue were related to glazed eyes and to all the cues affected by sleep deprivation (P < 0.01). Ratings of rash/eczema or tense lips were not significantly affected by sleep deprivation, nor associated with judgements of fatigue. In addition, sleep-deprived individuals looked sadder than after normal sleep, and sadness was related to looking fatigued (P < 0.01). The results show that sleep deprivation affects features relating to the eyes, mouth, and skin, and that these features function as cues of sleep loss to other people. Because these facial regions are important in the communication between humans, facial cues of sleep deprivation and fatigue may carry social consequences for the sleep deprived individual in everyday life.

  6. BDNF in sleep, insomnia, and sleep deprivation.

    PubMed

    Schmitt, Karen; Holsboer-Trachsler, Edith; Eckert, Anne

    2016-01-01

    The protein brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family of growth factors involved in plasticity of neurons in several brain regions. There are numerous evidence that BDNF expression is decreased by experiencing psychological stress and that, accordingly, a lack of neurotrophic support causes major depression. Furthermore, disruption in sleep homeostatic processes results in higher stress vulnerability and is often associated with stress-related mental disorders. Recently, we reported, for the first time, a relationship between BDNF and insomnia and sleep deprivation (SD). Using a biphasic stress model as explanation approach, we discuss here the hypothesis that chronic stress might induce a deregulation of the hypothalamic-pituitary-adrenal system. In the long-term it leads to sleep disturbance and depression as well as decreased BDNF levels, whereas acute stress like SD can be used as therapeutic intervention in some insomniac or depressed patients as compensatory process to normalize BDNF levels. Indeed, partial SD (PSD) induced a fast increase in BDNF serum levels within hours after PSD which is similar to effects seen after ketamine infusion, another fast-acting antidepressant intervention, while traditional antidepressants are characterized by a major delay until treatment response as well as delayed BDNF level increase. Key messages Brain-derived neurotrophic factor (BDNF) plays a key role in the pathophysiology of stress-related mood disorders. The interplay of stress and sleep impacts on BDNF level. Partial sleep deprivation (PSD) shows a fast action on BDNF level increase.

  7. Sleep Deprivation and Recovery Sleep Prior to a Noxious Inflammatory Insult Influence Characteristics and Duration of Pain

    PubMed Central

    Vanini, Giancarlo

    2016-01-01

    Study Objectives: Insufficient sleep and chronic pain are public health epidemics. Sleep loss worsens pain and predicts the development of chronic pain. Whether previous, acute sleep loss and recovery sleep determine pain levels and duration remains poorly understood. This study tested whether acute sleep deprivation and recovery sleep prior to formalin injection alter post-injection pain levels and duration. Methods: Male Sprague-Dawley rats (n = 48) underwent sleep deprivation or ad libitum sleep for 9 hours. Thereafter, rats received a subcutaneous injection of formalin or saline into a hind paw. In the recovery sleep group, rats were allowed 24 h between sleep deprivation and the injection of formalin. Mechanical and thermal nociception were assessed using the von Frey test and Hargreaves' method. Nociceptive measures were performed at 1, 3, 7, 10, 14, 17 and 21 days post-injection. Results: Formalin caused bilateral mechanical hypersensitivity (allodynia) that persisted for up to 21 days post-injection. Sleep deprivation significantly enhanced bilateral allodynia. There was a synergistic interaction when sleep deprivation preceded a formalin injection. Rats allowed a recovery sleep period prior to formalin injection developed allodynia only in the injected limb, with higher mechanical thresholds (less allodynia) and a shorter recovery period. There were no persistent changes in thermal nociception. Conclusion: The data suggest that acute sleep loss preceding an inflammatory insult enhances pain and can contribute to chronic pain. The results encourage studies in a model of surgical pain to test whether enhancing sleep reduces pain levels and duration. Citation: Vanini G. Sleep deprivation and recovery sleep prior to a noxious inflammatory insult influence characteristics and duration of pain. SLEEP 2016;39(1):133–142. PMID:26237772

  8. Impact of Acute Sleep Deprivation on Sarcasm Detection

    PubMed Central

    Mary, Alison; Slama, Hichem; Cleeremans, Axel; Peigneux, Philippe; Kissine, Mikhail

    2015-01-01

    There is growing evidence that sleep plays a pivotal role on health, cognition and emotional regulation. However, the interplay between sleep and social cognition remains an uncharted research area. In particular, little is known about the impact of sleep deprivation on sarcasm detection, an ability which, once altered, may hamper everyday social interactions. The aim of this study is to determine whether sleep-deprived participants are as able as sleep-rested participants to adopt another perspective in gauging sarcastic statements. At 9am, after a whole night of sleep (n = 15) or a sleep deprivation night (n = 15), participants had to read the description of an event happening to a group of friends. An ambiguous voicemail message left by one of the friends on another's phone was then presented, and participants had to decide whether the recipient would perceive the message as sincere or as sarcastic. Messages were uttered with a neutral intonation and were either: (1) sarcastic from both the participant’s and the addressee’s perspectives (i.e. both had access to the relevant background knowledge to gauge the message as sarcastic), (2) sarcastic from the participant’s but not from the addressee’s perspective (i.e. the addressee lacked context knowledge to detect sarcasm) or (3) sincere. A fourth category consisted in messages sarcastic from both the participant’s and from the addressee’s perspective, uttered with a sarcastic tone. Although sleep-deprived participants were as accurate as sleep-rested participants in interpreting the voice message, they were also slower. Blunted reaction time was not fully explained by generalized cognitive slowing after sleep deprivation; rather, it could reflect a compensatory mechanism supporting normative accuracy level in sarcasm understanding. Introducing prosodic cues compensated for increased processing difficulties in sarcasm detection after sleep deprivation. Our findings support the hypothesis that sleep

  9. Sleep deprivation impairs the accurate recognition of human emotions.

    PubMed

    van der Helm, Els; Gujar, Ninad; Walker, Matthew P

    2010-03-01

    Investigate the impact of sleep deprivation on the ability to recognize the intensity of human facial emotions. Randomized total sleep-deprivation or sleep-rested conditions, involving between-group and within-group repeated measures analysis. Experimental laboratory study. Thirty-seven healthy participants, (21 females) aged 18-25 y, were randomly assigned to the sleep control (SC: n = 17) or total sleep deprivation group (TSD: n = 20). Participants performed an emotional face recognition task, in which they evaluated 3 different affective face categories: Sad, Happy, and Angry, each ranging in a gradient from neutral to increasingly emotional. In the TSD group, the task was performed once under conditions of sleep deprivation, and twice under sleep-rested conditions following different durations of sleep recovery. In the SC group, the task was performed twice under sleep-rested conditions, controlling for repeatability. In the TSD group, when sleep-deprived, there was a marked and significant blunting in the recognition of Angry and Happy affective expressions in the moderate (but not extreme) emotional intensity range; differences that were most reliable and significant in female participants. No change in the recognition of Sad expressions was observed. These recognition deficits were, however, ameliorated following one night of recovery sleep. No changes in task performance were observed in the SC group. Sleep deprivation selectively impairs the accurate judgment of human facial emotions, especially threat relevant (Anger) and reward relevant (Happy) categories, an effect observed most significantly in females. Such findings suggest that sleep loss impairs discrete affective neural systems, disrupting the identification of salient affective social cues.

  10. Deconstructing and Reconstructing Cognitive Performance in Sleep Deprivation

    PubMed Central

    Jackson, Melinda L.; Gunzelmann, Glenn; Whitney, Paul; Hinson, John M.; Belenky, Gregory; Rabat, Arnaud; Van Dongen, Hans P. A.

    2012-01-01

    Summary Mitigation of cognitive impairment due to sleep deprivation in operational settings is critical for safety and productivity. Achievements in this area are hampered by limited knowledge about the effects of sleep loss on actual job tasks. Sleep deprivation has different effects on different cognitive performance tasks, but the mechanisms behind this task-specificity are poorly understood. In this context it is important to recognize that cognitive performance is not a unitary process, but involves a number of component processes. There is emerging evidence that these component processes are differentially affected by sleep loss. Experiments have been conducted to decompose sleep-deprived performance into underlying cognitive processes using cognitive-behavioral, neuroimaging and cognitive modeling techniques. Furthermore, computational modeling in cognitive architectures has been employed to simulate sleep-deprived cognitive performance on the basis of the constituent cognitive processes. These efforts are beginning to enable quantitative prediction of the effects of sleep deprivation across different task contexts. This paper reviews a rapidly evolving area of research, and outlines a theoretical framework in which the effects of sleep loss on cognition may be understood from the deficits in the underlying neurobiology to the applied consequences in real-world job tasks. PMID:22884948

  11. Deconstructing and reconstructing cognitive performance in sleep deprivation.

    PubMed

    Jackson, Melinda L; Gunzelmann, Glenn; Whitney, Paul; Hinson, John M; Belenky, Gregory; Rabat, Arnaud; Van Dongen, Hans P A

    2013-06-01

    Mitigation of cognitive impairment due to sleep deprivation in operational settings is critical for safety and productivity. Achievements in this area are hampered by limited knowledge about the effects of sleep loss on actual job tasks. Sleep deprivation has different effects on different cognitive performance tasks, but the mechanisms behind this task-specificity are poorly understood. In this context it is important to recognize that cognitive performance is not a unitary process, but involves a number of component processes. There is emerging evidence that these component processes are differentially affected by sleep loss. Experiments have been conducted to decompose sleep-deprived performance into underlying cognitive processes using cognitive-behavioral, neuroimaging and cognitive modeling techniques. Furthermore, computational modeling in cognitive architectures has been employed to simulate sleep-deprived cognitive performance on the basis of the constituent cognitive processes. These efforts are beginning to enable quantitative prediction of the effects of sleep deprivation across different task contexts. This paper reviews a rapidly evolving area of research, and outlines a theoretical framework in which the effects of sleep loss on cognition may be understood from the deficits in the underlying neurobiology to the applied consequences in real-world job tasks. Copyright © 2012 Elsevier Ltd. All rights reserved.

  12. Total sleep deprivation decreases flow experience and mood status

    PubMed Central

    Kaida, Kosuke; Niki, Kazuhisa

    2014-01-01

    Background The purpose of this study was to examine the effect of sleep deprivation on flow experience. Methods Sixteen healthy male volunteers of mean age 21.4±1.59 (21–24) years participated in two experimental conditions, ie, sleep-deprivation and normal sleep. In the sleep-deprived condition, participants stayed awake at home for 36 hours (from 8 am until 10 pm the next day) beginning on the day prior to an experimental day. In both conditions, participants carried out a simple reaction time (psychomotor vigilance) task and responded to a questionnaire measuring flow experience and mood status. Results Flow experience was reduced after one night of total sleep deprivation. Sleep loss also decreased positive mood, increased negative mood, and decreased psychomotor performance. Conclusion Sleep deprivation has a strong impact on mental and behavioral states associated with the maintenance of flow, namely subjective well-being. PMID:24376356

  13. Selective REM Sleep Deprivation Improves Expectation-Related Placebo Analgesia

    PubMed Central

    Chouchou, Florian; Chauny, Jean-Marc; Rainville, Pierre; Lavigne, Gilles J.

    2015-01-01

    The placebo effect is a neurobiological and psychophysiological process known to influence perceived pain relief. Optimization of placebo analgesia may contribute to the clinical efficacy and effectiveness of medication for acute and chronic pain management. We know that the placebo effect operates through two main mechanisms, expectations and learning, which is also influenced by sleep. Moreover, a recent study suggested that rapid eye movement (REM) sleep is associated with modulation of expectation-mediated placebo analgesia. We examined placebo analgesia following pharmacological REM sleep deprivation and we tested the hypothesis that relief expectations and placebo analgesia would be improved by experimental REM sleep deprivation in healthy volunteers. Following an adaptive night in a sleep laboratory, 26 healthy volunteers underwent classical experimental placebo analgesic conditioning in the evening combined with pharmacological REM sleep deprivation (clonidine: 13 volunteers or inert control pill: 13 volunteers). Medication was administered in a double-blind manner at bedtime, and placebo analgesia was tested in the morning. Results revealed that 1) placebo analgesia improved with REM sleep deprivation; 2) pain relief expectations did not differ between REM sleep deprivation and control groups; and 3) REM sleep moderated the relationship between pain relief expectations and placebo analgesia. These results support the putative role of REM sleep in modulating placebo analgesia. The mechanisms involved in these improvements in placebo analgesia and pain relief following selective REM sleep deprivation should be further investigated. PMID:26678391

  14. Selective REM Sleep Deprivation Improves Expectation-Related Placebo Analgesia.

    PubMed

    Chouchou, Florian; Chauny, Jean-Marc; Rainville, Pierre; Lavigne, Gilles J

    2015-01-01

    The placebo effect is a neurobiological and psychophysiological process known to influence perceived pain relief. Optimization of placebo analgesia may contribute to the clinical efficacy and effectiveness of medication for acute and chronic pain management. We know that the placebo effect operates through two main mechanisms, expectations and learning, which is also influenced by sleep. Moreover, a recent study suggested that rapid eye movement (REM) sleep is associated with modulation of expectation-mediated placebo analgesia. We examined placebo analgesia following pharmacological REM sleep deprivation and we tested the hypothesis that relief expectations and placebo analgesia would be improved by experimental REM sleep deprivation in healthy volunteers. Following an adaptive night in a sleep laboratory, 26 healthy volunteers underwent classical experimental placebo analgesic conditioning in the evening combined with pharmacological REM sleep deprivation (clonidine: 13 volunteers or inert control pill: 13 volunteers). Medication was administered in a double-blind manner at bedtime, and placebo analgesia was tested in the morning. Results revealed that 1) placebo analgesia improved with REM sleep deprivation; 2) pain relief expectations did not differ between REM sleep deprivation and control groups; and 3) REM sleep moderated the relationship between pain relief expectations and placebo analgesia. These results support the putative role of REM sleep in modulating placebo analgesia. The mechanisms involved in these improvements in placebo analgesia and pain relief following selective REM sleep deprivation should be further investigated.

  15. Acute sleep deprivation enhances post-infection sleep and promotes survival during bacterial infection in Drosophila.

    PubMed

    Kuo, Tzu-Hsing; Williams, Julie A

    2014-05-01

    Sleep is known to increase as an acute response to infection. However, the function of this behavioral response in host defense is not well understood. To address this problem, we evaluated the effect of acute sleep deprivation on post-infection sleep and immune function in Drosophila. Laboratory. Drosophila melanogaster. Flies were subjected to sleep deprivation before (early DEP) or after (late DEP) bacterial infection. Relative to a non-deprived control, flies subjected to early DEP had enhanced sleep after infection as well as increased bacterial clearance and survival outcome. Flies subjected to late DEP experienced enhanced sleep following the deprivation period, and showed a modest improvement in survival outcome. Continuous DEP (early and late DEP) throughout infection also enhanced sleep later during infection and improved survival. However, improved survival in flies subjected to late or continuous DEP did not occur until after flies had experienced sleep. During infection, both early and late DEP enhanced NFκB transcriptional activity as measured by a luciferase reporter (κB-luc) in living flies. Early DEP also increased NFκB activity prior to infection. Flies that were deficient in expression of either the Relish or Dif NFκB transcription factors showed normal responses to early DEP. However, the effect of early DEP on post-infection sleep and survival was abolished in double mutants, which indicates that Relish and Dif have redundant roles in this process. Acute sleep deprivation elevated NFκB-dependent activity, increased post-infection sleep, and improved survival during bacterial infection.

  16. The effect of REM sleep deprivation on motivation for food reward.

    PubMed

    Hanlon, Erin C; Andrzejewski, Matthew E; Harder, Bridgette K; Kelley, Ann E; Benca, Ruth M

    2005-08-30

    Prolonged sleep deprivation in rats produces a characteristic syndrome consisting of an increase in food intake yet a decrease in weight. Moreover, the increase in food intake generally precedes the weight loss, suggesting that sleep deprivation may affect appetitive behaviors. Using the multiple platform method to produce rapid eye movement (REM) sleep deprivation, we investigated the effect of REM sleep deprivation (REMSD) on motivation for food reward utilizing food-reinforced operant tasks. In acquisition or maintenance of an operant task, REM sleep-deprived rats, with or without simultaneous food restriction, decreased responding for sucrose pellet reward in comparison to controls, despite the fact that all REM sleep-deprived rats lost weight. Furthermore, the overall response deficit of the REM sleep-deprived rats was due to a within-session decline in responding. REM sleep-deprived rats showed evidence of understanding the contingency of the task comparable to controls throughout deprivation period, suggesting that the decrements in responding were not primarily related to deficits in learning or memory. Rather, REM sleep deprivation appears to alter systems involved in motivational processes, reward, and/or attention.

  17. Notch signaling modulates sleep homeostasis and learning after sleep deprivation in Drosophila.

    PubMed

    Seugnet, Laurent; Suzuki, Yasuko; Merlin, Gabriel; Gottschalk, Laura; Duntley, Stephen P; Shaw, Paul J

    2011-05-24

    The role of the transmembrane receptor Notch in the adult brain is poorly understood. Here, we provide evidence that bunched, a negative regulator of Notch, is involved in sleep homeostasis. Genetic evidence indicates that interfering with bunched activity in the mushroom bodies (MBs) abolishes sleep homeostasis. Combining bunched and Delta loss-of-function mutations rescues normal homeostasis, suggesting that Notch signaling may be involved in regulating sensitivity to sleep loss. Preventing the downregulation of Delta by overexpressing a wild-type transgene in MBs reduces sleep homeostasis and, importantly, prevents learning impairments induced by sleep deprivation. Similar resistance to sleep loss is observed with Notch(spl-1) gain-of-function mutants. Immunohistochemistry reveals that the Notch receptor is expressed in glia, whereas Delta is localized in neurons. Importantly, the expression in glia of the intracellular domain of Notch, a dominant activated form of the receptor, is sufficient to prevent learning deficits after sleep deprivation. Together, these results identify a novel neuron-glia signaling pathway dependent on Notch and regulated by bunched. These data highlight the emerging role of neuron-glia interactions in regulating both sleep and learning impairments associated with sleep loss. Copyright © 2011 Elsevier Ltd. All rights reserved.

  18. Sleep Deprivation and Recovery Sleep Prior to a Noxious Inflammatory Insult Influence Characteristics and Duration of Pain.

    PubMed

    Vanini, Giancarlo

    2016-01-01

    Insufficient sleep and chronic pain are public health epidemics. Sleep loss worsens pain and predicts the development of chronic pain. Whether previous, acute sleep loss and recovery sleep determine pain levels and duration remains poorly understood. This study tested whether acute sleep deprivation and recovery sleep prior to formalin injection alter post-injection pain levels and duration. Male Sprague-Dawley rats (n = 48) underwent sleep deprivation or ad libitum sleep for 9 hours. Thereafter, rats received a subcutaneous injection of formalin or saline into a hind paw. In the recovery sleep group, rats were allowed 24 h between sleep deprivation and the injection of formalin. Mechanical and thermal nociception were assessed using the von Frey test and Hargreaves' method. Nociceptive measures were performed at 1, 3, 7, 10, 14, 17 and 21 days post-injection. Formalin caused bilateral mechanical hypersensitivity (allodynia) that persisted for up to 21 days post-injection. Sleep deprivation significantly enhanced bilateral allodynia. There was a synergistic interaction when sleep deprivation preceded a formalin injection. Rats allowed a recovery sleep period prior to formalin injection developed allodynia only in the injected limb, with higher mechanical thresholds (less allodynia) and a shorter recovery period. There were no persistent changes in thermal nociception. The data suggest that acute sleep loss preceding an inflammatory insult enhances pain and can contribute to chronic pain. The results encourage studies in a model of surgical pain to test whether enhancing sleep reduces pain levels and duration. © 2016 Associated Professional Sleep Societies, LLC.

  19. The effects of sleep deprivation on emotional empathy.

    PubMed

    Guadagni, Veronica; Burles, Ford; Ferrara, Michele; Iaria, Giuseppe

    2014-12-01

    Previous studies have shown that sleep loss has a detrimental effect on the ability of the individuals to process emotional information. In this study, we tested the hypothesis that this negative effect extends to the ability of experiencing emotions while observing other individuals, i.e. emotional empathy. To test this hypothesis, we assessed emotional empathy in 37 healthy volunteers who were assigned randomly to one of three experimental groups: one group was tested before and after a night of total sleep deprivation (sleep deprivation group), a second group was tested before and after a usual night of sleep spent at home (sleep group) and the third group was tested twice during the same day (day group). Emotional empathy was assessed by using two parallel versions of a computerized test measuring direct (i.e. explicit evaluation of empathic concern) and indirect (i.e. the observer's reported physiological arousal) emotional empathy. The results revealed that the post measurements of both direct and indirect emotional empathy of participants in the sleep deprivation group were significantly lower than those of the sleep and day groups; post measurement scores of participants in the day and sleep groups did not differ significantly for either direct or indirect emotional empathy. These data are consistent with previous studies showing the negative effect of sleep deprivation on the processing of emotional information, and extend these effects to emotional empathy. The findings reported in our study are relevant to healthy individuals with poor sleep habits, as well as clinical populations suffering from sleep disturbances. © 2014 European Sleep Research Society.

  20. Evoked Electrical and Cerebral Vascular Responses Following Sleep Deprivation

    PubMed Central

    Schei, Jennifer L.; Rector, David M.

    2011-01-01

    Neuronal activity elicits vascular dilation, delivering additional blood and metabolites to the activated region. With increasing neural activity, vessels stretch and may become less compliant. Most functional imaging studies assume that limits to vascular expansion are not normally reached except under pathological conditions, with the possibility that metabolism could outpace supply. However, we previously demonstrated that evoked hemodynamic responses were larger during quiet sleep when compared to both waking and REM sleep, suggesting that high basal activity during wake may elicit blunted evoked hemodynamic responses due to vascular expansion limits. We hypothesized that extended brain activity through sleep deprivation will further dilate blood vessels, and exacerbate the blunted evoked hemodynamic responses observed during wake, and dampen responses in subsequent sleep. We measured evoked electrical and hemodynamic responses from rats using auditory clicks (0.5 s, 10 Hz, 2–13 s random ISIs) for one hour following 2, 4, or 6 hours of sleep deprivation. Time-of-day matched controls were recorded continuously for 7 hours. Within quiet sleep periods following deprivation, ERP amplitude did not differ; however, the evoked vascular response was smaller with longer sleep deprivation periods. These results suggest that prolonged neural activity periods through sleep deprivation may diminish vascular compliance as indicated by the blunted vascular response. Subsequent sleep may allow vessels to relax, restoring their ability to deliver blood. These results also suggest that severe sleep deprivation or chronic sleep disturbances could push the vasculature to critical limits, leading to metabolic deficit and the potential for tissue trauma. PMID:21854966

  1. Sleep mechanisms: Sleep deprivation and detection of changing levels of consciousness

    NASA Technical Reports Server (NTRS)

    Dement, W. C.; Barchas, J. D.

    1972-01-01

    An attempt was made to obtain information relevant to assessing the need to sleep and make up for lost sleep. Physiological and behavioral parameters were used as measuring parameters. Sleep deprivation in a restricted environment, derivation of data relevant to determining sleepiness from EEG, and the development of the Sanford Sleepiness Scale were discussed.

  2. A Novel BHLHE41 Variant is Associated with Short Sleep and Resistance to Sleep Deprivation in Humans

    PubMed Central

    Pellegrino, Renata; Kavakli, Ibrahim Halil; Goel, Namni; Cardinale, Christopher J.; Dinges, David F.; Kuna, Samuel T.; Maislin, Greg; Van Dongen, Hans P.A.; Tufik, Sergio; Hogenesch, John B.; Hakonarson, Hakon; Pack, Allan I.

    2014-01-01

    Study Objectives: Earlier work described a mutation in DEC2 also known as BHLHE41 (basic helix-loophelix family member e41) as causal in a family of short sleepers, who needed just 6 h sleep per night. We evaluated whether there were other variants of this gene in two well-phenotyped cohorts. Design: Sequencing of the BHLHE41 gene, electroencephalographic data, and delta power analysis and functional studies using cell-based luciferase. Results: We identified new variants of the BHLHE41 gene in two cohorts who had either acute sleep deprivation (n = 200) or chronic partial sleep deprivation (n = 217). One variant, Y362H, at another location in the same exon occurred in one twin in a dizygotic twin pair and was associated with reduced sleep duration, less recovery sleep following sleep deprivation, and fewer performance lapses during sleep deprivation than the homozygous twin. Both twins had almost identical amounts of non rapid eye movement (NREM) sleep. This variant reduced the ability of BHLHE41 to suppress CLOCK/BMAL1 and NPAS2/BMAL1 transactivation in vitro. Another variant in the same exome had no effect on sleep or response to sleep deprivation and no effect on CLOCK/BMAL1 transactivation. Random mutagenesis identified a number of other variants of BHLHE41 that affect its function. Conclusions: There are a number of mutations of BHLHE41. Mutations reduce total sleep while maintaining NREM sleep and provide resistance to the effects of sleep loss. Mutations that affect sleep also modify the normal inhibition of BHLHE41 of CLOCK/BMAL1 transactivation. Thus, clock mechanisms are likely involved in setting sleep length and the magnitude of sleep homeostasis. Citation: Pellegrino R, Kavakli IH, Goel N, Cardinale CJ, Dinges DF, Kuna ST, Maislin G, Van Dongen HP, Tufik S, Hogenesch JB, Hakonarson H, Pack AI. A novel BHLHE41 variant is associated with short sleep and resistance to sleep deprivation in humans. SLEEP 2014;37(8):1327-1336. PMID:25083013

  3. A novel BHLHE41 variant is associated with short sleep and resistance to sleep deprivation in humans.

    PubMed

    Pellegrino, Renata; Kavakli, Ibrahim Halil; Goel, Namni; Cardinale, Christopher J; Dinges, David F; Kuna, Samuel T; Maislin, Greg; Van Dongen, Hans P A; Tufik, Sergio; Hogenesch, John B; Hakonarson, Hakon; Pack, Allan I

    2014-08-01

    Earlier work described a mutation in DEC2 also known as BHLHE41 (basic helix-loophelix family member e41) as causal in a family of short sleepers, who needed just 6 h sleep per night. We evaluated whether there were other variants of this gene in two well-phenotyped cohorts. Sequencing of the BHLHE41 gene, electroencephalographic data, and delta power analysis and functional studies using cell-based luciferase. We identified new variants of the BHLHE41 gene in two cohorts who had either acute sleep deprivation (n = 200) or chronic partial sleep deprivation (n = 217). One variant, Y362H, at another location in the same exon occurred in one twin in a dizygotic twin pair and was associated with reduced sleep duration, less recovery sleep following sleep deprivation, and fewer performance lapses during sleep deprivation than the homozygous twin. Both twins had almost identical amounts of non rapid eye movement (NREM) sleep. This variant reduced the ability of BHLHE41 to suppress CLOCK/BMAL1 and NPAS2/BMAL1 transactivation in vitro. Another variant in the same exome had no effect on sleep or response to sleep deprivation and no effect on CLOCK/BMAL1 transactivation. Random mutagenesis identified a number of other variants of BHLHE41 that affect its function. There are a number of mutations of BHLHE41. Mutations reduce total sleep while maintaining NREM sleep and provide resistance to the effects of sleep loss. Mutations that affect sleep also modify the normal inhibition of BHLHE41 of CLOCK/BMAL1 transactivation. Thus, clock mechanisms are likely involved in setting sleep length and the magnitude of sleep homeostasis. Pellegrino R, Kavakli IH, Goel N, Cardinale CJ, Dinges DF, Kuna ST, Maislin G, Van Dongen HP, Tufik S, Hogenesch JB, Hakonarson H, Pack AI. A novel BHLHE41 variant is associated with short sleep and resistance to sleep deprivation in humans. SLEEP 2014;37(8):1327-1336.

  4. Sleep deprivation affects extinction but not acquisition memory in honeybees.

    PubMed

    Hussaini, Syed Abid; Bogusch, Lisa; Landgraf, Tim; Menzel, Randolf

    2009-11-01

    Sleep-like behavior has been studied in honeybees before, but the relationship between sleep and memory formation has not been explored. Here we describe a new approach to address the question if sleep in bees, like in other animals, improves memory consolidation. Restrained bees were observed by a web camera, and their antennal activities were used as indicators of sleep. We found that the bees sleep more during the dark phase of the day compared with the light phase. Sleep phases were characterized by two distinct patterns of antennal activities: symmetrical activity, more prominent during the dark phase; and asymmetrical activity, more common during the light phase. Sleep-deprived bees showed rebound the following day, confirming effective deprivation of sleep. After appetitive conditioning of the bees to various olfactory stimuli, we observed their sleep. Bees conditioned to odor with sugar reward showed lesser sleep compared with bees that were exposed to either reward alone or air alone. Next, we asked whether sleep deprivation affects memory consolidation. While sleep deprivation had no effect on retention scores after odor acquisition, retention for extinction learning was significantly reduced, indicating that consolidation of extinction memory but not acquisition memory was affected by sleep deprivation.

  5. Sleep Deprivation Reveals Altered Brain Perfusion Patterns in Somnambulism.

    PubMed

    Dang-Vu, Thien Thanh; Zadra, Antonio; Labelle, Marc-Antoine; Petit, Dominique; Soucy, Jean-Paul; Montplaisir, Jacques

    2015-01-01

    Despite its high prevalence, relatively little is known about the pathophysiology of somnambulism. Increasing evidence indicates that somnambulism is associated with functional abnormalities during wakefulness and that sleep deprivation constitutes an important drive that facilitates sleepwalking in predisposed patients. Here, we studied the neural mechanisms associated with somnambulism using Single Photon Emission Computed Tomography (SPECT) with 99mTc-Ethylene Cysteinate Dimer (ECD), during wakefulness and after sleep deprivation. Ten adult sleepwalkers and twelve controls with normal sleep were scanned using 99mTc-ECD SPECT in morning wakefulness after a full night of sleep. Eight of the sleepwalkers and nine of the controls were also scanned during wakefulness after a night of total sleep deprivation. Between-group comparisons of regional cerebral blood flow (rCBF) were performed to characterize brain activity patterns during wakefulness in sleepwalkers. During wakefulness following a night of total sleep deprivation, rCBF was decreased bilaterally in the inferior temporal gyrus in sleepwalkers compared to controls. Functional neural abnormalities can be observed during wakefulness in somnambulism, particularly after sleep deprivation and in the inferior temporal cortex. Sleep deprivation thus not only facilitates the occurrence of sleepwalking episodes, but also uncovers patterns of neural dysfunction that characterize sleepwalkers during wakefulness.

  6. Sleep Deprivation Reveals Altered Brain Perfusion Patterns in Somnambulism

    PubMed Central

    Dang-Vu, Thien Thanh; Zadra, Antonio; Labelle, Marc-Antoine; Petit, Dominique; Soucy, Jean-Paul; Montplaisir, Jacques

    2015-01-01

    Background Despite its high prevalence, relatively little is known about the pathophysiology of somnambulism. Increasing evidence indicates that somnambulism is associated with functional abnormalities during wakefulness and that sleep deprivation constitutes an important drive that facilitates sleepwalking in predisposed patients. Here, we studied the neural mechanisms associated with somnambulism using Single Photon Emission Computed Tomography (SPECT) with 99mTc-Ethylene Cysteinate Dimer (ECD), during wakefulness and after sleep deprivation. Methods Ten adult sleepwalkers and twelve controls with normal sleep were scanned using 99mTc-ECD SPECT in morning wakefulness after a full night of sleep. Eight of the sleepwalkers and nine of the controls were also scanned during wakefulness after a night of total sleep deprivation. Between-group comparisons of regional cerebral blood flow (rCBF) were performed to characterize brain activity patterns during wakefulness in sleepwalkers. Results During wakefulness following a night of total sleep deprivation, rCBF was decreased bilaterally in the inferior temporal gyrus in sleepwalkers compared to controls. Conclusions Functional neural abnormalities can be observed during wakefulness in somnambulism, particularly after sleep deprivation and in the inferior temporal cortex. Sleep deprivation thus not only facilitates the occurrence of sleepwalking episodes, but also uncovers patterns of neural dysfunction that characterize sleepwalkers during wakefulness. PMID:26241047

  7. The prospective association between sleep deprivation and depression among adolescents.

    PubMed

    Roberts, Robert E; Duong, Hao T

    2014-02-01

    To examine the prospective, reciprocal association between sleep deprivation and depression among adolescents. A community-based two-wave cohort study. A metropolitan area with a population of over 4 million. 4,175 youths 11-17 at baseline, and 3,134 of these followed up a year later. Depression is measured using both symptoms of depression and DSM-IV major depression. Sleep deprivation is defined as ≤ 6 h of sleep per night. Sleep deprivation at baseline predicted both measures of depression at follow-up, controlling for depression at baseline. Examining the reciprocal association, major depression at baseline, but not symptoms predicted sleep deprivation at follow-up. These results are the first to document reciprocal effects for major depression and sleep deprivation among adolescents using prospective data. The data suggest reduced quantity of sleep increases risk for major depression, which in turn increases risk for decreased sleep.

  8. Countermeasures for sleep loss and deprivation.

    PubMed

    Kushida, Clete A

    2006-09-01

    Sleep deprivation is ubiquitous and carries profound consequences in terms of personal and public health and safety. There is no substitute for a good night's sleep. Sleep that is optimal in quality and quantity for individuals, factoring in their age and personal sleep requirements, will minimize sleep debt and maximize daytime performance. Therefore, setting aside an adequate amount of time for sleep should be a priority; sleep should not be sacrificed at the expense of other activities of daily living. Nevertheless, there are certain therapeutic countermeasures available for individuals who are unable to obtain adequate sleep because of medical or sleep-related conditions (eg, narcolepsy, obstructive sleep apnea) when excessive daytime sleepiness is the main feature of the condition, or residual sleepiness despite treatment for the main conditions is present. These therapeutic countermeasures may also be considered in situations in which occupational constraints (eg, rotating shift work, military duty) dictate that constant or heightened vigilance is important or critical to work performance, crucial decision making, and/or survival. Exploration of the causes of sleep loss or deprivation, whether it is voluntary, or work or family induced, and/or the effects of a medical or sleep disorder, is a necessary first step in the evaluation of a patient who has significant daytime fatigue or sleepiness. Wake-promoting substances and medications such as caffeine, modafinil, methylphenidate, and dextroamphetamine may be considered in situations in which sleep loss is unavoidable or persists despite treatment of an underlying disorder that is characterized by or associated with daytime fatigue or sleepiness.

  9. Deprivation and Recovery of Sleep in Succession Enhances Reflexive Motor Behavior

    PubMed Central

    Sprenger, Andreas; Weber, Frederik D.; Machner, Bjoern; Talamo, Silke; Scheffelmeier, Sabine; Bethke, Judith; Helmchen, Christoph; Gais, Steffen; Kimmig, Hubert; Born, Jan

    2015-01-01

    Sleep deprivation impairs inhibitory control over reflexive behavior, and this impairment is commonly assumed to dissipate after recovery sleep. Contrary to this belief, here we show that fast reflexive behaviors, when practiced during sleep deprivation, is consolidated across recovery sleep and, thereby, becomes preserved. As a model for the study of sleep effects on prefrontal cortex-mediated inhibitory control in humans, we examined reflexive saccadic eye movements (express saccades), as well as speeded 2-choice finger motor responses. Different groups of subjects were trained on a standard prosaccade gap paradigm before periods of nocturnal sleep and sleep deprivation. Saccade performance was retested in the next morning and again 24 h later. The rate of express saccades was not affected by sleep after training, but slightly increased after sleep deprivation. Surprisingly, this increase augmented even further after recovery sleep and was still present 4 weeks later. Additional experiments revealed that the short testing after sleep deprivation was sufficient to increase express saccades across recovery sleep. An increase in speeded responses across recovery sleep was likewise found for finger motor responses. Our findings indicate that recovery sleep can consolidate motor disinhibition for behaviors practiced during prior sleep deprivation, thereby persistently enhancing response automatization. PMID:26048955

  10. Deprivation and Recovery of Sleep in Succession Enhances Reflexive Motor Behavior.

    PubMed

    Sprenger, Andreas; Weber, Frederik D; Machner, Bjoern; Talamo, Silke; Scheffelmeier, Sabine; Bethke, Judith; Helmchen, Christoph; Gais, Steffen; Kimmig, Hubert; Born, Jan

    2015-11-01

    Sleep deprivation impairs inhibitory control over reflexive behavior, and this impairment is commonly assumed to dissipate after recovery sleep. Contrary to this belief, here we show that fast reflexive behaviors, when practiced during sleep deprivation, is consolidated across recovery sleep and, thereby, becomes preserved. As a model for the study of sleep effects on prefrontal cortex-mediated inhibitory control in humans, we examined reflexive saccadic eye movements (express saccades), as well as speeded 2-choice finger motor responses. Different groups of subjects were trained on a standard prosaccade gap paradigm before periods of nocturnal sleep and sleep deprivation. Saccade performance was retested in the next morning and again 24 h later. The rate of express saccades was not affected by sleep after training, but slightly increased after sleep deprivation. Surprisingly, this increase augmented even further after recovery sleep and was still present 4 weeks later. Additional experiments revealed that the short testing after sleep deprivation was sufficient to increase express saccades across recovery sleep. An increase in speeded responses across recovery sleep was likewise found for finger motor responses. Our findings indicate that recovery sleep can consolidate motor disinhibition for behaviors practiced during prior sleep deprivation, thereby persistently enhancing response automatization. © The Author 2015. Published by Oxford University Press.

  11. Sleep Duration and Area-Level Deprivation in Twins

    PubMed Central

    Watson, Nathaniel F.; Horn, Erin; Duncan, Glen E.; Buchwald, Dedra; Vitiello, Michael V.; Turkheimer, Eric

    2016-01-01

    Study Objectives: We used quantitative genetic models to assess whether area-level deprivation as indicated by the Singh Index predicts shorter sleep duration and modifies its underlying genetic and environmental contributions. Methods: Participants were 4,218 adult twin pairs (2,377 monozygotic and 1,841 dizygotic) from the University of Washington Twin Registry. Participants self-reported habitual sleep duration. The Singh Index was determined by linking geocoding addresses to 17 indicators at the census-tract level using data from Census of Washington State and Census Tract Cartographic Boundary Files from 2000 and 2010. Data were analyzed using univariate and bivariate genetic decomposition and quantitative genetic interaction models that assessed A (additive genetics), C (common environment), and E (unique environment) main effects of the Singh Index on sleep duration and allowed the magnitude of residual ACE variance components in sleep duration to vary with the Index. Results: The sample had a mean age of 38.2 y (standard deviation [SD] = 18), and was predominantly female (62%) and Caucasian (91%). Mean sleep duration was 7.38 h (SD = 1.20) and the mean Singh Index score was 0.00 (SD = 0.89). The heritability of sleep duration was 39% and the Singh Index was 12%. The uncontrolled phenotypic regression of sleep duration on the Singh Index showed a significant negative relationship between area-level deprivation and sleep length (b = −0.080, P < 0.001). Every 1 SD in Singh Index was associated with a ∼4.5 min change in sleep duration. For the quasi-causal bivariate model, there was a significant main effect of E (b0E = −0.063; standard error [SE] = 0.30; P < 0.05). Residual variance components unique to sleep duration were significant for both A (b0Au = 0.734; SE = 0.020; P < 0.001) and E (b0Eu = 0.934; SE = 0.013; P < 0.001). Conclusions: Area-level deprivation has a quasi-causal association with sleep duration, with greater deprivation being related to

  12. Cardiovascular reactivity to acute psychological stress following sleep deprivation.

    PubMed

    Franzen, Peter L; Gianaros, Peter J; Marsland, Anna L; Hall, Martica H; Siegle, Greg J; Dahl, Ronald E; Buysse, Daniel J

    2011-10-01

    Psychological stress and sleep disturbances are highly prevalent and are both implicated in the etiology of cardiovascular diseases. Given the common co-occurrence of psychological distress and sleep disturbances including short sleep duration, this study examined the combined effects of these two factors on blood pressure reactivity to immediate mental challenge tasks after well-rested and sleep-deprived experimental conditions. Participants (n = 20) were healthy young adults free from current or past sleep, psychiatric, or major medical disorders. Using a within-subjects crossover design, we examined acute stress reactivity under two experimental conditions: after a night of normal sleep in the laboratory and after a night of total sleep deprivation. Two standardized psychological stress tasks were administered, a Stroop color-word naming interference task and a speech task, which were preceded by a prestress baseline period and followed by a poststress recovery period. Each period was 10 minutes in duration, and blood pressure recordings were collected every 2.5 minutes throughout each period. Mean blood pressure responses during stress and recovery periods were examined with a mixed-effects analysis of covariance, controlling for baseline blood pressure. There was a significant interaction between sleep deprivation and stress on systolic blood pressure (F(2,82.7) = 4.05, p = .02). Systolic blood pressure was higher in the sleep deprivation condition compared with the normal sleep condition during the speech task and during the two baseline periods. Sleep deprivation amplified systolic blood pressure increases to psychological stress. Sleep loss may increase cardiovascular risk by dysregulating stress physiology.

  13. Sex-dependent effects of sleep deprivation on myocardial sensitivity to ischemic injury.

    PubMed

    Zoladz, Phillip R; Krivenko, Anna; Eisenmann, Eric D; Bui, Albert D; Seeley, Sarah L; Fry, Megan E; Johnson, Brandon L; Rorabaugh, Boyd R

    2016-01-01

    Sleep deprivation is associated with increased risk of myocardial infarction. However, it is unknown whether the effects of sleep deprivation are limited to increasing the likelihood of experiencing a myocardial infarction or if sleep deprivation also increases the extent of myocardial injury. In this study, rats were deprived of paradoxical sleep for 96 h using the platform-over-water method. Control rats were subjected to the same condition except the control platform was large enough for the rats to sleep. Hearts from sleep deprived and control rats were subjected to 20 min ischemia on a Langendorff isolated heart system. Infarct size and post ischemic recovery of contractile function were unaffected by sleep deprivation in male hearts. In contrast, hearts from sleep-deprived females exhibited significantly larger infarcts than hearts from control females. Post ischemic recovery of rate pressure product and + dP/dT were significantly attenuated by sleep deprivation in female hearts, and post ischemic recovery of end diastolic pressure was significantly elevated in hearts from sleep deprived females compared to control females, indicating that post ischemic recovery of both systolic and diastolic function were worsened by sleep deprivation. These data provide evidence that sleep deprivation increases the extent of ischemia-induced injury in a sex-dependent manner.

  14. Physiological responses of men during sleep deprivation.

    DOT National Transportation Integrated Search

    1970-05-01

    The effects of 84 hours of sleep deprivation were examined in a group of six young men and compared with a group of six controls. Subjects were studied in pairs, one sleep-deprived and one control. Primary attention was given to the responses to acut...

  15. Health Effects of Sleep Deprivation,

    DTIC Science & Technology

    1990-06-01

    of an inordinate sleep loss (as hunger and thirst prevent us from going too long without food and water). Because of this, it takes great personal...drug-refractory depression. Neuropsychology 13:111-116, 1985. 82. Dowd PJ: Sleep deprivation effects on the vestibular habituation process. J Apply

  16. Sleep Deprivation Influences Circadian Gene Expression in the Lateral Habenula.

    PubMed

    Zhang, Beilin; Gao, Yanxia; Li, Yang; Yang, Jing; Zhao, Hua

    2016-01-01

    Sleep is governed by homeostasis and the circadian clock. Clock genes play an important role in the generation and maintenance of circadian rhythms but are also involved in regulating sleep homeostasis. The lateral habenular nucleus (LHb) has been implicated in sleep-wake regulation, since LHb gene expression demonstrates circadian oscillation characteristics. This study focuses on the participation of LHb clock genes in regulating sleep homeostasis, as the nature of their involvement is unclear. In this study, we observed changes in sleep pattern following sleep deprivation in LHb-lesioned rats using EEG recording techniques. And then the changes of clock gene expression (Per1, Per2, and Bmal1) in the LHb after 6 hours of sleep deprivation were detected by using real-time quantitative PCR (qPCR). We found that sleep deprivation increased the length of Non-Rapid Eye Movement Sleep (NREMS) and decreased wakefulness. LHb-lesioning decreased the amplitude of reduced wake time and increased NREMS following sleep deprivation in rats. qPCR results demonstrated that Per2 expression was elevated after sleep deprivation, while the other two genes were unaffected. Following sleep recovery, Per2 expression was comparable to the control group. This study provides the basis for further research on the role of LHb Per2 gene in the regulation of sleep homeostasis.

  17. Circadian Modulation of Consolidated Memory Retrieval Following Sleep Deprivation in Drosophila

    PubMed Central

    Glou, Eric Le; Seugnet, Laurent; Shaw, Paul J.; Preat, Thomas; Goguel, Valérie

    2012-01-01

    Objectives: Several lines of evidence indicate that sleep plays a critical role in learning and memory. The aim of this study was to evaluate anesthesia resistant memory following sleep deprivation in Drosophila. Design: Four to 16 h after aversive olfactory training, flies were sleep deprived for 4 h. Memory was assessed 24 h after training. Training, sleep deprivation, and memory tests were performed at different times during the day to evaluate the importance of the time of day for memory formation. The role of circadian rhythms was further evaluated using circadian clock mutants. Results Memory was disrupted when flies were exposed to 4 h of sleep deprivation during the consolidation phase. Interestingly, normal memory was observed following sleep deprivation when the memory test was performed during the 2 h preceding lights-off, a period characterized by maximum wake in flies. We also show that anesthesia resistant memory was less sensitive to sleep deprivation in flies with disrupted circadian rhythms. Conclusions Our results indicate that anesthesia resistant memory, a consolidated memory less costly than long-term memory, is sensitive to sleep deprivation. In addition, we provide evidence that circadian factors influence memory vulnerability to sleep deprivation and memory retrieval. Taken together, the data show that memories weakened by sleep deprivation can be retrieved if the animals are tested at the optimal circadian time. Citation: Le Glou E; Seugnet L; Shaw PJ; Preat T; Goguel V. Circadian modulation of consolidated memory retrieval following sleep deprivation in Drosophila. SLEEP 2012;35(10):1377-1384. PMID:23024436

  18. Sleep extension increases IGF-I concentrations before and during sleep deprivation in healthy young men.

    PubMed

    Chennaoui, Mounir; Arnal, Pierrick J; Drogou, Catherine; Sauvet, Fabien; Gomez-Merino, Danielle

    2016-09-01

    Sleep deprivation is known to suppress circulating trophic factors such as insulin-like growth factor (IGF)-I and brain-derived neurotrophic factor (BDNF). This experiment examined the effect of an intervention involving 6 nights of extended sleep before total sleep deprivation on this catabolic profile. In a randomized crossover design, 14 young men (age range: 26-37 years) were either in an extended (EXT; time in bed: 2100-0700 h) or habitual (HAB: 2230-0700 h) sleep condition, followed by 3 days in the laboratory with blood sampling at baseline (B), after 24 h of sleep deprivation (24h-SD), and after 1 night of recovery sleep (R). In the EXT condition compared with the HAB condition, free IGF-I levels were significantly higher at B, 24h-SD, and R (P < 0.001), and those of total IGF-I at B and 24h-SD (P < 0.05). EXT did not influence growth hormone, IGF binding protein 3, BDNF, insulin, and glucose levels. The only effect of 24 h of sleep deprivation was for insulin levels, which were significantly higher after R compared with B. In a healthy adult, additional sleep over 1 week increased blood concentrations of the anabolic factor IGF-I before and during 24 h of sleep deprivation and after the subsequent recovery night without effects on BDNF. With further research, these findings may prove to be important in guiding effective lifestyle modifications to limit physical or cognitive deficits associated with IGF-I decrease with age.

  19. Sleep Duration and Area-Level Deprivation in Twins.

    PubMed

    Watson, Nathaniel F; Horn, Erin; Duncan, Glen E; Buchwald, Dedra; Vitiello, Michael V; Turkheimer, Eric

    2016-01-01

    We used quantitative genetic models to assess whether area-level deprivation as indicated by the Singh Index predicts shorter sleep duration and modifies its underlying genetic and environmental contributions. Participants were 4,218 adult twin pairs (2,377 monozygotic and 1,841 dizygotic) from the University of Washington Twin Registry. Participants self-reported habitual sleep duration. The Singh Index was determined by linking geocoding addresses to 17 indicators at the census-tract level using data from Census of Washington State and Census Tract Cartographic Boundary Files from 2000 and 2010. Data were analyzed using univariate and bivariate genetic decomposition and quantitative genetic interaction models that assessed A (additive genetics), C (common environment), and E (unique environment) main effects of the Singh Index on sleep duration and allowed the magnitude of residual ACE variance components in sleep duration to vary with the Index. The sample had a mean age of 38.2 y (standard deviation [SD] = 18), and was predominantly female (62%) and Caucasian (91%). Mean sleep duration was 7.38 h (SD = 1.20) and the mean Singh Index score was 0.00 (SD = 0.89). The heritability of sleep duration was 39% and the Singh Index was 12%. The uncontrolled phenotypic regression of sleep duration on the Singh Index showed a significant negative relationship between area-level deprivation and sleep length (b = -0.080, P < 0.001). Every 1 SD in Singh Index was associated with a ∼4.5 min change in sleep duration. For the quasi-causal bivariate model, there was a significant main effect of E (b(0E) = -0.063; standard error [SE] = 0.30; P < 0.05). Residual variance components unique to sleep duration were significant for both A (b(0Au) = 0.734; SE = 0.020; P < 0.001) and E (b(0Eu) = 0.934; SE = 0.013; P < 0.001). Area-level deprivation has a quasi-causal association with sleep duration, with greater deprivation being related to shorter sleep. As area-level deprivation

  20. Individual Differences in Response to Sleep Deprivation: Assessment of Fatigue Following Sleep Loss

    NASA Technical Reports Server (NTRS)

    Carskadon, Mary A.

    1997-01-01

    Previous work has indicated that a small but significant number of participants in sleep deprivation studies or in simulated shift work experiments manifests an exaggerated performance decrement when they reach a critical point in the experiment, usually near the trough of the circadian cycle or the middle of the night. Those who show this exaggerated response do not appear to differ from other non-nal volunteers in any substantial way according to usual screening criteria or baseline values. The present study aims to examine factors that may provide the basis for this extreme response. We propose that a preexisting sleep deficit-as manifested by low values on the Multiple Sleep Latency Test (MSLT)-may account for extreme responders. It has been shown that among normal volunteers screened for a variety of studies, approximately 20 to 25 percent show low (< 6 minutes) MSLT scores on a consistent basis, whereas a like proportion shows consistently high MSLT scores (> 13 minutes). Additionally, studies by this group have indicated that subjects with low MSLT scores may suffer from chronic insufficient sleep, as further substantiated by the finding that they have consistently higher nocturnal sleep efficiency and that their MSLT scores rise to normal values when sleep is extended. We hypothesize that the short MSLT subjects have a significant long-term sleep deficit that leads to a marked intolerance for sleep deprivation or shift work. We further suggest that this sleep debt may signify an increased sleep need in these individuals that is not met either due to personal preference or to societal pressures (or both). If this speculation is accurate, then we predict that the tolerance for sleep deprivation in such individuals can be increased by "pretreatment" with sleep extension. Thus, the present study is designed to test the following two hypotheses: (1) subjects with nominal sleep patterns who have low MSLT scores (e.g., Sleepy subjects) will show an exaggerated

  1. Individual Differences in Response to Sleep Deprivation: Assessment of Fatigue Following Sleep Loss

    NASA Technical Reports Server (NTRS)

    Carskadon, Mary A.

    1997-01-01

    Previous work has indicated that a small but significant number of participants in sleep deprivation studies or in simulated shift work experiments manifests an exaggerated performance decrement when they reach a critical point in the experiment, usually near the trough of the circadian cycle or the middle of the night. Those who show this exaggerated response do not appear to differ from other non-nal volunteers in any substantial way according to usual screening criteria or baseline values. The present study aims to examine factors that may provide the basis for this extreme response. We propose that a preexisting sleep deficit-as manifested by low values on the Multiple Sleep Latency Test (MSLT)-may account for extreme responders. Roth and colleagues (1993) have shown that among normal volunteers screened for a variety of studies, approximately 20 to 25 percent show low (< 6 minutes) MSLT scores on a consistent basis, whereas a like proportion shows consistently high MSLT scores (> 13 minutes). Additionally, studies by this group have indicated that subjects with low MSLT scores may suffer from chronic insufficient sleep (Roth et al., 1993), as further substantiated by the finding that they have consistently higher nocturnal sleep efficiency and that their MSLT scores rise to normal values when sleep is extended (Roehrs et al., 1996). We hypothesize that the short MSLT subjects have a significant long-term sleep deficit that leads to a marked intolerance for sleep deprivation or shift work. We further suggest that this sleep debt may signify an increased sleep need in these individuals that is not met either due to personal preference or to societal pressures (or both). If this speculation is accurate, then we predict that the tolerance for sleep deprivation in such individuals can be increased by "pretreatment" with sleep extension. Thus, the present study is designed to test the following two hypotheses: subjects with nominal sleep patterns who have low MSLT

  2. Individual Differences in Response to Sleep Deprivation: Assessment of Fatigue Following Sleep Loss

    NASA Technical Reports Server (NTRS)

    Carskadon, Mary A.

    1997-01-01

    Previous work has indicated that a small but significant number of participants in sleep deprivation studies or in simulated shift work experiments manifests an exaggerated performance decrement when they reach a critical point in the experiment, usually near the trough of the circadian cycle or the middle of the night. Those who show this exaggerated response do not appear to differ from other normal volunteers in any substantial way according to usual screening criteria or baseline values. The present study aims to examine factors that may provide the basis for this extreme response. We propose that a preexisting sleep deficit-as manifested by low values on the Multiple Sleep Latency Test (MSLT)-may account for extreme responders. Roth and colleagues (1993) have shown that among normal volunteers screened for a variety of studies, approximately 20 to 25 percent show low (< or = 6 minutes) MSLT scores on a consistent basis, whereas a like proportion shows consistently high MSLT scores (> or = 13 minutes). Additionally, studies by this group have indicated that subjects with low MSLT scores may suffer from chronic insufficient sleep (Roth et al., 1993), as further substantiated by the finding that they have consistently higher nocturnal sleep efficiency and that their MSLT scores rise to normal values when sleep is extended (Roehrs et al., 1996). We hypothesize that the short MSLT subjects have a significant long-term sleep deficit that leads to a marked intolerance for sleep deprivation or shift work. We further suggest that this sleep debt may signify an increased sleep need in these individuals that is not met either due to personal preference or to societal pressures (or both). If this speculation is accurate, then we predict that the tolerance for sleep deprivation in such individuals can be increased by "pretreatment" with sleep extension. Thus, the present study is designed to test the following two hypotheses: subjects with nominal sleep patterns who have

  3. Sleep deprivation effects on object discrimination task in zebrafish (Danio rerio).

    PubMed

    Pinheiro-da-Silva, Jaquelinne; Silva, Priscila Fernandes; Nogueira, Marcelo Borges; Luchiari, Ana Carolina

    2017-03-01

    The zebrafish is an ideal vertebrate model for neurobehavioral studies with translational relevance to humans. Many aspects of sleep have been studied, but we still do not understand how and why sleep deprivation alters behavioral and physiological processes. A number of hypotheses suggest its role in memory consolidation. In this respect, the aim of this study was to analyze the effects of sleep deprivation on memory in zebrafish (Danio rerio), using an object discrimination paradigm. Four treatments were tested: control, partial sleep deprivation, total sleep deprivation by light pulses, and total sleep deprivation by extended light. The control group explored the new object more than the known object, indicating clear discrimination. The partially sleep-deprived group explored the new object more than the other object in the discrimination phase, suggesting a certain degree of discriminative performance. By contrast, both total sleep deprivation groups equally explored all objects, regardless of their novelty. It seems that only one night of sleep deprivation is enough to affect discriminative response in zebrafish, indicating its negative impact on cognitive processes. We suggest that this study could be a useful screening tool for cognitive dysfunction and a better understanding of the effect of sleep-wake cycles on cognition.

  4. Circadian modulation of consolidated memory retrieval following sleep deprivation in Drosophila.

    PubMed

    Le Glou, Eric; Seugnet, Laurent; Shaw, Paul J; Preat, Thomas; Goguel, Valérie

    2012-10-01

    Several lines of evidence indicate that sleep plays a critical role in learning and memory. The aim of this study was to evaluate anesthesia resistant memory following sleep deprivation in Drosophila. Four to 16 h after aversive olfactory training, flies were sleep deprived for 4 h. Memory was assessed 24 h after training. Training, sleep deprivation, and memory tests were performed at different times during the day to evaluate the importance of the time of day for memory formation. The role of circadian rhythms was further evaluated using circadian clock mutants. Memory was disrupted when flies were exposed to 4 h of sleep deprivation during the consolidation phase. Interestingly, normal memory was observed following sleep deprivation when the memory test was performed during the 2 h preceding lights-off, a period characterized by maximum wake in flies. We also show that anesthesia resistant memory was less sensitive to sleep deprivation in flies with disrupted circadian rhythms. Our results indicate that anesthesia resistant memory, a consolidated memory less costly than long-term memory, is sensitive to sleep deprivation. In addition, we provide evidence that circadian factors influence memory vulnerability to sleep deprivation and memory retrieval. Taken together, the data show that memories weakened by sleep deprivation can be retrieved if the animals are tested at the optimal circadian time.

  5. Effects of acute sleep deprivation and caffeine supplementation on anaerobic performance.

    PubMed

    Moore, Joss; McDonald, Ciaran; McIntyre, Alan; Carmody, Kevin; Donne, Bernard

    2018-01-01

    Athletes involved in team sports may be subject to varying degrees of sleep deprivation either before or after training and competition. Despite the belief among athletes and coaches of the importance of adequate sleep for ensuing performance, the effect of sleep loss on team-sport anaerobic performance remains unclear. There is conflicting evidence in the scientific literature as to the impact of acute sleep deprivation and caffeine supplementation on anaerobic performance indices. The purpose of this study is to investigate the effect of 24 hours of acute sleep deprivation on anaerobic performance and the effect of caffeine supplementation on anaerobic performance in the sleep deprived state. 11 club level games players (n=11, 25±4 yr, 178±7.5 cm, 80.2±10.4 kg, 15.1±5.6% body fat) participated in a repeated measures double-blinded placebo control trial. Following familiarisation, each participant returned for testing on three separate occasions. One of the testing sessions took place following a night of normal sleep and the other two sessions took place following 24 hours of sleep deprivation with supplementation of either placebo or 6 mg.kg- 1 of caffeine. During each testing session participants performed the vertical jump height, 20-m straight sprint, Illinois speed agility test and 5-m shuttle run. No significant differences were detected comparing non sleep deprived and sleep deprived interventions in any of the assessed outcome measures. There were also no significant differences observed in any of the outcome measures when comparing caffeine and placebo data in the sleep deprived state. In this cohort of athletes, a 24-h period of acute sleep deprivation did not have any significant impact on anaerobic performance. Caffeine also did not have any effect of on anaerobic performance in the sleep-deprived state.

  6. Psychological Effect of an Analogue Traumatic Event Reduced by Sleep Deprivation

    PubMed Central

    Porcheret, Kate; Holmes, Emily A.; Goodwin, Guy M.; Foster, Russell G.; Wulff, Katharina

    2015-01-01

    Study Objective: To examine the effect of sleep deprivation compared to sleep, immediately after experimental trauma stimuli on the development of intrusive memories to that trauma stimuli. Design: Participants were exposed to a film with traumatic content (trauma film). The immediate response to the trauma film was assessed, followed by either total sleep deprivation (sleep deprived group, N = 20) or sleep as usual (sleep group, N = 22). Twelve hours after the film viewing the initial psychological effect of the trauma film was measured and for the subsequent 6 days intrusive emotional memories related to the trauma film were recorded in daily life. Setting: Academic sleep laboratory and participants' home environment. Participants: Healthy paid volunteers. Measurements and results: On the first day after the trauma film, the psychological effect as assessed by the Impact of Event Scale – Revised was lower in the sleep deprived group compared to the sleep group. In addition, the sleep deprived group reported fewer intrusive emotional memories (mean 2.28, standard deviation [SD] 2.91) compared to the sleep group (mean 3.76, SD 3.35). Because habitual sleep/circadian patterns, psychological health, and immediate effect of the trauma film were similar at baseline for participants of both groups, the results cannot be accounted for by pre-existing inequalities between groups. Conclusions: Our findings suggest that sleep deprivation on one night, rather than sleeping, reduces emotional effect and intrusive memories following exposure to experimental trauma. Citation: Porcheret K, Holmes EA, Goodwin GM, Foster RG, Wulff K. Psychological effect of an analogue traumatic event reduced by sleep deprivation. SLEEP 2015;38(7):1017–1025. PMID:26118556

  7. Psychological Effect of an Analogue Traumatic Event Reduced by Sleep Deprivation.

    PubMed

    Porcheret, Kate; Holmes, Emily A; Goodwin, Guy M; Foster, Russell G; Wulff, Katharina

    2015-07-01

    To examine the effect of sleep deprivation compared to sleep, immediately after experimental trauma stimuli on the development of intrusive memories to that trauma stimuli. Participants were exposed to a film with traumatic content (trauma film). The immediate response to the trauma film was assessed, followed by either total sleep deprivation (sleep deprived group, N = 20) or sleep as usual (sleep group, N = 22). Twelve hours after the film viewing the initial psychological effect of the trauma film was measured and for the subsequent 6 days intrusive emotional memories related to the trauma film were recorded in daily life. Academic sleep laboratory and participants' home environment. Healthy paid volunteers. On the first day after the trauma film, the psychological effect as assessed by the Impact of Event Scale - Revised was lower in the sleep deprived group compared to the sleep group. In addition, the sleep deprived group reported fewer intrusive emotional memories (mean 2.28, standard deviation [SD] 2.91) compared to the sleep group (mean 3.76, SD 3.35). Because habitual sleep/circadian patterns, psychological health, and immediate effect of the trauma film were similar at baseline for participants of both groups, the results cannot be accounted for by pre-existing inequalities between groups. Our findings suggest that sleep deprivation on one night, rather than sleeping, reduces emotional effect and intrusive memories following exposure to experimental trauma. © 2015 Associated Professional Sleep Societies, LLC.

  8. Effects of Acute Sleep Deprivation Resulting from Night Shift Work on Young Doctors.

    PubMed

    Sanches, Inês; Teixeira, Fátima; dos Santos, José Moutinho; Ferreira, António Jorge

    2015-01-01

    To evaluate sleep deprivation and its effects on young physicians in relation to concentration capacity and psychomotor performance. Eighteen physicians aged 26 - 33 years were divided into 2 groups: non-sleep deprived group (with no night work) and sleep deprived group (minimum 12 hour of night work/week). We applied Pittsburgh Sleep Quality Index to screen the presence of sleep pathology and Epworth Sleepiness Scale to evaluate subjective daytime sleepiness; we used actigraphy and sleep diary to assess sleep hygiene and standard sleep-wake cycles. To demonstrate the effects of sleep deprivation, we applied Toulouse-Piéron's test (concentration test) and a battery of three reaction time tasks after the night duty. Sleep deprived group had higher daytime sleepiness on Epworth Sleepiness Scale (p < 0.05) and during week sleep deprivation was higher (p < 0.010). The mean duration of sleep during the period of night duty was 184.2 minutes to sleep deprived group and 397.7 minutes to non-sleep deprived group (p < 0.001). In the Toulouse-Piéron's test, the sleep deprived group had more omissions (p < 0.05) with a poorer result in concentration (p < 0.05). Psychomotor tests that evaluated response to simple stimuli revealed longer response latency (p < 0.05) and more errors (p < 0.05) in Sleep deprived group; in reaction to instruction test the sleep deprived group showed worse perfection index (p < 0.05); in the fine movements test there was no statistically significant difference between the groups. Acute sleep deprivation resulting from nocturnal work in medical professions is associated with a reduction in attention and concentration and delayed response to stimuli. This may compromise patient care as well as the physician's health and quality of life. It is essential to study the effects of acute sleep deprivation on the cognitive abilities and performance of health professionals.

  9. Resident Performance and Sleep Deprivation: A Review.

    ERIC Educational Resources Information Center

    Asken, Michael J.; Raham, David C.

    1983-01-01

    A review of the literature on resident performance and sleep deprivation suggests that current research is sparse and inconclusive, and existing research suggests potentially severe negative effects. It is proposed that justifications for sleep-depriving night call schedules remain untested, and their use as part of residency training should be…

  10. Total sleep deprivation does not significantly degrade semantic encoding.

    PubMed

    Honn, K A; Grant, D A; Hinson, J M; Whitney, P; Van Dongen, Hpa

    2018-01-17

    Sleep deprivation impairs performance on cognitive tasks, but it is unclear which cognitive processes it degrades. We administered a semantic matching task with variable stimulus onset asynchrony (SOA) and both speeded and self-paced trial blocks. The task was administered at the baseline and 24 hours later after 30.8 hours of total sleep deprivation (TSD) or matching well-rested control. After sleep deprivation, the 20% slowest response times (RTs) were significantly increased. However, the semantic encoding time component of the RTs remained at baseline level. Thus, the performance impairment induced by sleep deprivation on this task occurred in cognitive processes downstream of semantic encoding.

  11. The Effects of Sleep Deprivation on Soccer Skills.

    PubMed

    Pallesen, Ståle; Gundersen, Hilde Stokvold; Kristoffersen, Morten; Bjorvatn, Bjørn; Thun, Eirunn; Harris, Anette

    2017-08-01

    Many athletes sleep poorly due to stress, travel, and competition anxiety. In the present study, we investigated the effects of sleep deprivation on soccer skills (juggling, dribbling, ball control, continuous kicking, 20 and 40 m sprint, and 30 m sprint with changes of direction). In all, 19 male junior soccer players (14-19 years old) were recruited and participated in a cross-balanced experimental study comprising two conditions; habitual sleep and 24 hours sleep deprivation. In both conditions, testing took place between 8 a.m. and 10 a.m. Order of tests was counterbalanced. Each test was conducted once or twice in a sequence repeated three times. The results revealed a negative effect of sleep deprivation on the continuous kicking test. On one test, 30 meter sprint with directional changes, a significant condition × test repetition interaction was found, indicating a steeper learning curve in the sleep deprived condition from Test 1 to Test 2 and a steeper learning curve in the rested condition from Test 2 to Test 3. The results are discussed in terms of limitations and strengths, and recommendations for future studies are outlined.

  12. Genomic analysis of sleep deprivation reveals translational regulation in the hippocampus.

    PubMed

    Vecsey, Christopher G; Peixoto, Lucia; Choi, Jennifer H K; Wimmer, Mathieu; Jaganath, Devan; Hernandez, Pepe J; Blackwell, Jennifer; Meda, Karuna; Park, Alan J; Hannenhalli, Sridhar; Abel, Ted

    2012-10-17

    Sleep deprivation is a common problem of considerable health and economic impact in today's society. Sleep loss is associated with deleterious effects on cognitive functions such as memory and has a high comorbidity with many neurodegenerative and neuropsychiatric disorders. Therefore, it is crucial to understand the molecular basis of the effect of sleep deprivation in the brain. In this study, we combined genome-wide and traditional molecular biological approaches to determine the cellular and molecular impacts of sleep deprivation in the mouse hippocampus, a brain area crucial for many forms of memory. Microarray analysis examining the effects of 5 h of sleep deprivation on gene expression in the mouse hippocampus found 533 genes with altered expression. Bioinformatic analysis revealed that a prominent effect of sleep deprivation was to downregulate translation, potentially mediated through components of the insulin signaling pathway such as the mammalian target of rapamycin (mTOR), a key regulator of protein synthesis. Consistent with this analysis, sleep deprivation reduced levels of total and phosphorylated mTOR, and levels returned to baseline after 2.5 h of recovery sleep. Our findings represent the first genome-wide analysis of the effects of sleep deprivation on the mouse hippocampus, and they suggest that the detrimental effects of sleep deprivation may be mediated by reductions in protein synthesis via downregulation of mTOR. Because protein synthesis and mTOR activation are required for long-term memory formation, our study improves our understanding of the molecular mechanisms underlying the memory impairments induced by sleep deprivation.

  13. Sleep deprivation leads to mood deficits in healthy adolescents.

    PubMed

    Short, Michelle A; Louca, Mia

    2015-08-01

    The objectives of the study were to investigate the effects of 36 h of sleep deprivation on the discrete mood states of anger, depression, anxiety, confusion, fatigue, and vigour in healthy adolescents. Twelve healthy adolescent good sleepers (six male), aged 14-18 years (M = 16.17, standard deviation (SD) = 0.83), spent three consecutive nights in the sleep laboratory of the Centre for Sleep Research: two baseline nights with 10-h sleep opportunities and one night of total sleep deprivation. Every 2 h during wakefulness, they completed the Profile of Mood States - Short Form. Mood across two baseline days was compared to mood at the same clock time (0900 h to 1900 h) following one night without sleep. The subscales of depression, anger, confusion, anxiety, vigour, and fatigue were compared across days. All mood states significantly worsened following one night without sleep. Females showed a greater vulnerability to mood deficits following sleep loss, with greater depressed mood and anxiety following sleep deprivation only witnessed among female participants. While both males and females reported more confusion following sleep deprivation, the magnitude of this effect was greater for females. This study provides empirical support for the notion that sleep loss can causally affect mood states in healthy adolescents, with females having heightened vulnerability. Understanding the detrimental effects of insufficient sleep during adolescence is important, as it is a stage where sleep loss and mood dysregulation are highly prevalent. These findings escalate the importance of promoting sleep for the well-being of adolescents at this critical life phase. Copyright © 2015 Elsevier B.V. All rights reserved.

  14. Effect of 24 hours of sleep deprivation on auditory and linguistic perception: a comparison among young controls, sleep-deprived participants, dyslexic readers, and aging adults.

    PubMed

    Fostick, Leah; Babkoff, Harvey; Zukerman, Gil

    2014-06-01

    To test the effects of 24 hr of sleep deprivation on auditory and linguistic perception and to assess the magnitude of this effect by comparing such performance with that of aging adults on speech perception and with that of dyslexic readers on phonological awareness. Fifty-five sleep-deprived young adults were compared with 29 aging adults (older than 60 years) and with 18 young controls on auditory temporal order judgment (TOJ) and on speech perception tasks (Experiment 1). The sleep deprived were also compared with 51 dyslexic readers and with the young controls on TOJ and phonological awareness tasks (One-Minute Test for Pseudowords, Phoneme Deletion, Pig Latin, and Spoonerism; Experiment 2). Sleep deprivation resulted in longer TOJ thresholds, poorer speech perception, and poorer nonword reading compared with controls. The TOJ thresholds of the sleep deprived were comparable to those of the aging adults, but their pattern of speech performance differed. They also performed better on TOJ and phonological awareness than dyslexic readers. A variety of linguistic skills are affected by sleep deprivation. The comparison of sleep-deprived individuals with other groups with known difficulties in these linguistic skills might suggest that different groups exhibit common difficulties.

  15. The cumulative cost of additional wakefulness: dose-response effects on neurobehavioral functions and sleep physiology from chronic sleep restriction and total sleep deprivation

    NASA Technical Reports Server (NTRS)

    Van Dongen, Hans P A.; Maislin, Greg; Mullington, Janet M.; Dinges, David F.

    2003-01-01

    OBJECTIVES: To inform the debate over whether human sleep can be chronically reduced without consequences, we conducted a dose-response chronic sleep restriction experiment in which waking neurobehavioral and sleep physiological functions were monitored and compared to those for total sleep deprivation. DESIGN: The chronic sleep restriction experiment involved randomization to one of three sleep doses (4 h, 6 h, or 8 h time in bed per night), which were maintained for 14 consecutive days. The total sleep deprivation experiment involved 3 nights without sleep (0 h time in bed). Each study also involved 3 baseline (pre-deprivation) days and 3 recovery days. SETTING: Both experiments were conducted under standardized laboratory conditions with continuous behavioral, physiological and medical monitoring. PARTICIPANTS: A total of n = 48 healthy adults (ages 21-38) participated in the experiments. INTERVENTIONS: Noctumal sleep periods were restricted to 8 h, 6 h or 4 h per day for 14 days, or to 0 h for 3 days. All other sleep was prohibited. RESULTS: Chronic restriction of sleep periods to 4 h or 6 h per night over 14 consecutive days resulted in significant cumulative, dose-dependent deficits in cognitive performance on all tasks. Subjective sleepiness ratings showed an acute response to sleep restriction but only small further increases on subsequent days, and did not significantly differentiate the 6 h and 4 h conditions. Polysomnographic variables and delta power in the non-REM sleep EEG-a putative marker of sleep homeostasis--displayed an acute response to sleep restriction with negligible further changes across the 14 restricted nights. Comparison of chronic sleep restriction to total sleep deprivation showed that the latter resulted in disproportionately large waking neurobehavioral and sleep delta power responses relative to how much sleep was lost. A statistical model revealed that, regardless of the mode of sleep deprivation, lapses in behavioral alertness

  16. Sleep deprivation compromises resting-state emotional regulatory processes: An EEG study.

    PubMed

    Zhang, Jinxiao; Lau, Esther Yuet Ying; Hsiao, Janet H

    2018-03-01

    Resting-state spontaneous neural activities consume far more biological energy than stimulus-induced activities, suggesting their significance. However, existing studies of sleep loss and emotional functioning have focused on how sleep deprivation modulates stimulus-induced emotional neural activities. The current study aimed to investigate the impacts of sleep deprivation on the brain network of emotional functioning using electroencephalogram during a resting state. Two established resting-state electroencephalogram indexes (i.e. frontal alpha asymmetry and frontal theta/beta ratio) were used to reflect the functioning of the emotion regulatory neural network. Participants completed an 8-min resting-state electroencephalogram recording after a well-rested night or 24 hr sleep deprivation. The Sleep Deprivation group had a heightened ratio of the power density in theta band to beta band (theta/beta ratio) in the frontal area than the Sleep Control group, suggesting an effective approach with reduced frontal cortical regulation of subcortical drive after sleep deprivation. There was also marginally more left-lateralized frontal alpha power (left frontal alpha asymmetry) in the Sleep Deprivation group compared with the Sleep Control group. Besides, higher theta/beta ratio and more left alpha lateralization were correlated with higher sleepiness and lower vigilance. The results converged in suggesting compromised emotional regulatory processes during resting state after sleep deprivation. Our work provided the first resting-state neural evidence for compromised emotional functioning after sleep loss, highlighting the significance of examining resting-state neural activities within the affective brain network as a default functional mode in investigating the sleep-emotion relationship. © 2018 European Sleep Research Society.

  17. Effects of Acute Sleep Deprivation on Motor and Reversal Learning in Mice

    PubMed Central

    Varga, Andrew W.; Kang, Mihwa; Ramesh, Priyanka V.; Klann, Eric

    2014-01-01

    Sleep supports the formation of a variety of declarative and non-declarative memories, and sleep deprivation often impairs these types of memories. In human subjects, natural sleep either during a nap or overnight leads to long-lasting improvements in visuomotor and fine motor tasks, but rodent models recapitulating these findings have been scarce. Here we present evidence that 5 hours of acute sleep deprivation impairs mouse skilled reach learning compared to a matched period of ad libitum sleep. In sleeping mice, the duration of total sleep time during the 5 hours of sleep opportunity or during the first bout of sleep did not correlate with ultimate gain in motor performance. In addition, we observed that reversal learning during the skilled reaching task was also affected by sleep deprivation. Consistent with this observation, 5 hours of sleep deprivation also impaired reversal learning in the water-based Y-maze. In conclusion, acute sleep deprivation negatively impacts subsequent motor and reversal learning and memory. PMID:25046627

  18. Acute Sleep Deprivation Blocks Short- and Long-Term Operant Memory in Aplysia.

    PubMed

    Krishnan, Harini C; Gandour, Catherine E; Ramos, Joshua L; Wrinkle, Mariah C; Sanchez-Pacheco, Joseph J; Lyons, Lisa C

    2016-12-01

    Insufficient sleep in individuals appears increasingly common due to the demands of modern work schedules and technology use. Consequently, there is a growing need to understand the interactions between sleep deprivation and memory. The current study determined the effects of acute sleep deprivation on short and long-term associative memory using the marine mollusk Aplysia californica , a relatively simple model system well known for studies of learning and memory. Aplysia were sleep deprived for 9 hours using context changes and tactile stimulation either prior to or after training for the operant learning paradigm, learning that food is inedible (LFI). The effects of sleep deprivation on short-term (STM) and long-term memory (LTM) were assessed. Acute sleep deprivation prior to LFI training impaired the induction of STM and LTM with persistent effects lasting at least 24 h. Sleep deprivation immediately after training blocked the consolidation of LTM. However, sleep deprivation following the period of molecular consolidation did not affect memory recall. Memory impairments were independent of handling-induced stress, as daytime handled control animals demonstrated no memory deficits. Additional training immediately after sleep deprivation failed to rescue the induction of memory, but additional training alleviated the persistent impairment in memory induction when training occurred 24 h following sleep deprivation. Acute sleep deprivation inhibited the induction and consolidation, but not the recall of memory. These behavioral studies establish Aplysia as an effective model system for studying the interactions between sleep and memory formation. © 2016 Associated Professional Sleep Societies, LLC.

  19. Acute Sleep Deprivation Blocks Short- and Long-Term Operant Memory in Aplysia

    PubMed Central

    Krishnan, Harini C.; Gandour, Catherine E.; Ramos, Joshua L.; Wrinkle, Mariah C.; Sanchez-Pacheco, Joseph J.; Lyons, Lisa C.

    2016-01-01

    Study Objectives: Insufficient sleep in individuals appears increasingly common due to the demands of modern work schedules and technology use. Consequently, there is a growing need to understand the interactions between sleep deprivation and memory. The current study determined the effects of acute sleep deprivation on short and long-term associative memory using the marine mollusk Aplysia californica, a relatively simple model system well known for studies of learning and memory. Methods: Aplysia were sleep deprived for 9 hours using context changes and tactile stimulation either prior to or after training for the operant learning paradigm, learning that food is inedible (LFI). The effects of sleep deprivation on short-term (STM) and long-term memory (LTM) were assessed. Results: Acute sleep deprivation prior to LFI training impaired the induction of STM and LTM with persistent effects lasting at least 24 h. Sleep deprivation immediately after training blocked the consolidation of LTM. However, sleep deprivation following the period of molecular consolidation did not affect memory recall. Memory impairments were independent of handling-induced stress, as daytime handled control animals demonstrated no memory deficits. Additional training immediately after sleep deprivation failed to rescue the induction of memory, but additional training alleviated the persistent impairment in memory induction when training occurred 24 h following sleep deprivation. Conclusions: Acute sleep deprivation inhibited the induction and consolidation, but not the recall of memory. These behavioral studies establish Aplysia as an effective model system for studying the interactions between sleep and memory formation. Citation: Krishnan HC, Gandour CE, Ramos JL, Wrinkle MC, Sanchez-Pacheco JJ, Lyons LC. Acute sleep deprivation blocks short- and long-term operant memory in Aplysia. SLEEP 2016;39(12):2161–2171. PMID:27748243

  20. Estradiol and Progesterone Modulate Spontaneous Sleep Patterns and Recovery from Sleep Deprivation in Ovariectomized Rats

    PubMed Central

    Deurveilher, Samüel; Rusak, Benjamin; Semba, Kazue

    2009-01-01

    Study Objectives: Women undergo hormonal changes both naturally during their lives and as a result of sex hormone treatments. The objective of this study was to gain more knowledge about how these hormones affect sleep and responses to sleep loss. Design: Rats were ovariectomized and implanted subcutaneously with Silastic capsules containing oil vehicle, 17β-estradiol and/or progesterone. After 2 weeks, sleep/wake states were recorded during a 24-h baseline period, 6 h of total sleep deprivation induced by gentle handling during the light phase, and an 18-h recovery period. Measurements and Results: At baseline and particularly in the dark phase, ovariectomized rats treated with estradiol or estradiol plus progesterone spent more time awake at the expense of non-rapid eye movement sleep (NREMS) and/or REMS, whereas those given progesterone alone spent less time in REMS than ovariectomized rats receiving no hormones. Following sleep deprivation, all rats showed rebound increases in NREMS and REMS, but the relative increase in REMS was larger in females receiving hormones, especially high estradiol. In contrast, the normal increase in NREMS EEG delta power (an index of NREMS intensity) during recovery was attenuated by all hormone treatments. Conclusions: Estradiol promotes arousal in the active phase in sleep-satiated rats, but after sleep loss, both estradiol and progesterone selectively facilitate REMS rebound while reducing NREMS intensity. These results indicate that effects of ovarian hormones on recovery sleep differ from those on spontaneous sleep. The hormonal modulation of recovery sleep architecture may affect recovery of sleep related functions after sleep loss. Citation: Deurveilher S; Rusak B; Semba K. Estradiol and progesterone modulate spontaneous sleep patterns and recovery from sleep deprivation in ovariectomized rats. SLEEP 2009;32(7):865-877. PMID:19639749

  1. The Effects of Sleep Deprivation on Dissociable Prototype Learning Systems

    PubMed Central

    Maddox, W. Todd; Glass, Brian D.; Zeithamova, Dagmar; Savarie, Zachary R.; Bowen, Christopher; Matthews, Michael D.; Schnyer, David M.

    2011-01-01

    Background: The cognitive neural underpinnings of prototype learning are becoming clear. Evidence points to 2 different neural systems, depending on the learning parameters. A/not-A (AN) prototype learning is mediated by posterior brain regions that are involved in early perceptual learning, whereas A/B (AB) is mediated by frontal and medial temporal lobe regions. Study Objectives: To investigate the effects of sleep deprivation on AN and AB prototype learning and to use established prototype models to provide insights into the cognitive-processing locus of sleep-deprivation deficits. Design: Participants performed an AN and an AB prototype learning task twice, separated by a 24-hour period, with or without sleep between testing sessions. Participants: Eighteen West Point cadets participated in the sleep-deprivation group, and 17 West Point cadets participated in a control group. Measurements and Results: Sleep deprivation led to an AN, but not an AB, performance deficit. Prototype model analyses indicated that the AN deficit was due to changes in attentional focus and a decrease in confidence that is reflected in an increased bias to respond non-A. Conclusions: The findings suggest that AN, but not AB, prototype learning is affected by sleep deprivation. Prototype model analyses support the notion that the effect of sleep deprivation on AN is consistent with lapses in attentional focus that are more detrimental to AN than to AB. This finding adds to a growing body of work that suggests that different performance changes associated with sleep deprivation can be attributed to a common mechanism of changes in simple attention and vigilance. Citation: Maddox WT; Glass BD; Zeithamova D; Savarie ZR; Bowen C; Matthews MD; Schnyer DM. The effects of sleep deprivation on dissociable prototype learning systems. SLEEP 2011;34(3):253-260. PMID:21358842

  2. Free Recall of Word Lists under Total Sleep Deprivation and after Recovery Sleep

    PubMed Central

    de Almeida Valverde Zanini, Gislaine; Tufik, Sérgio; Andersen, Monica Levy; da Silva, Raquel Cristina Martins; Bueno, Orlando Francisco Amodeo; Rodrigues, Camila Cruz; Pompéia, Sabine

    2012-01-01

    Study Objectives: One task that has been used to assess memory effects of prior total sleep deprivation (TSD) is the immediate free recall of word lists; however, results have been mixed. A possible explanation for this is task impurity, since recall of words from different serial positions reflects use of distinct types of memory (last words: short-term memory; first and intermediate words: episodic memory). Here we studied the effects of 2 nights of TSD on immediate free recall of semantically unrelated word lists considering the serial position curve. Design: Random allocation to a 2-night TSD protocol followed by one night of recovery sleep or to a control group. Setting: Study conducted under continuous behavioral monitoring. Participants: 24 young, healthy male volunteers. Intervention: 2 nights of total sleep deprivation (TSD) and one night of recovery sleep. Measurements and Results: Participants were shown five 15 unrelated word-lists at baseline, after one and 2 nights of TSD, and after one night of recovery sleep. We also investigated the development of recall strategies (learning) and susceptibility to interference from previous lists. No free recall impairment occurred during TSD, irrespective of serial position. Interference was unchanged. Both groups developed recall strategies, but task learning occurred earlier in controls and was evident in the TSD group only after sleep recovery. Conclusion: Prior TSD spared episodic memory, short-term phonological memory, and interference, allowed the development of recall strategies, but may have decreased the advantage of using these strategies, which returned to normal after recovery sleep. Citation: Zanini GAV; Tufik S; Andersen ML; da Silva RCM; Bueno OFA; Rodrigues CC; Pompéia S. Free recall of word lists under total sleep deprivation and after recovery sleep. SLEEP 2012;35(2):223-230. PMID:22294812

  3. Stationary gaze entropy predicts lane departure events in sleep-deprived drivers.

    PubMed

    Shiferaw, Brook A; Downey, Luke A; Westlake, Justine; Stevens, Bronwyn; Rajaratnam, Shantha M W; Berlowitz, David J; Swann, Phillip; Howard, Mark E

    2018-02-02

    Performance decrement associated with sleep deprivation is a leading contributor to traffic accidents and fatalities. While current research has focused on eye blink parameters as physiological indicators of driver drowsiness, little is understood of how gaze behaviour alters as a result of sleep deprivation. In particular, the effect of sleep deprivation on gaze entropy has not been previously examined. In this randomised, repeated measures study, 9 (4 male, 5 female) healthy participants completed two driving sessions in a fully instrumented vehicle (1 after a night of sleep deprivation and 1 after normal sleep) on a closed track, during which eye movement activity and lane departure events were recorded. Following sleep deprivation, the rate of fixations reduced while blink rate and duration as well as saccade amplitude increased. In addition, stationary and transition entropy of gaze also increased following sleep deprivation as well as with amount of time driven. An increase in stationary gaze entropy in particular was associated with higher odds of a lane departure event occurrence. These results highlight how fatigue induced by sleep deprivation and time-on-task effects can impair drivers' visual awareness through disruption of gaze distribution and scanning patterns.

  4. Lithium Prevents REM Sleep Deprivation-Induced Impairments on Memory Consolidation

    PubMed Central

    Ota, Simone M.; Moreira, Karin Di Monteiro; Suchecki, Deborah; Oliveira, Maria Gabriela M.; Tiba, Paula A.

    2013-01-01

    Background: Pre-training rapid eye movement sleep (REMS) deprivation affects memory acquisition and/or consolidation. It also produces major REMS rebound at the cost of waking and slow wave sleep (SWS). Given that both SWS and REMS appear to be important for memory processes, REMS rebound after training may disrupt the organization of sleep cycles, i.e., excessive amount of REMS and/or little SWS after training could be harmful for memory formation. Objective: To examine whether lithium, a drug known to increase SWS and reduce REMS, could prevent the memory impairment induced by pre-training sleep deprivation. Design: Animals were divided in 2 groups: cage control (CC) and REMS-deprived (REMSDep), and then subdivided into 4 subgroups, treated either with vehicle or 1 of 3 doses of lithium (50, 100, and 150 mg/kg) 2 h before training on the multiple trial inhibitory avoidance task. Animals were tested 48 h later to make sure that the drug had been already metabolized and eliminated. Another set of animals was implanted with electrodes and submitted to the same experimental protocol for assessment of drug-induced sleep-wake changes. Subjects: Wistar male rats weighing 300-400 g. Results: Sleep deprived rats required more trials to learn the task and still showed a performance deficit during test, except from those treated with 150 mg/kg of lithium, which also reduced the time spent in REM sleep during sleep recovery. Conclusion: Lithium reduced rapid eye movement sleep and prevented memory impairment induced by sleep deprivation. These results indicate that these phenomena may be related, but cause-effect relationship cannot be ascertained. Citation: Ota SM; Moreira KDM; Suchecki D; Oliveira MGM; Tiba PA. Lithium prevents REM sleep deprivation-induced impairments on memory consolidation. SLEEP 2013;36(11):1677-1684. PMID:24179301

  5. Uncoupling proteins and sleep deprivation.

    PubMed

    Cirelli, C; Tononi, G

    2004-07-01

    In both humans and animals sleep deprivation (SD) produces an increase in food intake and in energy expenditure (EE). The increase in EE is a core element of the SD syndrome and, in rats, is negatively correlated with survival rate. However, the mechanisms involved are not understood. A large component of resting EE is accounted for by the mitochondrial proton leak, which is mediated by uncoupling proteins (UCPs). We measured UCP2, UCP3, and UCP5 mRNA levels in rats during the spontaneous sleep/waking cycle and after short (8 hours) and long (7 days) SD. During spontaneous sleep and waking there was no change in the level of mitochondrial uncoupling as measured by UCPs expression, either in the brain or in peripheral tissues. During SD, by contrast, UCP3 expression in skeletal muscle was elevated, but the increase was similar, compared to sleep, after both short-term and long-term SD. UCP2 expression, on the other hand, was strongly increased in the liver and skeletal muscle of long-term sleep deprived animals and much less so, or not at all, in yoked controls or in rats that lost only 8 hours of sleep. Since the skeletal muscle is the largest tissue in the body, an elevated muscular expression of UCP2 is likely to affect the overall resting EE and may thus contribute to its increase after SD.

  6. Effects of acute sleep deprivation on motor and reversal learning in mice.

    PubMed

    Varga, Andrew W; Kang, Mihwa; Ramesh, Priyanka V; Klann, Eric

    2014-10-01

    Sleep supports the formation of a variety of declarative and non-declarative memories, and sleep deprivation often impairs these types of memories. In human subjects, natural sleep either during a nap or overnight leads to long-lasting improvements in visuomotor and fine motor tasks, but rodent models recapitulating these findings have been scarce. Here we present evidence that 5h of acute sleep deprivation impairs mouse skilled reach learning compared to a matched period of ad libitum sleep. In sleeping mice, the duration of total sleep time during the 5h of sleep opportunity or during the first bout of sleep did not correlate with ultimate gain in motor performance. In addition, we observed that reversal learning during the skilled reaching task was also affected by sleep deprivation. Consistent with this observation, 5h of sleep deprivation also impaired reversal learning in the water-based Y-maze. In conclusion, acute sleep deprivation negatively impacts subsequent motor and reversal learning and memory. Copyright © 2014 Elsevier Inc. All rights reserved.

  7. Increased Automaticity and Altered Temporal Preparation Following Sleep Deprivation

    PubMed Central

    Kong, Danyang; Asplund, Christopher L.; Ling, Aiqing; Chee, Michael W.L.

    2015-01-01

    Study Objectives: Temporal expectation enables us to focus limited processing resources, thereby optimizing perceptual and motor processing for critical upcoming events. We investigated the effects of total sleep deprivation (TSD) on temporal expectation by evaluating the foreperiod and sequential effects during a psychomotor vigilance task (PVT). We also examined how these two measures were modulated by vulnerability to TSD. Design: Three 10-min visual PVT sessions using uniformly distributed foreperiods were conducted in the wake-maintenance zone the evening before sleep deprivation (ESD) and three more in the morning following approximately 22 h of TSD. TSD vulnerable and nonvulnerable groups were determined by a tertile split of participants based on the change in the number of behavioral lapses recorded during ESD and TSD. A subset of participants performed six additional 10-min modified auditory PVTs with exponentially distributed foreperiods during rested wakefulness (RW) and TSD to test the effect of temporal distribution on foreperiod and sequential effects. Setting: Sleep laboratory. Participants: There were 172 young healthy participants (90 males) with regular sleep patterns. Nineteen of these participants performed the modified auditory PVT. Measurements and Results: Despite behavioral lapses and slower response times, sleep deprived participants could still perceive the conditional probability of temporal events and modify their level of preparation accordingly. Both foreperiod and sequential effects were magnified following sleep deprivation in vulnerable individuals. Only the foreperiod effect increased in nonvulnerable individuals. Conclusions: The preservation of foreperiod and sequential effects suggests that implicit time perception and temporal preparedness are intact during total sleep deprivation. Individuals appear to reallocate their depleted preparatory resources to more probable event timings in ongoing trials, whereas vulnerable

  8. Flurbiprofen in rapid eye movement sleep deprivation induced hyperalgesia.

    PubMed

    Gürel, Elif Ezgi; Ural, Keremcan; Öztürk, Gülnur; Öztürk, Levent

    2014-04-10

    Rapid eye movement (REM) sleep deprivation induces hyperalgesia in healthy rats. Here, we evaluated the effects of flurbiprofen, an anti-inflammatory and neuroprotective agent, on the increased thermal responses observed in REM sleep deprived rats. Forty female rats were divided into four groups following 96-hour REM sleep deprivation: intraperitoneal injections of placebo, and flurbiprofen 5 mg/kg, 15 mg/kg and 40 mg/kg were made in CONT (n=10), FBP5, FBP15 and FBP40 groups respectively. Pain threshold measurements were performed three times at baseline (0.hour), at the end of REM sleep deprivation (96.hour) and at 1 h after injections (97.hour) by hot plate and tail-flick tests. REM sleep deprivation induced a significant decrease in pain thresholds of all rats (hotplate: 0.hour vs 96.hour, 9.75±2.85 vs 5.10±2.02, p<0.001; tail flick: 0.hour vs 96.hour, 11.92±4.62 vs 7.92±5.15, p<0.001). Flurbiprofen in 15 mg/kg and 40 mg/kg doses significantly improved pain tolerance measured by tail flick test (tail flick in FBP15 and FBP40 groups: 96.hour vs 97.hour, 7.01±4.97 vs 8.34±3.61 and 5.06±1.57 vs 7.04±2.49, p<0.05 for both). 96 h of REM sleep deprivation resulted in reduced pain thresholds in both hot plate and tail flick tests. Flurbiprofen was used for the first time in a rat model of REM sleep deprivation, and it provided anti-nociceptive effects in 15 mg/kg and 40 mg/kg doses. Flurbiprofen may have the potential for treatment of painful syndromes accompanying insomnia or sleep loss. Copyright © 2014 Elsevier Inc. All rights reserved.

  9. Sleep deprivation alters gene expression and antioxidant enzyme activity in mice splenocytes.

    PubMed

    Lungato, L; Marques, M S; Pereira, V G; Hix, S; Gazarini, M L; Tufik, S; D'Almeida, V

    2013-03-01

    Cellular defence against the formation of reactive oxygen species (ROS) involves a number of mechanisms in which antioxidant enzymes such as catalase (CAT) and superoxide dismutase (SOD) play an important role. The relation between sleep deprivation and oxidative stress has not yet been completely elucidated. Although some authors did not find evidence of this relationship, others found alterations in some oxidative stress markers in response to sleep deprivation. Thus, the objective of this study was to identify changes induced by sleep deprivation in the activity and gene expression of antioxidant enzymes in mice splenocytes, ideally corroborating a better understanding of the observed effects related to sleep deprivation, which could be triggered by oxidative imbalance. Splenocytes from mice sleep deprived for 72 h showed no significant difference in CAT and CuZnSOD gene expression compared with normal sleep mice. However, sleep-deprived mice did show higher MnSOD gene expression than the control group. Concerning enzymatic activity, CuZnSOD and MnSOD significantly increased after sleep deprivation, despite the expression in CuZnSOD remained unchanged. Moreover, CAT activity was significantly lower after sleep deprivation. The data suggest that the antioxidant system is triggered by sleep deprivation, which in turn could influence the splenocytes homoeostasis, thus interfering in physiological responses. © 2013 The Authors. Scandinavian Journal of Immunology © 2013 Blackwell Publishing Ltd.

  10. Unsupervised online classifier in sleep scoring for sleep deprivation studies.

    PubMed

    Libourel, Paul-Antoine; Corneyllie, Alexandra; Luppi, Pierre-Hervé; Chouvet, Guy; Gervasoni, Damien

    2015-05-01

    This study was designed to evaluate an unsupervised adaptive algorithm for real-time detection of sleep and wake states in rodents. We designed a Bayesian classifier that automatically extracts electroencephalogram (EEG) and electromyogram (EMG) features and categorizes non-overlapping 5-s epochs into one of the three major sleep and wake states without any human supervision. This sleep-scoring algorithm is coupled online with a new device to perform selective paradoxical sleep deprivation (PSD). Controlled laboratory settings for chronic polygraphic sleep recordings and selective PSD. Ten adult Sprague-Dawley rats instrumented for chronic polysomnographic recordings. The performance of the algorithm is evaluated by comparison with the score obtained by a human expert reader. Online detection of PS is then validated with a PSD protocol with duration of 72 hours. Our algorithm gave a high concordance with human scoring with an average κ coefficient > 70%. Notably, the specificity to detect PS reached 92%. Selective PSD using real-time detection of PS strongly reduced PS amounts, leaving only brief PS bouts necessary for the detection of PS in EEG and EMG signals (4.7 ± 0.7% over 72 h, versus 8.9 ± 0.5% in baseline), and was followed by a significant PS rebound (23.3 ± 3.3% over 150 minutes). Our fully unsupervised data-driven algorithm overcomes some limitations of the other automated methods such as the selection of representative descriptors or threshold settings. When used online and coupled with our sleep deprivation device, it represents a better option for selective PSD than other methods like the tedious gentle handling or the platform method. © 2015 Associated Professional Sleep Societies, LLC.

  11. Sleep Disturbance, Sleep Duration, and Inflammation: A Systematic Review and Meta-Analysis of Cohort Studies and Experimental Sleep Deprivation.

    PubMed

    Irwin, Michael R; Olmstead, Richard; Carroll, Judith E

    2016-07-01

    Sleep disturbance is associated with inflammatory disease risk and all-cause mortality. Here, we assess global evidence linking sleep disturbance, sleep duration, and inflammation in adult humans. A systematic search of English language publications was performed, with inclusion of primary research articles that characterized sleep disturbance and/or sleep duration or performed experimental sleep deprivation and assessed inflammation by levels of circulating markers. Effect sizes (ES) and 95% confidence intervals (CI) were extracted and pooled using a random effect model. A total of 72 studies (n > 50,000) were analyzed with assessment of C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor α (TNFα). Sleep disturbance was associated with higher levels of CRP (ES .12; 95% CI = .05-.19) and IL-6 (ES .20; 95% CI = .08-.31). Shorter sleep duration, but not the extreme of short sleep, was associated with higher levels of CRP (ES .09; 95% CI = .01-.17) but not IL-6 (ES .03; 95% CI: -.09 to .14). The extreme of long sleep duration was associated with higher levels of CRP (ES .17; 95% CI = .01-.34) and IL-6 (ES .11; 95% CI = .02-20). Neither sleep disturbances nor sleep duration was associated with TNFα. Neither experimental sleep deprivation nor sleep restriction was associated with CRP, IL-6, or TNFα. Some heterogeneity among studies was found, but there was no evidence of publication bias. Sleep disturbance and long sleep duration, but not short sleep duration, are associated with increases in markers of systemic inflammation. Copyright © 2016 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

  12. [Effects of chronic partial sleep deprivation on growth and learning/memory in young rats].

    PubMed

    Jiang, Fan; Shen, Xiao-Ming; Li, Sheng-Hui; Cui, Mao-Long; Zhang, Yin; Wang, Cheng; Yu, Xiao-Gang; Yan, Chong-Huai

    2009-02-01

    The effects of sleep deprivation on the immature brain remain unknown. Based on a computer controlled chronic sleep deprivation animal model, the effects of chronic partial sleep deprivation on growth, learning and memory in young rats were explored. Twelve weaned male Spraque-Dawley rats (3-week-old) were randomly divided into sleep deprivation, test control and blank control groups. Sleep deprivation was performed using computer-controlled "disc-over-water" technique at 8-11 am daily, for 14 days. The temperature and weights were measured every 7 days. Morris water maze was used to test spatial learning and memory abilities before and 7 and 14 days after sleep deprivation. After 14 days of sleep deprivation, the rats were sacrificed for weighting their major organs. After 14 days of sleep deprivation, the rats' temperature increased significantly. During the sleep deprivation, the rate of weight gain in the sleep deprivation group was much slower than that in the test control and blank control groups. The thymus of the rats subjected to sleep deprivation was much lighter than that of the blank control group. After 7 days of sleep deprivation, the rats showed slower acquisition of reference memory, but were capable of successfully performing the task by repeated exposure to the test. Such impairment of reference memory was not seen 14 days after sleep deprivation. Chronic sleep deprivation can affect growth of immature rats, as well as their abilities to acquire spatial reference memory.

  13. The effects of sleep deprivation on dissociable prototype learning systems.

    PubMed

    Maddox, W Todd; Glass, Brian D; Zeithamova, Dagmar; Savarie, Zachary R; Bowen, Christopher; Matthews, Michael D; Schnyer, David M

    2011-03-01

    The cognitive neural underpinnings of prototype learning are becoming clear. Evidence points to 2 different neural systems, depending on the learning parameters. A/not-A (AN) prototype learning is mediated by posterior brain regions that are involved in early perceptual learning, whereas A/B (AB) is mediated by frontal and medial temporal lobe regions. To investigate the effects of sleep deprivation on AN and AB prototype learning and to use established prototype models to provide insights into the cognitive-processing locus of sleep-deprivation deficits. Participants performed an AN and an AB prototype learning task twice, separated by a 24-hour period, with or without sleep between testing sessions. Eighteen West Point cadets participated in the sleep-deprivation group, and 17 West Point cadets participated in a control group. Sleep deprivation led to an AN, but not an AB, performance deficit. Prototype model analyses indicated that the AN deficit was due to changes in attentional focus and a decrease in confidence that is reflected in an increased bias to respond non-A. The findings suggest that AN, but not AB, prototype learning is affected by sleep deprivation. Prototype model analyses support the notion that the effect of sleep deprivation on AN is consistent with lapses in attentional focus that are more detrimental to AN than to AB. This finding adds to a growing body of work that suggests that different performance changes associated with sleep deprivation can be attributed to a common mechanism of changes in simple attention and vigilance.

  14. Auditory Evoked Potentials as a Function of Sleep Deprivation and Recovery Sleep

    DTIC Science & Technology

    1985-09-29

    present research: They relate to the effects of: a) 48-hours of sleep deprivation on endogenous event related potentials (ERPs); b) circadian rhythms on...the study were: decreases in amplitude for N2, P3 and N2P3 across the reprivation period; a circadian rhythm was apparent for both ERP recordings and...of cortical evoked response potentials (ERPs)? 2) How do circadian rhythms affect ERPS under conditions of sleep deprivation? 3) How do different

  15. Transiently Increasing cAMP Levels Selectively in Hippocampal Excitatory Neurons during Sleep Deprivation Prevents Memory Deficits Caused by Sleep Loss

    PubMed Central

    Bruinenberg, Vibeke M.; Tudor, Jennifer C.; Ferri, Sarah L.; Baumann, Arnd; Meerlo, Peter

    2014-01-01

    The hippocampus is particularly sensitive to sleep loss. Although previous work has indicated that sleep deprivation impairs hippocampal cAMP signaling, it remains to be determined whether the cognitive deficits associated with sleep deprivation are caused by attenuated cAMP signaling in the hippocampus. Further, it is unclear which cell types are responsible for the memory impairments associated with sleep deprivation. Transgenic approaches lack the spatial resolution to manipulate specific signaling pathways selectively in the hippocampus, while pharmacological strategies are limited in terms of cell-type specificity. Therefore, we used a pharmacogenetic approach based on a virus-mediated expression of a Gαs-coupled Drosophila octopamine receptor selectively in mouse hippocampal excitatory neurons in vivo. With this approach, a systemic injection with the receptor ligand octopamine leads to increased cAMP levels in this specific set of hippocampal neurons. We assessed whether transiently increasing cAMP levels during sleep deprivation prevents memory consolidation deficits associated with sleep loss in an object–location task. Five hours of total sleep deprivation directly following training impaired the formation of object–location memories. Transiently increasing cAMP levels in hippocampal neurons during the course of sleep deprivation prevented these memory consolidation deficits. These findings demonstrate that attenuated cAMP signaling in hippocampal excitatory neurons is a critical component underlying the memory deficits in hippocampus-dependent learning tasks associated with sleep deprivation. PMID:25411499

  16. Lithium prevents REM sleep deprivation-induced impairments on memory consolidation.

    PubMed

    Ota, Simone M; Moreira, Karin Di Monteiro; Suchecki, Deborah; Oliveira, Maria Gabriela M; Tiba, Paula A

    2013-11-01

    Pre-training rapid eye movement sleep (REMS) deprivation affects memory acquisition and/or consolidation. It also produces major REMS rebound at the cost of waking and slow wave sleep (SWS). Given that both SWS and REMS appear to be important for memory processes, REMS rebound after training may disrupt the organization of sleep cycles, i.e., excessive amount of REMS and/or little SWS after training could be harmful for memory formation. To examine whether lithium, a drug known to increase SWS and reduce REMS, could prevent the memory impairment induced by pre-training sleep deprivation. Animals were divided in 2 groups: cage control (CC) and REMS-deprived (REMSDep), and then subdivided into 4 subgroups, treated either with vehicle or 1 of 3 doses of lithium (50, 100, and 150 mg/kg) 2 h before training on the multiple trial inhibitory avoidance task. Animals were tested 48 h later to make sure that the drug had been already metabolized and eliminated. Another set of animals was implanted with electrodes and submitted to the same experimental protocol for assessment of drug-induced sleep-wake changes. Wistar male rats weighing 300-400 g. Sleep deprived rats required more trials to learn the task and still showed a performance deficit during test, except from those treated with 150 mg/kg of lithium, which also reduced the time spent in REM sleep during sleep recovery. Lithium reduced rapid eye movement sleep and prevented memory impairment induced by sleep deprivation. These results indicate that these phenomena may be related, but cause-effect relationship cannot be ascertained.

  17. Quantitative physiologically based modeling of subjective fatigue during sleep deprivation.

    PubMed

    Fulcher, B D; Phillips, A J K; Robinson, P A

    2010-05-21

    A quantitative physiologically based model of the sleep-wake switch is used to predict variations in subjective fatigue-related measures during total sleep deprivation. The model includes the mutual inhibition of the sleep-active neurons in the hypothalamic ventrolateral preoptic area (VLPO) and the wake-active monoaminergic brainstem populations (MA), as well as circadian and homeostatic drives. We simulate sleep deprivation by introducing a drive to the MA, which we call wake effort, to maintain the system in a wakeful state. Physiologically this drive is proposed to be afferent from the cortex or the orexin group of the lateral hypothalamus. It is hypothesized that the need to exert this effort to maintain wakefulness at high homeostatic sleep pressure correlates with subjective fatigue levels. The model's output indeed exhibits good agreement with existing clinical time series of subjective fatigue-related measures, supporting this hypothesis. Subjective fatigue, adrenaline, and body temperature variations during two 72h sleep deprivation protocols are reproduced by the model. By distinguishing a motivation-dependent orexinergic contribution to the wake-effort drive, the model can be extended to interpret variation in performance levels during sleep deprivation in a way that is qualitatively consistent with existing, clinically derived results. The example of sleep deprivation thus demonstrates the ability of physiologically based sleep modeling to predict psychological measures from the underlying physiological interactions that produce them. Copyright (c) 2010 Elsevier Ltd. All rights reserved.

  18. Sleep deprivation impairs precision of waggle dance signaling in honey bees

    PubMed Central

    Klein, Barrett A.; Klein, Arno; Wray, Margaret K.; Mueller, Ulrich G.; Seeley, Thomas D.

    2010-01-01

    Sleep is essential for basic survival, and insufficient sleep leads to a variety of dysfunctions. In humans, one of the most profound consequences of sleep deprivation is imprecise or irrational communication, demonstrated by degradation in signaling as well as in receiving information. Communication in nonhuman animals may suffer analogous degradation of precision, perhaps with especially damaging consequences for social animals. However, society-specific consequences of sleep loss have rarely been explored, and no function of sleep has been ascribed to a truly social (eusocial) organism in the context of its society. Here we show that sleep-deprived honey bees (Apis mellifera) exhibit reduced precision when signaling direction information to food sources in their waggle dances. The deterioration of the honey bee's ability to communicate is expected to reduce the foraging efficiency of nestmates. This study demonstrates the impact of sleep deprivation on signaling in a eusocial animal. If the deterioration of signals made by sleep-deprived honey bees and humans is generalizable, then imprecise communication may be one detrimental effect of sleep loss shared by social organisms. PMID:21156830

  19. The Effect of One Night's Sleep Deprivation on Adolescent Neurobehavioral Performance

    PubMed Central

    Louca, Mia; Short, Michelle A.

    2014-01-01

    Study Objectives: To investigate the effects of one night's sleep deprivation on neurobehavioral functioning in adolescents. Design: Participants completed a neurobehavioral test battery measuring sustained attention, reaction speed, cognitive processing speed, sleepiness, and fatigue every 2 h during wakefulness. Baseline performance (defined as those test bouts between 09:00 and 19:00 on days 2 and 3, following two 10-h sleep opportunities) were compared to performance at the same clock time the day following total sleep deprivation. Setting: The sleep laboratory at the Centre for Sleep Research. Participants: Twelve healthy adolescents (6 male), aged 14-18 years (mean = 16.17, standard deviation = 0.83). Measurements and Results: Sustained attention, reaction speed, cognitive processing speed, and subjective sleepiness were all significantly worse following one night without sleep than following 10-h sleep opportunities (all main effects of day, P < 0.05). Sleep deprivation led to increased variability on objective performance measures. There were between-subjects differences in response to sleep loss that were task-specific, suggesting that adolescents may not only vary in terms of the degree to which they are affected by sleep loss but also the domains in which they are affected. Conclusions: These findings suggest that one night of total sleep deprivation has significant deleterious effects upon neurobehavioral performance and subjective sleepiness. These factors impair daytime functioning in adolescents, leaving them at greater risk of poor academic and social functioning and accidents and injuries. Citation: Louca M, Short MA. The effect of one night's sleep deprivation on adolescent neurobehavioral performance. SLEEP 2014;37(11):1799-1807. PMID:25364075

  20. HEALTH EFFECTS OF SLEEP DEPRIVATION ON NURSES WORKING SHIFTS.

    PubMed

    Stanojevic, Cedomirka; Simic, Svetlana; Milutinovic, Dragana

    2016-10-01

    Atypical work schedules cause reduced sleep, leading to drowsiness, fatigue, decline of cognitive performance and health problems among the members of the nursing staff. The study was aimed at reviewing current knowledge and attitudes concerning the impact of sleep disorders on health and cognitive functions among the members of the nursing staff. Sleep and Interpersonal Relations in Modern Society. The modern 24-hour society involves more and more employees (health services, police departments, public transport) in non-standard forms of work. In European Union countries, over 50% of the nursing staff work night shifts, while in the United States of America 55% of nursing staff work more than 40 hours a week, and 30-70% of nurses sleep less than six hours before their shift. Cognitive Effects of Sleep Deprivation. Sleep deprivation impairs the performance of tasks that require intensive and prolonged attention which increases the number of errors in patients care, and nurses are subject to incre- ased risk of traffic accidents. Sleep Deprivation and Health Disorders. Sleep deprived members of the nursing staff are at risk of obesity, diabetes, gastrointestinal disorders and cardiovascular disease. The risk factors for breast cancer are increased by 1.79 times. and there is a significantly higher risk for colorectal carcinoma. Too long or repeated shifts reduce the opportunity for sleep, shorten recovery time in nurses, thus endangering their safety and health as well as the quality of care and patients' safety. Bearing in mind the significance of the problerm it is necessary to conduct the surveys of sleep quality and health of nurses in the Republic of Serbia as well in order to tackle this issue which is insufficiently recognized.

  1. Classifying vulnerability to sleep deprivation using baseline measures of psychomotor vigilance.

    PubMed

    Patanaik, Amiya; Kwoh, Chee Keong; Chua, Eric C P; Gooley, Joshua J; Chee, Michael W L

    2015-05-01

    To identify measures derived from baseline psychomotor vigilance task (PVT) performance that can reliably predict vulnerability to sleep deprivation. Subjects underwent total sleep deprivation and completed a 10-min PVT every 1-2 h in a controlled laboratory setting. Participants were categorized as vulnerable or resistant to sleep deprivation, based on a median split of lapses that occurred following sleep deprivation. Standard reaction time, drift diffusion model (DDM), and wavelet metrics were derived from PVT response times collected at baseline. A support vector machine model that incorporated maximum relevance and minimum redundancy feature selection and wrapper-based heuristics was used to classify subjects as vulnerable or resistant using rested data. Two academic sleep laboratories. Independent samples of 135 (69 women, age 18 to 25 y), and 45 (3 women, age 22 to 32 y) healthy adults. In both datasets, DDM measures, number of consecutive reaction times that differ by more than 250 ms, and two wavelet features were selected by the model as features predictive of vulnerability to sleep deprivation. Using the best set of features selected in each dataset, classification accuracy was 77% and 82% using fivefold stratified cross-validation, respectively. In both datasets, DDM measures, number of consecutive reaction times that differ by more than 250 ms, and two wavelet features were selected by the model as features predictive of vulnerability to sleep deprivation. Using the best set of features selected in each dataset, classification accuracy was 77% and 82% using fivefold stratified cross-validation, respectively. Despite differences in experimental conditions across studies, drift diffusion model parameters associated reliably with individual differences in performance during total sleep deprivation. These results demonstrate the utility of drift diffusion modeling of baseline performance in estimating vulnerability to psychomotor vigilance decline

  2. Metabolic, Endocrine, and Immune Consequences of Sleep Deprivation

    PubMed Central

    AlDabal, Laila; BaHammam, Ahmed S

    2011-01-01

    Over the last three to four decades, it has been observed that the average total hours of sleep have decreased to less than seven hours per person per night. Concomitantly, global figures relating to obesity and diabetes mellitus have increased in an alarming fashion in adults and children, and it has been hypothesized that neuro-hormonal changes accompanying this behavioral sleep deprivation may lead to insulin resistance and, subsequently, to diabetes mellitus. Sleep deprivation has been associated with multiple physiological changes, including increased cortisol and ghrelin levels, decreased leptin levels and impaired glucose metabolism. Experimental studies have also shown an increase in inflammatory and pro-inflammatory markers, which are indicators of body stress, under sleep deprivation. This review elaborates further on this hypothesis, exploring the molecular basis for the link between both entities and the underlying pathophysiology that results in insulin resistance and diabetes mellitus. We review the results of experimental and epidemiological studies, specifically examining the relationship between sleep duration and the immune and endocrine systems. PMID:21754974

  3. Increased Automaticity and Altered Temporal Preparation Following Sleep Deprivation.

    PubMed

    Kong, Danyang; Asplund, Christopher L; Ling, Aiqing; Chee, Michael W L

    2015-08-01

    Temporal expectation enables us to focus limited processing resources, thereby optimizing perceptual and motor processing for critical upcoming events. We investigated the effects of total sleep deprivation (TSD) on temporal expectation by evaluating the foreperiod and sequential effects during a psychomotor vigilance task (PVT). We also examined how these two measures were modulated by vulnerability to TSD. Three 10-min visual PVT sessions using uniformly distributed foreperiods were conducted in the wake-maintenance zone the evening before sleep deprivation (ESD) and three more in the morning following approximately 22 h of TSD. TSD vulnerable and nonvulnerable groups were determined by a tertile split of participants based on the change in the number of behavioral lapses recorded during ESD and TSD. A subset of participants performed six additional 10-min modified auditory PVTs with exponentially distributed foreperiods during rested wakefulness (RW) and TSD to test the effect of temporal distribution on foreperiod and sequential effects. Sleep laboratory. There were 172 young healthy participants (90 males) with regular sleep patterns. Nineteen of these participants performed the modified auditory PVT. Despite behavioral lapses and slower response times, sleep deprived participants could still perceive the conditional probability of temporal events and modify their level of preparation accordingly. Both foreperiod and sequential effects were magnified following sleep deprivation in vulnerable individuals. Only the foreperiod effect increased in nonvulnerable individuals. The preservation of foreperiod and sequential effects suggests that implicit time perception and temporal preparedness are intact during total sleep deprivation. Individuals appear to reallocate their depleted preparatory resources to more probable event timings in ongoing trials, whereas vulnerable participants also rely more on automatic processes. © 2015 Associated Professional Sleep

  4. Monitoring sleep depth: analysis of bispectral index (BIS) based on polysomnographic recordings and sleep deprivation.

    PubMed

    Giménez, Sandra; Romero, Sergio; Alonso, Joan Francesc; Mañanas, Miguel Ángel; Pujol, Anna; Baxarias, Pilar; Antonijoan, Rosa Maria

    2017-02-01

    The assessment and management of sleep are increasingly recommended in the clinical practice. Polysomnography (PSG) is considered the gold standard test to monitor sleep objectively, but some practical and technical constraints exist due to environmental and patient considerations. Bispectral index (BIS) monitoring is commonly used in clinical practice for guiding anesthetic administration and provides an index based on relationships between EEG components. Due to similarities in EEG synchronization between anesthesia and sleep, several studies have assessed BIS as a sleep monitor with contradictory results. The aim of this study was to evaluate objectively both the feasibility and reliability of BIS for sleep monitoring through a robust methodology, which included full PSG recordings at a baseline situation and after 40 h of sleep deprivation. Results confirmed that the BIS index was highly correlated with the hypnogram (0.89 ± 0.02), showing a progressive decrease as sleep deepened, and an increase during REM sleep (awake: 91.77 ± 8.42; stage N1: 83.95 ± 11.05; stage N2: 71.71 ± 11.99; stage N3: 42.41 ± 9.14; REM: 80.11 ± 8.73). Mean and median BIS values were lower in the post-deprivation night than in the baseline night, showing statistical differences for the slow wave sleep (baseline: 42.41 ± 9.14 vs. post-deprivation: 39.49 ± 10.27; p = 0.02). BIS scores were able to discriminate properly between deep (N3) and light (N1, N2) sleep. BIS values during REM overlapped those of other sleep stages, although EMG activity provided by the BIS monitor could help to identify REM sleep if needed. In conclusion, BIS monitors could provide a useful measure of sleep depth in especially particular situations such as intensive care units, and they could be used as an alternative for sleep monitoring in order to reduce PSG-derived costs and to increase capacity in ambulatory care.

  5. Cerebral mGluR5 availability contributes to elevated sleep need and behavioral adjustment after sleep deprivation

    PubMed Central

    Hefti, Katharina; Saberi-Moghadam, Sohrab; Buck, Alfred; Ametamey, Simon M; Scheidegger, Milan; Franken, Paul; Henning, Anke; Seifritz, Erich

    2017-01-01

    Increased sleep time and intensity quantified as low-frequency brain electrical activity after sleep loss demonstrate that sleep need is homeostatically regulated, yet the underlying molecular mechanisms remain elusive. We here demonstrate that metabotropic glutamate receptors of subtype 5 (mGluR5) contribute to the molecular machinery governing sleep-wake homeostasis. Using positron emission tomography, magnetic resonance spectroscopy, and electroencephalography in humans, we find that increased mGluR5 availability after sleep loss tightly correlates with behavioral and electroencephalographic biomarkers of elevated sleep need. These changes are associated with altered cortical myo-inositol and glycine levels, suggesting sleep loss-induced modifications downstream of mGluR5 signaling. Knock-out mice without functional mGluR5 exhibit severe dysregulation of sleep-wake homeostasis, including lack of recovery sleep and impaired behavioral adjustment to a novel task after sleep deprivation. The data suggest that mGluR5 contribute to the brain's coping mechanisms with sleep deprivation and point to a novel target to improve disturbed wakefulness and sleep. PMID:28980941

  6. Cerebral mGluR5 availability contributes to elevated sleep need and behavioral adjustment after sleep deprivation.

    PubMed

    Holst, Sebastian C; Sousek, Alexandra; Hefti, Katharina; Saberi-Moghadam, Sohrab; Buck, Alfred; Ametamey, Simon M; Scheidegger, Milan; Franken, Paul; Henning, Anke; Seifritz, Erich; Tafti, Mehdi; Landolt, Hans-Peter

    2017-10-05

    Increased sleep time and intensity quantified as low-frequency brain electrical activity after sleep loss demonstrate that sleep need is homeostatically regulated, yet the underlying molecular mechanisms remain elusive. We here demonstrate that metabotropic glutamate receptors of subtype 5 (mGluR5) contribute to the molecular machinery governing sleep-wake homeostasis. Using positron emission tomography, magnetic resonance spectroscopy, and electroencephalography in humans, we find that increased mGluR5 availability after sleep loss tightly correlates with behavioral and electroencephalographic biomarkers of elevated sleep need. These changes are associated with altered cortical myo-inositol and glycine levels, suggesting sleep loss-induced modifications downstream of mGluR5 signaling. Knock-out mice without functional mGluR5 exhibit severe dysregulation of sleep-wake homeostasis, including lack of recovery sleep and impaired behavioral adjustment to a novel task after sleep deprivation. The data suggest that mGluR5 contribute to the brain's coping mechanisms with sleep deprivation and point to a novel target to improve disturbed wakefulness and sleep.

  7. Transiently increasing cAMP levels selectively in hippocampal excitatory neurons during sleep deprivation prevents memory deficits caused by sleep loss.

    PubMed

    Havekes, Robbert; Bruinenberg, Vibeke M; Tudor, Jennifer C; Ferri, Sarah L; Baumann, Arnd; Meerlo, Peter; Abel, Ted

    2014-11-19

    The hippocampus is particularly sensitive to sleep loss. Although previous work has indicated that sleep deprivation impairs hippocampal cAMP signaling, it remains to be determined whether the cognitive deficits associated with sleep deprivation are caused by attenuated cAMP signaling in the hippocampus. Further, it is unclear which cell types are responsible for the memory impairments associated with sleep deprivation. Transgenic approaches lack the spatial resolution to manipulate specific signaling pathways selectively in the hippocampus, while pharmacological strategies are limited in terms of cell-type specificity. Therefore, we used a pharmacogenetic approach based on a virus-mediated expression of a Gαs-coupled Drosophila octopamine receptor selectively in mouse hippocampal excitatory neurons in vivo. With this approach, a systemic injection with the receptor ligand octopamine leads to increased cAMP levels in this specific set of hippocampal neurons. We assessed whether transiently increasing cAMP levels during sleep deprivation prevents memory consolidation deficits associated with sleep loss in an object-location task. Five hours of total sleep deprivation directly following training impaired the formation of object-location memories. Transiently increasing cAMP levels in hippocampal neurons during the course of sleep deprivation prevented these memory consolidation deficits. These findings demonstrate that attenuated cAMP signaling in hippocampal excitatory neurons is a critical component underlying the memory deficits in hippocampus-dependent learning tasks associated with sleep deprivation. Copyright © 2014 the authors 0270-6474/14/3415715-07$15.00/0.

  8. Sleep deprivation influences some but not all processes of supervisory attention

    NASA Technical Reports Server (NTRS)

    Jennings, J. R.; Monk, T. H.; van der Molen, M. W.

    2003-01-01

    Does one night of sleep deprivation alter processes of supervisory attention in general or only a specific subset of such processes? Twenty college-aged volunteers, half female, performed a choice reaction time task. A cue indicated that compatible (e.g., right button, right-pointing arrow) or incompatible (e.g., left button, right-pointing arrow) responses were to be given to a stimulus that followed 50 or 500 ms later. The paradigm assessed response inhibition, task-shifting skill, and task strategy-processes inherent in supervisory attention. Performance, along with heart rate, was assessed for 12 hr following normal sleep or a night of complete sleep deprivation. Sleep deprivation altered neither preparation for task shifting nor response inhibition. The ability to use preparatory bias to speed performance did decrease with sleep deprivation. Sleep deprivation appears to selectively affect this supervisory attention process, which is perceived as an active effort to cope with a challenging task.

  9. Sleep deprivation influences some but not all processes of supervisory attention.

    PubMed

    Jennings, J R; Monk, T H; van der Molen, M W

    2003-09-01

    Does one night of sleep deprivation alter processes of supervisory attention in general or only a specific subset of such processes? Twenty college-aged volunteers, half female, performed a choice reaction time task. A cue indicated that compatible (e.g., right button, right-pointing arrow) or incompatible (e.g., left button, right-pointing arrow) responses were to be given to a stimulus that followed 50 or 500 ms later. The paradigm assessed response inhibition, task-shifting skill, and task strategy-processes inherent in supervisory attention. Performance, along with heart rate, was assessed for 12 hr following normal sleep or a night of complete sleep deprivation. Sleep deprivation altered neither preparation for task shifting nor response inhibition. The ability to use preparatory bias to speed performance did decrease with sleep deprivation. Sleep deprivation appears to selectively affect this supervisory attention process, which is perceived as an active effort to cope with a challenging task.

  10. Sleepless night, restless mind: Effects of sleep deprivation on mind wandering.

    PubMed

    Poh, Jia-Hou; Chong, Pearlynne L H; Chee, Michael W L

    2016-10-01

    Sleep deprivation can result in degradation of sustained attention through increased distraction by task-irrelevant exogenous stimuli. However, attentional failures in the sleep-deprived state could also be a result of task-unrelated thoughts (TUTs, or mind wandering). Here, well-rested and sleep-deprived participants performed a visual search task under high and low perceptual load conditions. Thought probes were administered at irregular intervals to gauge the frequency of TUTs and level of meta-awareness of mind wandering. Despite sleep-deprived participants reporting more TUTs, they also reported less awareness of TUTs. Although the frequency of TUTs decreased in the high load condition in well-rested participants, they were equally frequent across low and high perceptual load conditions in sleep-deprived participants. Together, these findings suggest that sleep deprivation can result in a loss of ability to allocate attentional resources according to task demands consistent with diminished executive control. This may have been exacerbated by reduced meta-awareness. (PsycINFO Database Record (c) 2016 APA, all rights reserved).

  11. Aging worsens the effects of sleep deprivation on postural control.

    PubMed

    Robillard, Rébecca; Prince, François; Filipini, Daniel; Carrier, Julie

    2011-01-01

    Falls increase with age and cause significant injuries in the elderly. This study aimed to determine whether age modulates the interactions between sleep deprivation and postural control and to evaluate how attention influences these interactions in the elderly. Fifteen young (24±2.7 y.o.) and 15 older adults (64±3.2 y.o.) stood still on a force plate after a night of sleep and after total sleep deprivation. Center of pressure range and velocity were measured with eyes open and with eyes closed while participants performed an interference task, a control task, and no cognitive task. Sleep deprivation increased the antero-posterior range of center of pressure in both age groups and center of pressure speed in older participants only. In elderly participants, the destabilizing effects of sleep deprivation were more pronounced with eyes closed. The interference task did not alter postural control beyond the destabilization induced by sleep loss in older subjects. It was concluded that sleep loss has greater destabilizing effects on postural control in older than in younger participants, and may therefore increase the risk of falls in the elderly.

  12. Aging Worsens the Effects of Sleep Deprivation on Postural Control

    PubMed Central

    Robillard, Rébecca; Prince, François; Filipini, Daniel; Carrier, Julie

    2011-01-01

    Falls increase with age and cause significant injuries in the elderly. This study aimed to determine whether age modulates the interactions between sleep deprivation and postural control and to evaluate how attention influences these interactions in the elderly. Fifteen young (24±2.7 y.o.) and 15 older adults (64±3.2 y.o.) stood still on a force plate after a night of sleep and after total sleep deprivation. Center of pressure range and velocity were measured with eyes open and with eyes closed while participants performed an interference task, a control task, and no cognitive task. Sleep deprivation increased the antero-posterior range of center of pressure in both age groups and center of pressure speed in older participants only. In elderly participants, the destabilizing effects of sleep deprivation were more pronounced with eyes closed. The interference task did not alter postural control beyond the destabilization induced by sleep loss in older subjects. It was concluded that sleep loss has greater destabilizing effects on postural control in older than in younger participants, and may therefore increase the risk of falls in the elderly. PMID:22163330

  13. Chronic sleep deprivation differentially affects short and long-term operant memory in Aplysia.

    PubMed

    Krishnan, Harini C; Noakes, Eric J; Lyons, Lisa C

    2016-10-01

    The induction, formation and maintenance of memory represent dynamic processes modulated by multiple factors including the circadian clock and sleep. Chronic sleep restriction has become common in modern society due to occupational and social demands. Given the impact of cognitive impairments associated with sleep deprivation, there is a vital need for a simple animal model in which to study the interactions between chronic sleep deprivation and memory. We used the marine mollusk Aplysia californica, with its simple nervous system, nocturnal sleep pattern and well-characterized learning paradigms, to assess the effects of two chronic sleep restriction paradigms on short-term (STM) and long-term (LTM) associative memory. The effects of sleep deprivation on memory were evaluated using the operant learning paradigm, learning that food is inedible, in which the animal associates a specific netted seaweed with failed swallowing attempts. We found that two nights of 6h sleep deprivation occurring during the first or last half of the night inhibited both STM and LTM. Moreover, the impairment in STM persisted for more than 24h. A milder, prolonged sleep deprivation paradigm consisting of 3 consecutive nights of 4h sleep deprivation also blocked STM, but had no effect on LTM. These experiments highlight differences in the sensitivity of STM and LTM to chronic sleep deprivation. Moreover, these results establish Aplysia as a valid model for studying the interactions between chronic sleep deprivation and associative memory paving the way for future studies delineating the mechanisms through which sleep restriction affects memory formation. Copyright © 2016 Elsevier Inc. All rights reserved.

  14. Chronic Sleep Deprivation Differentially Affects Short and Long-term Operant Memory in Aplysia

    PubMed Central

    Krishnan, Harini C.; Noakes, Eric J.; Lyons, Lisa C.

    2016-01-01

    The induction, formation and maintenance of memory represent dynamic processes modulated by multiple factors including the circadian clock and sleep. Chronic sleep restriction has become common in modern society due to occupational and social demands. Given the impact of cognitive impairments associated with sleep deprivation, there is a vital need for a simple animal model in which to study the interactions between chronic sleep deprivation and memory. We used the marine mollusk Aplysia californica, with its simple nervous system, nocturnal sleep pattern and well-characterized learning paradigms, to assess the effects of two chronic sleep restriction paradigms on short-term (STM) and long-term (LTM) associative memory. The effects of sleep deprivation on memory were evaluated using the operant learning paradigm, learning that food is inedible, in which the animal associates a specific netted seaweed with failed swallowing attempts. We found that two nights of 6 h sleep deprivation occurring during the first or last half of the night inhibited both STM and LTM. Moreover, the impairment in STM persisted for more than 24 hours. A milder, prolonged sleep deprivation paradigm consisting of 3 consecutive nights of 4 h sleep deprivation also blocked STM, but had no effect on LTM. These experiments highlight differences in the sensitivity of STM and LTM to chronic sleep deprivation. Moreover, these results establish Aplysia as a valid model for studying the interactions between chronic sleep deprivation and associative memory paving the way for future studies delineating the mechanisms through which sleep restriction affects memory formation. PMID:27555235

  15. AMPA receptors mediate passive avoidance deficits induced by sleep deprivation.

    PubMed

    Dubiela, Francisco Paulino; Queiroz, Claudio Marcos; Moreira, Karin Di Monteiro; Nobrega, Jose N; Sita, Luciane Valéria; Tufik, Sergio; Hipolide, Debora Cristina

    2013-11-15

    The present study addressed the effects of sleep deprivation (SD) on AMPA receptor (AMPAR) binding in brain regions associated with learning and memory, and investigated whether treatment with drugs acting on AMPAR could prevent passive avoidance deficits in sleep deprived animals. [(3)H]AMPA binding and GluR1 in situ hybridization signals were quantified in different brain regions of male Wistar rats either immediately after 96 h of sleep deprivation or after 24h of sleep recovery following 96 h of sleep deprivation. Another group of animals were sleep deprived and then treated with either the AMPAR potentiator, aniracetam (25, 50 and 100mg/kg, acute administration) or the AMPAR antagonist GYKI-52466 (5 and 10mg/kg, acute and chronic administration) before passive avoidance training. Task performance was evaluated 2h and 24h after training. A significant reduction in [(3)H]AMPA binding was found in the hippocampal formation of SD animals, while no alterations were observed in GluR1 mRNA levels. The highest dose of aniracetam (100mg/kg) reverted SD-induced impairment of passive avoidance performance in both retention tests, whereas GYKI-52466 treatment had no effect. Pharmacological enhancement of AMPAR function may revert hippocampal-dependent learning impairments produced after SD. We argue that such effects might be associated with reduced AMPAR binding in the hippocampus of sleep deprived animals. Copyright © 2013 Elsevier B.V. All rights reserved.

  16. Effects of partial sleep deprivation on slow waves during non-rapid eye movement sleep: A high density EEG investigation.

    PubMed

    Plante, David T; Goldstein, Michael R; Cook, Jesse D; Smith, Richard; Riedner, Brady A; Rumble, Meredith E; Jelenchick, Lauren; Roth, Andrea; Tononi, Giulio; Benca, Ruth M; Peterson, Michael J

    2016-02-01

    Changes in slow waves during non-rapid eye movement (NREM) sleep in response to acute total sleep deprivation are well-established measures of sleep homeostasis. This investigation utilized high-density electroencephalography (hdEEG) to examine topographic changes in slow waves during repeated partial sleep deprivation. Twenty-four participants underwent a 6-day sleep restriction protocol. Spectral and period-amplitude analyses of sleep hdEEG data were used to examine changes in slow wave energy, count, amplitude, and slope relative to baseline. Changes in slow wave energy were dependent on the quantity of NREM sleep utilized for analysis, with widespread increases during sleep restriction and recovery when comparing data from the first portion of the sleep period, but restricted to recovery sleep if the entire sleep episode was considered. Period-amplitude analysis was less dependent on the quantity of NREM sleep utilized, and demonstrated topographic changes in the count, amplitude, and distribution of slow waves, with frontal increases in slow wave amplitude, numbers of high-amplitude waves, and amplitude/slopes of low amplitude waves resulting from partial sleep deprivation. Topographic changes in slow waves occur across the course of partial sleep restriction and recovery. These results demonstrate a homeostatic response to partial sleep loss in humans. Copyright © 2015 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

  17. The effect of one night's sleep deprivation on adolescent neurobehavioral performance.

    PubMed

    Louca, Mia; Short, Michelle A

    2014-11-01

    To investigate the effects of one night's sleep deprivation on neurobehavioral functioning in adolescents. Participants completed a neurobehavioral test battery measuring sustained attention, reaction speed, cognitive processing speed, sleepiness, and fatigue every 2 h during wakefulness. Baseline performance (defined as those test bouts between 09:00 and 19:00 on days 2 and 3, following two 10-h sleep opportunities) were compared to performance at the same clock time the day following total sleep deprivation. The sleep laboratory at the Centre for Sleep Research. Twelve healthy adolescents (6 male), aged 14-18 years (mean = 16.17, standard deviation = 0.83). Sustained attention, reaction speed, cognitive processing speed, and subjective sleepiness were all significantly worse following one night without sleep than following 10-h sleep opportunities (all main effects of day, P < 0.05). Sleep deprivation led to increased variability on objective performance measures. There were between-subjects differences in response to sleep loss that were task-specific, suggesting that adolescents may not only vary in terms of the degree to which they are affected by sleep loss but also the domains in which they are affected. These findings suggest that one night of total sleep deprivation has significant deleterious effects upon neurobehavioral performance and subjective sleepiness. These factors impair daytime functioning in adolescents, leaving them at greater risk of poor academic and social functioning and accidents and injuries.

  18. Precipitating factors of somnambulism: impact of sleep deprivation and forced arousals.

    PubMed

    Pilon, Mathieu; Montplaisir, Jacques; Zadra, Antonio

    2008-06-10

    Experimental attempts to induce sleepwalking with forced arousals during slow-wave sleep (SWS) have yielded mixed results in children and have not been investigated in adult patients. We hypothesized that the combination of sleep deprivation and external stimulation would increase the probability of inducing somnambulistic episodes in sleepwalkers recorded in the sleep laboratory. The main goal of this study was to assess the effects of forced arousals from auditory stimuli (AS) in adult sleepwalkers and control subjects during normal sleep and following post-sleep deprivation recovery sleep. Ten sleepwalkers and 10 controls were investigated. After a baseline night, participants were presented with AS at predetermined sleep stages either during normal sleep or recovery sleep following 25 hours of sleep deprivation. One week later, the conditions with AS were reversed. No somnambulistic episodes were induced in controls. When compared to the effects of AS during sleepwalkers' normal sleep, the presentation of AS during sleepwalkers' recovery sleep significantly increased their efficacy in experimentally inducing somnambulistic events and a significantly greater proportion of sleepwalkers (100%) experienced at least one induced episode during recovery SWS as compared to normal SWS (30%). There was no significant difference between the mean intensity of AS that induced episodes during sleepwalkers' SWS and the mean intensity of AS that awakened sleepwalkers and controls from SWS. Sleep deprivation and forced arousals during slow-wave sleep can induce somnambulistic episodes in predisposed adults. The results highlight the potential value of this protocol in establishing a video-polysomnographically based diagnosis for sleepwalking.

  19. Sleep Deprivation Promotes Habitual Control over Goal-Directed Control: Behavioral and Neuroimaging Evidence.

    PubMed

    Chen, Jie; Liang, Jie; Lin, Xiao; Zhang, Yang; Zhang, Yan; Lu, Lin; Shi, Jie

    2017-12-06

    Sleep is one of the most fundamental processes of life, playing an important role in the regulation of brain function. The long-term lack of sleep can cause memory impairments, declines in learning ability, and executive dysfunction. In the present study, we evaluated the effects of sleep deprivation on instrumental learning behavior, particularly goal-directed and habitual actions in humans, and investigated the underlying neural mechanisms. Healthy college students of either gender were enrolled and randomly divided into sleep deprivation group and sleep control group. fMRI data were collected. We found that one night of sleep deprivation led to greater responsiveness to stimuli that were associated with devalued outcomes in the slips-of-action test, indicating a deficit in the formation of goal-directed control and an overreliance on habits. Furthermore, sleep deprivation had no effect on the expression of acquired goal-directed action. The level of goal-directed action after sleep deprivation was positively correlated with baseline working memory capacity. The neuroimaging data indicated that goal-directed learning mainly recruited the ventromedial PFC (vmPFC), the activation of which was less pronounced during goal-directed learning after sleep deprivation. Activation of the vmPFC during goal-directed learning during training was positively correlated with the level of goal-directed action performance. The present study suggests that people rely predominantly on habits at the expense of goal-directed control after sleep deprivation, and this process involves the vmPFC. These results contribute to a better understanding of the effects of sleep loss on decision-making. SIGNIFICANCE STATEMENT Understanding the cognitive consequences of sleep deprivation has become extremely important over the past half century, given the continued decline in sleep duration in industrialized societies. Our results provide novel evidence that goal-directed action may be

  20. The Impact of Partial Sleep Deprivation on Moral Reasoning in Military Officers

    PubMed Central

    Olsen, Olav Kjellevold; Pallesen, Ståle; Eid, Jarle

    2010-01-01

    Study Objectives: The present study explores the impact of long-term partial sleep deprivation on the activation of moral justice schemas, which are suggested to play a prominent role in moral reasoning and the formation of moral judgments and behavior. Design: Participants judged 5 dilemmas in rested and partially sleep deprived condition, in a counterbalanced design. Setting: In classroom and field exercises at the Norwegian Naval Academy and the Norwegian Army Academy. Participants: Seventy-one Norwegian naval and army officer cadets. Measurements and Results: The results showed that the officers' ability to conduct mature and principally oriented moral reasoning was severely impaired during partial sleep deprivation compared to the rested state. At the same time, the officers became substantially more rules-oriented in the sleep deprived condition, while self-oriented moral reasoning did not change. Interaction effects showed that those officers who displayed high levels of mature moral reasoning (n = 24) in the rested condition, lost much of this capacity during sleep deprivation in favor of a strong increase in rules-oriented moral reasoning as well as self-orientation. Conversely, officers at low levels of mature moral reasoning in rested condition (n = 23) were unaffected by sleep deprivation. Conclusions: The present data show that long-term partial sleep deprivation has an impact on the activation of moral justice schemas, and consequently on the ability to make moral justice judgments. Citation: Olsen OK; Pallesen S; Eid J. The impact of partial sleep deprivation on moral reasoning in military officers. SLEEP 2010;33(8):1086-1090. PMID:20815191

  1. Phosphorous31 magnetic resonance spectroscopy after total sleep deprivation in healthy adult men.

    PubMed

    Dorsey, Cynthia M; Lukas, Scott E; Moore, Constance M; Tartarini, Wendy L; Parow, Aimee M; Villafuerte, Rosemond A; Renshaw, Perry F

    2003-08-01

    To investigate chemical changes in the brains of healthy adults after sleep deprivation and recovery sleep, using phosphorous magnetic resonance spectroscopy. Three consecutive nights (baseline, sleep deprivation, recovery) were spent in the laboratory. Objective sleep measures were assessed on the baseline and recovery nights using polysomnography. Phosphorous magnetic resonance spectroscopy scans took place beginning at 7 am to 8 am on the morning after each of the 3 nights. Sleep laboratory in a private psychiatric teaching hospital. Eleven healthy young men. Following a baseline night of sleep, subjects underwent a night of total sleep deprivation, which involved supervision to ensure the absence of sleep but was not polysomnographically monitored. No significant changes in any measure of brain chemistry were observed the morning after a night of total sleep deprivation. However, after the recovery night, significant increases in total and beta-nucleoside triphosphate and decreases in phospholipid catabolism, measured by an increase in the concentration of glycerylphosphorylcholine, were observed. Chemical changes paralleled some changes in objective sleep measures. Significant chemical changes in the brain were observed following recovery sleep after 1 night of total sleep deprivation. The specific process underlying these changes is unclear due to the large brain region sampled in this exploratory study, but changes may reflect sleep inertia or some aspect of the homeostatic sleep mechanism that underlies the depletion and restoration of sleep. Phosphorous magnetic resonance spectroscopy is a technique that may be of value in further exploration of such sleep-wake functions.

  2. Sleep deprivation and accidental fall risk in children.

    PubMed

    Boto, Leonor Reis; Crispim, João Núncio; de Melo, Isabel Saraiva; Juvandes, Carla; Rodrigues, Teresa; Azeredo, Paula; Ferreira, Rosário

    2012-01-01

    To look for an association between sleep deprivation and risk of accidental falls (AF) in children. A questionnaire was applied to two groups of children aged 1-14 years, encompassing children observed in an emergency room for AF (G1) and children attending health care visits (HV) (G2). Collected data included demographic characteristics, medical history, previous week's sleep pattern (PWSP), sleep duration and sleep pattern in the preceding 24 h, mechanism of fall, and injury severity. acute or chronic disease or exposure to drugs interfering with sleep. Statistical analyses included Fisher's exact test, Pearson Chi-square, Fisher-Freeman-Halton test, T and Mann-Whitney tests for independent samples, and multivariate logistic regression (α=5%). We obtained 1756 questionnaires in G1 and 277 in G2. Of those, 834 in G1 and 267 in G2 were analyzed. We found an increased risk of AF in boys (OR 1.6; 95% CI 1.2-2.4). After controlling for age, gender, summer holidays, parental education and profession, lack of naps and PWSP were associated with increased risk (OR 2.1; 95% CI 1.3-3.3 and OR 2.7; 95% CI 1.2-6.1). In 3-5 year-old children there was an association between AF and a shorter than usual sleep duration in the previous 24 h (p=0.02). To our knowledge, our study is the largest so far to assess the association between sleep deprivation and childhood injury. It evidences a protective effect of naps in children. Sleep duration of less than 8 h increases risk of AF. Pre-schoolers may be particularly susceptible to sleep deprivation. Copyright © 2011 Elsevier B.V. All rights reserved.

  3. Acute sleep deprivation increases food purchasing in men.

    PubMed

    Chapman, Colin D; Nilsson, Emil K; Nilsson, Victor C; Cedernaes, Jonathan; Rångtell, Frida H; Vogel, Heike; Dickson, Suzanne L; Broman, Jan-Erik; Hogenkamp, Pleunie S; Schiöth, Helgi B; Benedict, Christian

    2013-12-01

    To investigate if acute sleep deprivation affects food purchasing choices in a mock supermarket. On the morning after one night of total sleep deprivation (TSD) or after one night of sleep, 14 normal-weight men were given a fixed budget (300 SEK-approximately 50 USD). They were instructed to purchase as much as they could out of a possible 40 items, including 20 high-caloric foods (>2 kcal/g) and 20 low-caloric foods (<2 kcal/g). The prices of the high-caloric foods were then varied (75%, 100% (reference price), and 125%) to determine if TSD affects the flexibility of food purchasing. Before the task, participants received a standardized breakfast, thereby minimizing the potential confound produced by hunger. In addition, morning plasma concentrations of the orexigenic hormone ghrelin were measured under fasting conditions. Independent of both type of food offered and price condition, sleep-deprived men purchased significantly more calories (+9%) and grams (+18%) of food than they did after one night of sleep (both P < 0.05). Morning plasma ghrelin concentrations were also higher after TSD (P < 0.05). However, this increase did not correlate with the effects of TSD on food purchasing. This experiment demonstrates that acute sleep loss alters food purchasing behavior in men. Copyright © 2013 The Obesity Society.

  4. Impact of monetary incentives on cognitive performance and error monitoring following sleep deprivation.

    PubMed

    Hsieh, Shulan; Li, Tzu-Hsien; Tsai, Ling-Ling

    2010-04-01

    To examine whether monetary incentives attenuate the negative effects of sleep deprivation on cognitive performance in a flanker task that requires higher-level cognitive-control processes, including error monitoring. Twenty-four healthy adults aged 18 to 23 years were randomly divided into 2 subject groups: one received and the other did not receive monetary incentives for performance accuracy. Both subject groups performed a flanker task and underwent electroencephalographic recordings for event-related brain potentials after normal sleep and after 1 night of total sleep deprivation in a within-subject, counterbalanced, repeated-measures study design. Monetary incentives significantly enhanced the response accuracy and reaction time variability under both normal sleep and sleep-deprived conditions, and they reduced the effects of sleep deprivation on the subjective effort level, the amplitude of the error-related negativity (an error-related event-related potential component), and the latency of the P300 (an event-related potential variable related to attention processes). However, monetary incentives could not attenuate the effects of sleep deprivation on any measures of behavior performance, such as the response accuracy, reaction time variability, or posterror accuracy adjustments; nor could they reduce the effects of sleep deprivation on the amplitude of the Pe, another error-related event-related potential component. This study shows that motivation incentives selectively reduce the effects of total sleep deprivation on some brain activities, but they cannot attenuate the effects of sleep deprivation on performance decrements in tasks that require high-level cognitive-control processes. Thus, monetary incentives and sleep deprivation may act through both common and different mechanisms to affect cognitive performance.

  5. Neuroimmunologic aspects of sleep and sleep loss

    NASA Technical Reports Server (NTRS)

    Rogers, N. L.; Szuba, M. P.; Staab, J. P.; Evans, D. L.; Dinges, D. F.

    2001-01-01

    The complex and intimate interactions between the sleep and immune systems have been the focus of study for several years. Immune factors, particularly the interleukins, regulate sleep and in turn are altered by sleep and sleep deprivation. The sleep-wake cycle likewise regulates normal functioning of the immune system. Although a large number of studies have focused on the relationship between the immune system and sleep, relatively few studies have examined the effects of sleep deprivation on immune parameters. Studies of sleep deprivation's effects are important for several reasons. First, in the 21st century, various societal pressures require humans to work longer and sleep less. Sleep deprivation is becoming an occupational hazard in many industries. Second, to garner a greater understanding of the regulatory effects of sleep on the immune system, one must understand the consequences of sleep deprivation on the immune system. Significant detrimental effects on immune functioning can be seen after a few days of total sleep deprivation or even several days of partial sleep deprivation. Interestingly, not all of the changes in immune physiology that occur as a result of sleep deprivation appear to be negative. Numerous medical disorders involving the immune system are associated with changes in the sleep-wake physiology--either being caused by sleep dysfunction or being exacerbated by sleep disruption. These disorders include infectious diseases, fibromyalgia, cancers, and major depressive disorder. In this article, we will describe the relationships between sleep physiology and the immune system, in states of health and disease. Interspersed will be proposals for future research that may illuminate the clinical relevance of the relationships between sleeping, sleep loss and immune function in humans. Copyright 2001 by W.B. Saunders Company.

  6. Double Trouble? The Effects of Sleep Deprivation and Chronotype on Adolescent Affect

    ERIC Educational Resources Information Center

    Dagys, Natasha; McGlinchey, Eleanor L.; Talbot, Lisa S.; Kaplan, Katherine A.; Dahl, Ronald E.; Harvey, Allison G.

    2012-01-01

    Background: Two understudied risk factors that have been linked to emotional difficulties in adolescence are chronotype and sleep deprivation. This study extended past research by using an experimental design to investigate the role of sleep deprivation and chronotype on emotion in adolescents. It was hypothesized that sleep deprivation and an…

  7. The homeostatic and circadian sleep recovery responses after total sleep deprivation in mice.

    PubMed

    Dispersyn, Garance; Sauvet, Fabien; Gomez-Merino, Danielle; Ciret, Sylvain; Drogou, Catherine; Leger, Damien; Gallopin, Thierry; Chennaoui, Mounir

    2017-10-01

    Many studies on sleep deprivation effects lack data regarding the recovery period. We investigated the 2-day homeostatic and circadian sleep recovery response to 24 h of total sleep deprivation (TSD) induced by brief rotation of an activity wheel. Eight mice were implanted with telemetry transmitters (DSI F40-EET) that recorded simultaneously their electroencephalography (EEG), locomotor activity and temperature during 24 h of baseline (BSL), TSD and 2 days of recovery (D1 and D2). In a second experiment, two groups of five non-implanted mice underwent TSD or ad libitum sleep, after which they were killed, adrenal glands were weighed and blood was collected for analysis of corticosterone concentration. During TSD mice were awake at least 97% of the time, with a consecutive sleep rebound during D1 that persisted during D2. This was characterized by increases of non-rapid eye movement (NREM) sleep (44.2 ± 6.9% for D1 and 43.0 ± 7.7% for D2 versus 33.8 ± 9.2% for BSL) and the relative delta band power (179.2 ± 34.4% for D1 and 81.9 ± 11.2% for D2). Greater NREM and REM sleep amounts were observed during the 'light' periods. Temperature and locomotor activity characteristics were unchanged during D1 and D2 versus BSL. In non-implanted mice, corticosterone levels as well as adrenal gland and overall body weights did not differ between TSD and ad libitum sleep groups. In conclusion, 24 h of TSD in an activity wheel without stress responses influence homeostatic sleep regulation with no effect on the circadian regulation over at least 2 days of recovery in mice. © 2017 European Sleep Research Society.

  8. L-carnitine prevents memory impairment induced by chronic REM-sleep deprivation.

    PubMed

    Alzoubi, Karem H; Rababa'h, Abeer M; Owaisi, Amani; Khabour, Omar F

    2017-05-01

    Sleep deprivation (SD) negatively impacts memory, which was related to oxidative stress induced damage. L-carnitine is a naturally occurring compound, synthesized endogenously in mammalian species and known to possess antioxidant properties. In this study, the effect of L-carnitine on learning and memory impairment induced by rapid eye movement sleep (REM-sleep) deprivation was investigated. REM-sleep deprivation was induced using modified multiple platform model (8h/day, for 6 weeks). Simultaneously, L-carnitine was administered (300mg/kg/day) intraperitoneally for 6 weeks. Thereafter, the radial arm water maze (RAWM) was used to assess spatial learning and memory. Additionally, the hippocampus levels of antioxidant biomarkers/enzymes: reduced glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG ratio, glutathione peroxidase (GPx), catalase, and superoxide dismutase (SOD) and thiobarbituric acid reactive substance (TBARS) were assessed. The results showed that chronic REM-sleep deprivation impaired both short- and long-term memory (P<0.05), whereas L-carnitine treatment protected against this effect. Furthermore, L-carnitine normalized chronic REM-sleep deprivation induced reduction in the hippocampus ratio of GSH/GSSG, activity of catalase, GPx, and SOD. No change was observed in TBARS among tested groups (P>0.05). In conclusion, chronic REM-sleep deprivation induced memory impairment, and treatment with L-carnitine prevented this impairment through normalizing antioxidant mechanisms in the hippocampus. Copyright © 2017 Elsevier Inc. All rights reserved.

  9. Novel application of brain-targeting polyphenol compounds in sleep deprivation-induced cognitive dysfunction

    PubMed Central

    Zhao, Wei; Wang, Jun; Bi, Weina; Ferruzzi, Mario; Yemul, Shrishailam; Freire, Daniel; Mazzola, Paolo; Ho, Lap; Dubner, Lauren; Pasinetti, Giulio Maria

    2016-01-01

    Sleep deprivation produces deficits in hippocampal synaptic plasticity and hippocampal-dependent memory storage. Recent evidence suggests that sleep deprivation disrupts memory consolidation through multiple mechanisms, including the down-regulation of the cAMP-response element-binding protein (CREB) and of mammalian target of rapamycin (mTOR) signaling. In this study, we tested the effects of a Bioactive Dietary Polyphenol Preparation (BDPP), comprised of grape seed polyphenol extract, Concord grape juice, and resveratrol, on the attenuation of sleep deprivation-induced cognitive impairment. We found that BDPP significantly improves sleep deprivation-induced contextual memory deficits, possibly through the activation of CREB and mTOR signaling pathways. We also identified brain-available polyphenol metabolites from BDPP, among which quercetin-3-O-glucuronide activates CREB signaling and malvidin-3-O-glucoside activates mTOR signaling. In combination, quercetin and malvidin-glucoside significantly attenuated sleep deprivation-induced cognitive impairment in -a mouse model of acute sleep deprivation. Our data suggests the feasibility of using select brain-targeting polyphenol compounds derived from BDPP as potential therapeutic agents in promoting resilience against sleep deprivation-induced cognitive dysfunction. PMID:26235983

  10. Sleep Deprivation, Allergy Symptoms, and Negatively Reinforced Problem Behavior.

    ERIC Educational Resources Information Center

    Kennedy, Craig H.; Meyer, Kim A.

    1996-01-01

    A study of the relationship between presence or absence of sleep deprivation, allergy symptoms, and the rate and function of problem behavior in three adolescents with moderate to profound mental retardation found that problem behavior was negatively reinforced by escape from instruction, and both allergy symptoms and sleep deprivation influenced…

  11. Changes in Plasma Lipids during Exposure to Total Sleep Deprivation.

    PubMed

    Chua, Eric Chern-Pin; Shui, Guanghou; Cazenave-Gassiot, Amaury; Wenk, Markus R; Gooley, Joshua J

    2015-11-01

    The effects of sleep loss on plasma lipids, which play an important role in energy homeostasis and signaling, have not been systematically examined. Our aim was to identify lipid species in plasma that increase or decrease reliably during exposure to total sleep deprivation. Twenty individuals underwent sleep deprivation in a laboratory setting. Blood was drawn every 4 h and mass spectrometry techniques were used to analyze concentrations of 263 lipid species in plasma, including glycerolipids, glycerophospholipids, sphingolipids, and sterols. Chronobiology and Sleep Laboratory, Duke-NUS Graduate Medical School. Healthy ethnic-Chinese males aged 21-28 y (n = 20). Subjects were kept awake for 40 consecutive hours. Each metabolite time series was modeled as a sum of sinusoidal (circadian) and linear components, and we assessed whether the slope of the linear component differed from zero. More than a third of all individually analyzed lipid profiles exhibited a circadian rhythm and/or a linear change in concentration during sleep deprivation. Twenty-five lipid species showed a linear and predominantly unidirectional trend in concentration levels that was consistent across participants. Choline plasmalogen levels decreased, whereas several phosphatidylcholine (PC) species and triacylglycerides (TAG) carrying polyunsaturated fatty acids increased. The decrease in choline plasmalogen levels during sleep deprivation is consistent with prior work demonstrating that these lipids are susceptible to degradation by oxidative stress. The increase in phosphatidylcholines and triacylglycerides suggests that sleep loss might modulate lipid metabolism, which has potential implications for metabolic health in individuals who do not achieve adequate sleep. © 2015 Associated Professional Sleep Societies, LLC.

  12. Free recall of word lists under total sleep deprivation and after recovery sleep.

    PubMed

    de Almeida Valverde Zanini, Gislaine; Tufik, Sérgio; Andersen, Monica Levy; da Silva, Raquel Cristina Martins; Bueno, Orlando Francisco Amodeo; Rodrigues, Camila Cruz; Pompéia, Sabine

    2012-02-01

    One task that has been used to assess memory effects of prior total sleep deprivation (TSD) is the immediate free recall of word lists; however, results have been mixed. A possible explanation for this is task impurity, since recall of words from different serial positions reflects use of distinct types of memory (last words: short-term memory; first and intermediate words: episodic memory). Here we studied the effects of 2 nights of TSD on immediate free recall of semantically unrelated word lists considering the serial position curve. Random allocation to a 2-night TSD protocol followed by one night of recovery sleep or to a control group. Study conducted under continuous behavioral monitoring. 24 young, healthy male volunteers. 2 nights of total sleep deprivation (TSD) and one night of recovery sleep. Participants were shown five 15 unrelated word-lists at baseline, after one and 2 nights of TSD, and after one night of recovery sleep. We also investigated the development of recall strategies (learning) and susceptibility to interference from previous lists. No free recall impairment occurred during TSD, irrespective of serial position. Interference was unchanged. Both groups developed recall strategies, but task learning occurred earlier in controls and was evident in the TSD group only after sleep recovery. Prior TSD spared episodic memory, short-term phonological memory, and interference, allowed the development of recall strategies, but may have decreased the advantage of using these strategies, which returned to normal after recovery sleep.

  13. Identification of genes associated with resilience/vulnerability to sleep deprivation and starvation in Drosophila.

    PubMed

    Thimgan, Matthew S; Seugnet, Laurent; Turk, John; Shaw, Paul J

    2015-05-01

    Flies mutant for the canonical clock protein cycle (cyc(01)) exhibit a sleep rebound that is ∼10 times larger than wild-type flies and die after only 10 h of sleep deprivation. Surprisingly, when starved, cyc(01) mutants can remain awake for 28 h without demonstrating negative outcomes. Thus, we hypothesized that identifying transcripts that are differentially regulated between waking induced by sleep deprivation and waking induced by starvation would identify genes that underlie the deleterious effects of sleep deprivation and/or protect flies from the negative consequences of waking. We used partial complementary DNA microarrays to identify transcripts that are differentially expressed between cyc(01) mutants that had been sleep deprived or starved for 7 h. We then used genetics to determine whether disrupting genes involved in lipid metabolism would exhibit alterations in their response to sleep deprivation. Laboratory. Drosophila melanogaster. Sleep deprivation and starvation. We identified 84 genes with transcript levels that were differentially modulated by 7 h of sleep deprivation and starvation in cyc(01) mutants and were confirmed in independent samples using quantitative polymerase chain reaction. Several of these genes were predicted to be lipid metabolism genes, including bubblegum, cueball, and CG4500, which based on our data we have renamed heimdall (hll). Using lipidomics we confirmed that knockdown of hll using RNA interference significantly decreased lipid stores. Importantly, genetically modifying bubblegum, cueball, or hll resulted in sleep rebound alterations following sleep deprivation compared to genetic background controls. We have identified a set of genes that may confer resilience/vulnerability to sleep deprivation and demonstrate that genes involved in lipid metabolism modulate sleep homeostasis. © 2015 Associated Professional Sleep Societies, LLC.

  14. Melatonin attenuates dextran sodium sulfate induced colitis with sleep deprivation: possible mechanism by microarray analysis.

    PubMed

    Chung, Sook Hee; Park, Young Sook; Kim, Ok Soon; Kim, Ja Hyun; Baik, Haing Woon; Hong, Young Ok; Kim, Sang Su; Shin, Jae-Ho; Jun, Jin-Hyun; Jo, Yunju; Ahn, Sang Bong; Jo, Young Kwan; Son, Byoung Kwan; Kim, Seong Hwan

    2014-06-01

    Inflammatory bowel disease is a chronic inflammatory condition of the gastrointestinal tract. It can be aggravated by stress, like sleep deprivation, and improved by anti-inflammatory agents, like melatonin. We aimed to investigate the effects of sleep deprivation and melatonin on inflammation. We also investigated genes regulated by sleep deprivation and melatonin. In the 2% DSS induced colitis mice model, sleep deprivation was induced using modified multiple platform water bath. Melatonin was injected after induction of colitis and colitis with sleep deprivation. Also mRNA was isolated from the colon of mice and analyzed via microarray and real-time PCR. Sleep deprivation induced reduction of body weight, and it was difficult for half of the mice to survive. Sleep deprivation aggravated, and melatonin attenuated the severity of colitis. In microarrays and real-time PCR of mice colon tissues, mRNA of adiponectin and aquaporin 8 were downregulated by sleep deprivation and upregulated by melatonin. However, mRNA of E2F transcription factor (E2F2) and histocompatibility class II antigen A, beta 1 (H2-Ab1) were upregulated by sleep deprivation and downregulated by melatonin. Melatonin improves and sleep deprivation aggravates inflammation of colitis in mice. Adiponectin, aquaporin 8, E2F2 and H2-Ab1 may be involved in the inflammatory change aggravated by sleep deprivation and attenuated by melatonin.

  15. Sleep deprivation impairs memory by attenuating mTORC1-dependent protein synthesis.

    PubMed

    Tudor, Jennifer C; Davis, Emily J; Peixoto, Lucia; Wimmer, Mathieu E; van Tilborg, Erik; Park, Alan J; Poplawski, Shane G; Chung, Caroline W; Havekes, Robbert; Huang, Jiayan; Gatti, Evelina; Pierre, Philippe; Abel, Ted

    2016-04-26

    Sleep deprivation is a public health epidemic that causes wide-ranging deleterious consequences, including impaired memory and cognition. Protein synthesis in hippocampal neurons promotes memory and cognition. The kinase complex mammalian target of rapamycin complex 1 (mTORC1) stimulates protein synthesis by phosphorylating and inhibiting the eukaryotic translation initiation factor 4E-binding protein 2 (4EBP2). We investigated the involvement of the mTORC1-4EBP2 axis in the molecular mechanisms mediating the cognitive deficits caused by sleep deprivation in mice. Using an in vivo protein translation assay, we found that loss of sleep impaired protein synthesis in the hippocampus. Five hours of sleep loss attenuated both mTORC1-mediated phosphorylation of 4EBP2 and the interaction between eukaryotic initiation factor 4E (eIF4E) and eIF4G in the hippocampi of sleep-deprived mice. Increasing the abundance of 4EBP2 in hippocampal excitatory neurons before sleep deprivation increased the abundance of phosphorylated 4EBP2, restored the amount of eIF4E-eIF4G interaction and hippocampal protein synthesis to that seen in mice that were not sleep-deprived, and prevented the hippocampus-dependent memory deficits associated with sleep loss. These findings collectively demonstrate that 4EBP2-regulated protein synthesis is a critical mediator of the memory deficits caused by sleep deprivation. Copyright © 2016, American Association for the Advancement of Science.

  16. The impact of sleep deprivation in military surgical teams: a systematic review.

    PubMed

    Parker, Rachael Sv; Parker, P

    2017-06-01

    Fatigue in military operations leads to safety and operational problems due to a decrease in alertness and performance. The primary method of counteracting the effects of sleep deprivation is to increase nightly sleep time, which in operational situations is not always feasible. History has taught us that surgeons and surgical teams are finite resources that cannot operate on patients indefinitely. A systematic review was conducted using the search terms ' sleep ' and ' deprivation ' examining the impact of sleep deprivation on cognitive performance in military surgical teams. Studies examining outcomes on intensive care patients and subjects with comorbidities were not addressed in this review. Sleep deprivation in any ' out-of-hours ' surgery has a significant impact on overall morbidity and mortality. Sleep deprivation in surgeons and surgical trainees negatively impacts cognitive performance and puts their own and patients' health at risk. All published research lacks consensus when defining ' sleep deprivation ' and ' rested ' states. It is recognised that it would be unethical to conduct a well-designed randomised controlled trial, to determine the effects of fatigue on performance in surgery; however, there is a paucity between surrogate markers and applying simulated results to actual clinical performance. This requires further research. Recommended methods of combating fatigue include: prophylactically ' sleep-banking ' prior to known periods of sleep deprivation, napping, use of stimulant or alerting substances such as modafinil, coordinated work schedules to reduce circadian desynchronisation and regular breaks with enforced rest periods. A forward surgical team will become combat-ineffective after 48 hours of continuous operations. This systematic review recommends implementing on-call periods of no more than 12 hours in duration, with adequate rest periods every 24 hours. Drug therapies and sleep banking may, in the short term, prevent negative

  17. Tailoring Gut Microbiota for Enhanced Resilience and Performance Under Sleep-Deprived Conditions

    DTIC Science & Technology

    2016-08-01

    psychological disorders, we have developed a hypothesis that sleep deprivation initially degrades the functional and structural integrity of the...obesity. Interestingly, perturbation of gut microbiota presents a pattern of metabolic abnormalities mirroring those induced by sleep deprivation. In...sleep deprivation initially causes degradation in the functional and structural integrity of the gastrointestinal tract. Data generated will be

  18. The behavioral and health consequences of sleep deprivation among U.S. high school students: relative deprivation matters.

    PubMed

    Meldrum, Ryan Charles; Restivo, Emily

    2014-06-01

    To evaluate whether the strength of the association between sleep deprivation and negative behavioral and health outcomes varies according to the relative amount of sleep deprivation experienced by adolescents. 2011 Youth Risk Behavior Survey data of high school students (N=15,364) were analyzed. Associations were examined on weighted data using logistic regression. Twelve outcomes were examined, ranging from weapon carrying to obesity. The primary independent variable was a self-reported measure of average number of hours slept on school nights. Participants who reported deprivations in sleep were at an increased risk of a number of negative outcomes. However, this varied considerably across different degrees of sleep deprivation. For each of the outcomes considered, those who slept less than 5h were more likely to report negative outcomes (adjusted odds ratios ranging from 1.38 to 2.72; p<.05 across all models) relative to sleeping 8 or more hours. However, less extreme forms of sleep deprivation were, in many instances, unrelated to the outcomes considered. Among U.S. high school students, deficits in sleep are significantly and substantively associated with a variety of negative outcomes, and this association is particularly pronounced for students achieving fewer than 5h of sleep at night. Copyright © 2014 Elsevier Inc. All rights reserved.

  19. Sleep deprivation selectively disrupts top-down adaptation to cognitive conflict in the Stroop test.

    PubMed

    Gevers, Wim; Deliens, Gaetane; Hoffmann, Sophie; Notebaert, Wim; Peigneux, Philippe

    2015-12-01

    Sleep deprivation is known to exert detrimental effects on various cognitive domains, including attention, vigilance and working memory. Seemingly at odds with these findings, prior studies repeatedly failed to evidence an impact of prior sleep deprivation on cognitive interference in the Stroop test, a hallmark paradigm in the study of cognitive control abilities. The present study investigated further the effect of sleep deprivation on cognitive control using an adapted version of the Stroop test that allows to segregate top-down (attentional reconfiguration on incongruent items) and bottom-up (facilitated processing after repetitions in responses and/or features of stimuli) components of performance. Participants underwent a regular night of sleep or a night of total sleep deprivation before cognitive testing. Results disclosed that sleep deprivation selectively impairs top-down adaptation mechanisms: cognitive control no longer increased upon detection of response conflict at the preceding trial. In parallel, bottom-up abilities were found unaffected by sleep deprivation: beneficial effects of stimulus and response repetitions persisted. Changes in vigilance states due to sleep deprivation selectively impact on cognitive control in the Stroop test by affecting top-down, but not bottom-up, mechanisms that guide adaptive behaviours. © 2015 European Sleep Research Society.

  20. Selective neuronal lapses precede human cognitive lapses following sleep deprivation.

    PubMed

    Nir, Yuval; Andrillon, Thomas; Marmelshtein, Amit; Suthana, Nanthia; Cirelli, Chiara; Tononi, Giulio; Fried, Itzhak

    2017-12-01

    Sleep deprivation is a major source of morbidity with widespread health effects, including increased risk of hypertension, diabetes, obesity, heart attack, and stroke. Moreover, sleep deprivation brings about vehicle accidents and medical errors and is therefore an urgent topic of investigation. During sleep deprivation, homeostatic and circadian processes interact to build up sleep pressure, which results in slow behavioral performance (cognitive lapses) typically attributed to attentional thalamic and frontoparietal circuits, but the underlying mechanisms remain unclear. Recently, through study of electroencephalograms (EEGs) in humans and local field potentials (LFPs) in nonhuman primates and rodents it was found that, during sleep deprivation, regional 'sleep-like' slow and theta (slow/theta) waves co-occur with impaired behavioral performance during wakefulness. Here we used intracranial electrodes to record single-neuron activities and LFPs in human neurosurgical patients performing a face/nonface categorization psychomotor vigilance task (PVT) over multiple experimental sessions, including a session after full-night sleep deprivation. We find that, just before cognitive lapses, the selective spiking responses of individual neurons in the medial temporal lobe (MTL) are attenuated, delayed, and lengthened. These 'neuronal lapses' are evident on a trial-by-trial basis when comparing the slowest behavioral PVT reaction times to the fastest. Furthermore, during cognitive lapses, LFPs exhibit a relative local increase in slow/theta activity that is correlated with degraded single-neuron responses and with baseline theta activity. Our results show that cognitive lapses involve local state-dependent changes in neuronal activity already present in the MTL.

  1. β-Amyloid accumulation in the human brain after one night of sleep deprivation.

    PubMed

    Shokri-Kojori, Ehsan; Wang, Gene-Jack; Wiers, Corinde E; Demiral, Sukru B; Guo, Min; Kim, Sung Won; Lindgren, Elsa; Ramirez, Veronica; Zehra, Amna; Freeman, Clara; Miller, Gregg; Manza, Peter; Srivastava, Tansha; De Santi, Susan; Tomasi, Dardo; Benveniste, Helene; Volkow, Nora D

    2018-04-24

    The effects of acute sleep deprivation on β-amyloid (Aβ) clearance in the human brain have not been documented. Here we used PET and 18 F-florbetaben to measure brain Aβ burden (ABB) in 20 healthy controls tested after a night of rested sleep (baseline) and after a night of sleep deprivation. We show that one night of sleep deprivation, relative to baseline, resulted in a significant increase in Aβ burden in the right hippocampus and thalamus. These increases were associated with mood worsening following sleep deprivation, but were not related to the genetic risk (APOE genotype) for Alzheimer's disease. Additionally, baseline ABB in a range of subcortical regions and the precuneus was inversely associated with reported night sleep hours. APOE genotyping was also linked to subcortical ABB, suggesting that different Alzheimer's disease risk factors might independently affect ABB in nearby brain regions. In summary, our findings show adverse effects of one-night sleep deprivation on brain ABB and expand on prior findings of higher Aβ accumulation with chronic less sleep. Copyright © 2018 the Author(s). Published by PNAS.

  2. Partial sleep deprivation impacts impulsive action but not impulsive decision-making.

    PubMed

    Demos, K E; Hart, C N; Sweet, L H; Mailloux, K A; Trautvetter, J; Williams, S E; Wing, R R; McCaffery, J M

    2016-10-01

    Sleep deprivation may lead to increased impulsivity, however, previous literature has focused on examining effects of total sleep deprivation (TSD) rather than the more common condition, partial sleep deprivation (PSD) or 'short sleep'. Moreover, it has been unclear whether PSD impacts impulse-related cognitive processes, and specifically if it differentially affects impulsive action versus impulsive decision-making. We sought to determine if short compared to long sleep (6 vs. 9h/night) impacts impulsive action via behavioral inhibition (Go/No-Go), and/or impulsive decision-making processes of risk taking (Balloon Analogue Risk Task [BART]) and preferences for immediate over delayed rewards (Delay Discounting). In a within-subject design, 34 participants (71% female, mean age=37.0years, SD=10.54) were assigned to four consecutive nights of 6h/night (short sleep) and 9h/night (long sleep) in their own home in random counterbalanced order. Sleep was measured via wrist-worn actigraphs to confirm adherence to the sleep schedules (mean short sleep=5.9h, SD=0.3; mean long sleep=8.6h, SD=0.3, p<0.001). The Go/No-Go, BART, and Delay Discounting tasks were completed following both sleep conditions. Participants had more inhibition errors on the Go/No-Go task after short (mean false alarms=19.79%, SD=14.51) versus long sleep (mean=15.97%, SD=9.51, p=0.039). This effect was strongest in participants reporting longer habitual time in bed (p=0.04). There were no differences in performance following long- versus short-sleep for either delay discounting or the BART (p's>0.4). Overall, these results indicate that four days of PSD diminishes behavioral inhibition abilities, but may not alter impulsive decision-making. These findings contribute to the emerging understanding of how partial sleep deprivation, currently an epidemic, impacts cognitive ability. Future research should continue to explore the connection between PSD and cognitive functions, and ways to minimize the

  3. Hypersynchronous delta waves and somnambulism: brain topography and effect of sleep deprivation.

    PubMed

    Pilon, Mathieu; Zadra, Antonio; Joncas, Steve; Montplaisir, Jacques

    2006-01-01

    Hypersynchronous delta activity (HSD) is usually described as several continuous high-voltage delta waves (> or = 150 microV) in the sleep electroencephalogram of somnambulistic patients. However, studies have yielded varied and contradictory results. The goal of the present study was to evaluate HSD over different electroencephalographic derivations during the non-rapid eye movement (NREM) sleep of somnambulistic patients and controls during normal sleep and following 38 hours of sleep deprivation, as well as prior to sleepwalking episodes. N/A. Sleep disorders clinic. Ten adult sleepwalkers and 10 sex- and age-matched control subjects were investigated polysomnographically during a baseline night and following 38 hours of sleep deprivation. N/A. During normal sleep, sleepwalkers had a significantly higher ratio of HSD over the time spent in stage 2, 3 and 4 on frontal and central derivations when compared with controls. Sleep deprivation resulted in a significant increase in the ratio of the time in HSD over the time in stage 4 on the frontal lead in both groups and on the central lead in controls. There was no evidence for a temporal accumulation of HSD prior to the episodes. HSD shows a clear frontocentral gradient across all subjects during both baseline and recovery sleep and has relatively low specificity for the diagnosis of NREM parasomnias. Increases in HSD after sleep deprivation may reflect an enhancement of the homeostatic process underlying sleep regulation.

  4. Identification of Genes Associated with Resilience/Vulnerability to Sleep Deprivation and Starvation in Drosophila

    PubMed Central

    Thimgan, Matthew S.; Seugnet, Laurent; Turk, John; Shaw, Paul J.

    2015-01-01

    Background and Study Objectives: Flies mutant for the canonical clock protein cycle (cyc01) exhibit a sleep rebound that is ∼10 times larger than wild-type flies and die after only 10 h of sleep deprivation. Surprisingly, when starved, cyc01 mutants can remain awake for 28 h without demonstrating negative outcomes. Thus, we hypothesized that identifying transcripts that are differentially regulated between waking induced by sleep deprivation and waking induced by starvation would identify genes that underlie the deleterious effects of sleep deprivation and/or protect flies from the negative consequences of waking. Design: We used partial complementary DNA microarrays to identify transcripts that are differentially expressed between cyc01 mutants that had been sleep deprived or starved for 7 h. We then used genetics to determine whether disrupting genes involved in lipid metabolism would exhibit alterations in their response to sleep deprivation. Setting: Laboratory. Patients or Participants: Drosophila melanogaster. Interventions: Sleep deprivation and starvation. Measurements and Results: We identified 84 genes with transcript levels that were differentially modulated by 7 h of sleep deprivation and starvation in cyc01 mutants and were confirmed in independent samples using quantitative polymerase chain reaction. Several of these genes were predicted to be lipid metabolism genes, including bubblegum, cueball, and CG4500, which based on our data we have renamed heimdall (hll). Using lipidomics we confirmed that knockdown of hll using RNA interference significantly decreased lipid stores. Importantly, genetically modifying bubblegum, cueball, or hll resulted in sleep rebound alterations following sleep deprivation compared to genetic background controls. Conclusions: We have identified a set of genes that may confer resilience/vulnerability to sleep deprivation and demonstrate that genes involved in lipid metabolism modulate sleep homeostasis. Citation: Thimgan MS

  5. Feedback Blunting: Total Sleep Deprivation Impairs Decision Making that Requires Updating Based on Feedback.

    PubMed

    Whitney, Paul; Hinson, John M; Jackson, Melinda L; Van Dongen, Hans P A

    2015-05-01

    To better understand the sometimes catastrophic effects of sleep loss on naturalistic decision making, we investigated effects of sleep deprivation on decision making in a reversal learning paradigm requiring acquisition and updating of information based on outcome feedback. Subjects were randomized to a sleep deprivation or control condition, with performance testing at baseline, after 2 nights of total sleep deprivation (or rested control), and following 2 nights of recovery sleep. Subjects performed a decision task involving initial learning of go and no go response sets followed by unannounced reversal of contingencies, requiring use of outcome feedback for decisions. A working memory scanning task and psychomotor vigilance test were also administered. Six consecutive days and nights in a controlled laboratory environment with continuous behavioral monitoring. Twenty-six subjects (22-40 y of age; 10 women). Thirteen subjects were randomized to a 62-h total sleep deprivation condition; the others were controls. Unlike controls, sleep deprived subjects had difficulty with initial learning of go and no go stimuli sets and had profound impairment adapting to reversal. Skin conductance responses to outcome feedback were diminished, indicating blunted affective reactions to feedback accompanying sleep deprivation. Working memory scanning performance was not significantly affected by sleep deprivation. And although sleep deprived subjects showed expected attentional lapses, these could not account for impairments in reversal learning decision making. Sleep deprivation is particularly problematic for decision making involving uncertainty and unexpected change. Blunted reactions to feedback while sleep deprived underlie failures to adapt to uncertainty and changing contingencies. Thus, an error may register, but with diminished effect because of reduced affective valence of the feedback or because the feedback is not cognitively bound with the choice. This has important

  6. Effects of sleep deprivation on cognitive and physical performance in university students.

    PubMed

    Patrick, Yusuf; Lee, Alice; Raha, Oishik; Pillai, Kavya; Gupta, Shubham; Sethi, Sonika; Mukeshimana, Felicite; Gerard, Lothaire; Moghal, Mohammad U; Saleh, Sohag N; Smith, Susan F; Morrell, Mary J; Moss, James

    2017-01-01

    Sleep deprivation is common among university students, and has been associated with poor academic performance and physical dysfunction. However, current literature has a narrow focus in regard to domains tested, this study aimed to investigate the effects of a night of sleep deprivation on cognitive and physical performance in students. A randomized controlled crossover study was carried out with 64 participants [58% male ( n  = 37); 22 ± 4 years old (mean ± SD)]. Participants were randomized into two conditions: normal sleep or one night sleep deprivation. Sleep deprivation was monitored using an online time-stamped questionnaire at 45 min intervals, completed in the participants' homes. The outcomes were cognitive: working memory (Simon game© derivative), executive function (Stroop test); and physical: reaction time (ruler drop testing), lung function (spirometry), rate of perceived exertion, heart rate, and blood pressure during submaximal cardiopulmonary exercise testing. Data were analysed using paired two-tailed T tests and MANOVA. Reaction time and systolic blood pressure post-exercise were significantly increased following sleep deprivation (mean ± SD change: reaction time: 0.15 ± 0.04 s, p  = 0.003; systolic BP: 6 ± 17 mmHg, p  = 0.012). No significant differences were found in other variables. Reaction time and vascular response to exercise were significantly affected by sleep deprivation in university students, whilst other cognitive and cardiopulmonary measures showed no significant changes. These findings indicate that acute sleep deprivation can have an impact on physical but not cognitive ability in young healthy university students. Further research is needed to identify mechanisms of change and the impact of longer term sleep deprivation in this population.

  7. Feedback Blunting: Total Sleep Deprivation Impairs Decision Making that Requires Updating Based on Feedback

    PubMed Central

    Whitney, Paul; Hinson, John M.; Jackson, Melinda L.; Van Dongen, Hans P.A.

    2015-01-01

    Study Objectives: To better understand the sometimes catastrophic effects of sleep loss on naturalistic decision making, we investigated effects of sleep deprivation on decision making in a reversal learning paradigm requiring acquisition and updating of information based on outcome feedback. Design: Subjects were randomized to a sleep deprivation or control condition, with performance testing at baseline, after 2 nights of total sleep deprivation (or rested control), and following 2 nights of recovery sleep. Subjects performed a decision task involving initial learning of go and no go response sets followed by unannounced reversal of contingencies, requiring use of outcome feedback for decisions. A working memory scanning task and psychomotor vigilance test were also administered. Setting: Six consecutive days and nights in a controlled laboratory environment with continuous behavioral monitoring. Subjects: Twenty-six subjects (22–40 y of age; 10 women). Interventions: Thirteen subjects were randomized to a 62-h total sleep deprivation condition; the others were controls. Results: Unlike controls, sleep deprived subjects had difficulty with initial learning of go and no go stimuli sets and had profound impairment adapting to reversal. Skin conductance responses to outcome feedback were diminished, indicating blunted affective reactions to feedback accompanying sleep deprivation. Working memory scanning performance was not significantly affected by sleep deprivation. And although sleep deprived subjects showed expected attentional lapses, these could not account for impairments in reversal learning decision making. Conclusions: Sleep deprivation is particularly problematic for decision making involving uncertainty and unexpected change. Blunted reactions to feedback while sleep deprived underlie failures to adapt to uncertainty and changing contingencies. Thus, an error may register, but with diminished effect because of reduced affective valence of the feedback

  8. Oculomotor impairment during chronic partial sleep deprivation.

    PubMed

    Russo, M; Thomas, M; Thorne, D; Sing, H; Redmond, D; Rowland, L; Johnson, D; Hall, S; Krichmar, J; Balkin, T

    2003-04-01

    The effects of chronic partial sleep (sleep deprivation) and extended sleep (sleep augmentation) followed by recovery sleep on oculomotor function were evaluated in normal subjects to explore the usefulness of oculomotor assessment for alertness monitoring in fitness-for-duty testing. Sixty-six commercial drivers (24-62 years, 50m/16f) participated in a 15 day study composed of 3 training days with 8h time in bed per night, 7 experimental days with subjects randomly assigned to either 3, 5, 7, or 9h time in bed, and 3 recovery nights with 8h time in bed. Data from 57 subjects were used. Saccadic velocity (SV), initial pupil diameter (IPD), latency to pupil constriction (CL), and amplitude of pupil constriction (CA) were assessed and correlated with the sleep latency test (SLT), the Stanford sleepiness scale (SSS), and simulated driving performance. Regression analyses showed that SV slowed significantly in the 3 and 5h groups, IPD decreased significantly in the 9h group, and CL increased significantly in the 3h group. SLT and SSS significantly correlated with SV, IPD, CL, and driving accidents for the 3h group, and with CL for the 5h group. Analyses also showed a significant negative correlation between decreasing SV and increasing driving accidents in the 3h group and a significant negative correlation between IPD and driving accidents for the 7h group. The results demonstrate a sensitivity primarily of SV to sleepiness, and a correlation of SV and IPD to impaired simulated driving performance, providing evidence for the potential utility of oculomotor indicators in the detection of excessive sleepiness and deterioration of complex motor performance with chronic partial sleep restriction. This paper shows a relationship between sleep deprivation and oculomotor measures, and suggests a potential utility for oculometrics in assessing operational performance readiness under sleep restricted conditions.

  9. The effect of 60-h sleep deprivation on cardiovascular regulation and body temperature.

    PubMed

    Vaara, Jani; Kyröläinen, Heikki; Koivu, Mikko; Tulppo, Mikko; Finni, Taija

    2009-02-01

    This study examined cardiovascular regulation and body temperature (BT) during 60 h of sleep deprivation in 20 young healthy cadets. Heart rate variability was measured during an active orthostatic test (AOT). Measurements were performed each day in the morning and evening after 2, 14, 26, 38, 50 and 60 h of sleep deprivation. In AOT, in the sitting and standing positions, heart rate decreased (P < 0.001), while high frequency and low frequency power increased (P < 0.05-0.001) during sleep deprivation. Body temperature also decreased (P < 0.001), but no changes were detected in blood pressure. In conclusion, the accumulation of 60 h of sleep loss resulted in increased vagal outflow, as evidenced by decreased heart rate. In addition, BT decreased during sleep deprivation. Thus, sleep deprivation causes alterations in autonomic regulation of the heart, and in thermoregulation.

  10. Cold hands, warm feet: sleep deprivation disrupts thermoregulation and its association with vigilance.

    PubMed

    Romeijn, Nico; Verweij, Ilse M; Koeleman, Anne; Mooij, Anne; Steimke, Rosa; Virkkala, Jussi; van der Werf, Ysbrand; Van Someren, Eus J W

    2012-12-01

    Vigilance is affected by induced and spontaneous skin temperature fluctuations. Whereas sleep deprivation strongly affects vigilance, no previous study examined in detail its effect on human skin temperature fluctuations and their association with vigilance. In a repeated-measures constant routine design, skin temperatures were assessed continuously from 14 locations while performance was assessed using a reaction time task, including eyes-open video monitoring, performed five times a day for 2 days, after a normal sleep or sleep deprivation night. Participants were seated in a dimly lit, temperature-controlled laboratory. Eight healthy young adults (five males, age 22.0 ± 1.8 yr (mean ± standard deviation)). One night of sleep deprivation. Mixed-effect regression models were used to evaluate the effect of sleep deprivation on skin temperature gradients of the upper (ear-mastoid), middle (hand-arm), and lower (foot-leg) body, and on the association between fluctuations in performance and in temperature gradients. Sleep deprivation induced a marked dissociation of thermoregulatory skin temperature gradients, indicative of attenuated heat loss from the hands co-occurring with enhanced heat loss from the feet. Sleep deprivation moreover attenuated the association between fluctuations in performance and temperature gradients; the association was best preserved for the upper body gradient. Sleep deprivation disrupts coordination of fluctuations in thermoregulatory skin temperature gradients. The dissociation of middle and lower body temperature gradients may therefore be evaluated as a marker for sleep debt, and the upper body gradient as a possible aid in vigilance assessment when sleep debt is unknown. Importantly, our findings suggest that sleep deprivation affects the coordination between skin blood flow fluctuations and the baroreceptor-mediated cardiovascular regulation that prevents venous pooling of blood in the lower limbs when there is the orthostatic

  11. Sleepless in Adolescence: Prospective Data on Sleep Deprivation, Health and Functioning

    ERIC Educational Resources Information Center

    Roberts, Robert E.; Roberts, Catherine Ramsay; Duong, Hao T.

    2009-01-01

    We estimate prevalence, incidence and persistence of short sleep or sleep deprivation in a two wave cohort study of 4175 youths 11-17 years old at baseline and 3134 of these a year later. Data were collected using computer interviews and questionnaires. Sleep deprivation was defined as 6 h or less per night during the past 4 weeks. Weighted…

  12. Short-Term Total Sleep-Deprivation Impairs Contextual Fear Memory, and Contextual Fear-Conditioning Reduces REM Sleep in Moderately Anxious Swiss Mice

    PubMed Central

    Qureshi, Munazah F.; Jha, Sushil K.

    2017-01-01

    The conditioning tasks have been widely used to model fear and anxiety and to study their association with sleep. Many reports suggest that sleep plays a vital role in the consolidation of fear memory. Studies have also demonstrated that fear-conditioning influences sleep differently in mice strains having a low or high anxiety level. It is, therefore, necessary to know, how sleep influences fear-conditioning and how fear-conditioning induces changes in sleep architecture in moderate anxious strains. We have used Swiss mice, a moderate anxious strain, to study the effects of: (i) sleep deprivation on contextual fear conditioned memory, and also (ii) contextual fear conditioning on sleep architecture. Animals were divided into three groups: (a) non-sleep deprived (NSD); (b) stress control (SC); and (c) sleep-deprived (SD) groups. The SD animals were SD for 5 h soon after training. We found that the NSD and SC animals showed 60.57% and 58.12% freezing on the testing day, while SD animals showed significantly less freezing (17.13% only; p < 0.001) on the testing day. Further, we observed that contextual fear-conditioning did not alter the total amount of wakefulness and non-rapid eye movement (NREM) sleep. REM sleep, however, significantly decreased in NSD and SC animals on the training and testing days. Interestingly, REM sleep did not decrease in the SD animals on the testing day. Our results suggest that short-term sleep deprivation impairs fear memory in moderate anxious mice. It also suggests that NREM sleep, but not REM sleep, may have an obligatory role in memory consolidation. PMID:29238297

  13. Sustained attention performance during sleep deprivation: evidence of state instability

    NASA Technical Reports Server (NTRS)

    Doran, S. M.; Van Dongen, H. P.; Dinges, D. F.

    2001-01-01

    Nathaniel Kleitman was the first to observe that sleep deprivation in humans did not eliminate the ability to perform neurobehavioral functions, but it did make it difficult to maintain stable performance for more than a few minutes. To investigate variability in performance as a function of sleep deprivation, n = 13 subjects were tested every 2 hours on a 10-minute, sustained-attention, psychomotor vigilance task (PVT) throughout 88 hours of total sleep deprivation (TSD condition), and compared to a control group of n = 15 subjects who were permitted a 2-hour nap every 12 hours (NAP condition) throughout the 88-hour period. PVT reaction time means and standard deviations increased markedly among subjects and within each individual subject in the TSD condition relative to the NAP condition. TSD subjects also had increasingly greater performance variability as a function of time on task after 18 hours of wakefulness. During sleep deprivation, variability in PVT performance reflected a combination of normal timely responses, errors of omission (i.e., lapses), and errors of commission (i.e., responding when no stimulus was present). Errors of omission and errors of commission were highly intercorrelated across deprivation in the TSD condition (r = 0.85, p = 0.0001), suggesting that performance instability is more likely to include compensatory effort than a lack of motivation. The marked increases in PVT performance variability as sleep loss continued supports the "state instability" hypothesis, which posits that performance during sleep deprivation is increasingly variable due to the influence of sleep initiating mechanisms on the endogenous capacity to maintain attention and alertness, thereby creating an unstable state that fluctuates within seconds and that cannot be characterized as either fully awake or asleep.

  14. Too tired to inspire or be inspired: Sleep deprivation and charismatic leadership.

    PubMed

    Barnes, Christopher M; Guarana, Cristiano L; Nauman, Shazia; Kong, Dejun Tony

    2016-08-01

    We draw from theory on sleep and affect regulation to extend the emotional labor model of leadership. We examine both leader and follower sleep as important antecedents of attributions of charismatic leadership. In Study 1, we manipulate the sleep of leaders, and find that leader emotional labor in the form of deep acting (but not surface acting or authentically experienced positive affect) mediates the harmful effect of leader sleep deprivation on follower ratings of charismatic leadership. In Study 2, we manipulate the sleep of followers, and find that follower experienced positive affect mediates the harmful effect of follower sleep deprivation on follower ratings of charismatic leadership of the leader. Thus, both leader and follower sleep deprivation harm attributions of charismatic leadership, with the regulation and experience of affect as causal mechanisms. (PsycINFO Database Record (c) 2016 APA, all rights reserved).

  15. Partial sleep deprivation impacts impulsive action but not impulsive decision-making

    PubMed Central

    Demos, K.E.; Hart, C.N.; Sweet, LH.; Mailloux, K.A.; Trautvetter, J.; Williams, S.E.; Wing, R.R.; McCaffery, J.M.

    2017-01-01

    Sleep deprivation may lead to increased impulsivity, however, previous literature has focused on examining effects of total sleep deprivation (TSD) rather than the more common condition, partial sleep deprivation (PSD) or ‘short sleep’. Moreover, it has been unclear whether PSD impacts impulse-related cognitive processes, and specifically if it differentially affects impulsive action versus impulsive decision-making. We sought to determine if short compared to long sleep (6 vs. 9 h/night) impacts impulsive action via behavioral inhibition (Go/No-Go), and/or impulsive decision-making processes of risk taking (Balloon Analogue Risk Task [BART]) and preferences for immediate over delayed rewards (Delay Discounting). In a within-subject design, 34 participants (71% female, mean age = 37.0 years, SD = 10.54) were assigned to four consecutive nights of 6 h/night (short sleep) and 9 h/night (long sleep) in their own home in random counterbalanced order. Sleep was measured via wrist-worn actigraphs to confirm adherence to the sleep schedules (mean short sleep = 5.9 h, SD = 0.3; mean long sleep = 8.6 h, SD = 0.3, p < 0.001). The Go/No-Go, BART, and Delay Discounting tasks were completed following both sleep conditions. Participants had more inhibition errors on the Go/No-Go task after short (mean false alarms = 19.79%, SD = 14.51) versus long sleep (mean = 15.97%, SD = 9.51, p = 0.039). This effect was strongest in participants reporting longer habitual time in bed (p = 0.04). There were no differences in performance following long- versus short-sleep for either delay discounting or the BART (p’s > 0.4). Overall, these results indicate that four days of PSD diminishes behavioral inhibition abilities, but may not alter impulsive decision-making. These findings contribute to the emerging understanding of how partial sleep deprivation, currently an epidemic, impacts cognitive ability. Future research should continue to explore the connection between PSD and cognitive

  16. Double trouble? The effects of sleep deprivation and chronotype on adolescent affect.

    PubMed

    Dagys, Natasha; McGlinchey, Eleanor L; Talbot, Lisa S; Kaplan, Katherine A; Dahl, Ronald E; Harvey, Allison G

    2012-06-01

      Two understudied risk factors that have been linked to emotional difficulties in adolescence are chronotype and sleep deprivation. This study extended past research by using an experimental design to investigate the role of sleep deprivation and chronotype on emotion in adolescents. It was hypothesized that sleep deprivation and an evening chronotype would be associated with decreased positive affect (PA), increased negative affect (NA), and lower positivity ratios.   Forty-seven healthy adolescents (aged 10-15 for girls, 11-16 for boys) participated in a sleep deprivation and a rested condition. A subsample of 24 adolescents was selected on the basis of extreme morningness or eveningness scores (based on outer quartiles of scores on the Children's Morningness-Eveningness Preferences Scale). PA and NA were measured using the Positive and Negative Affect Schedule for Children, and positivity ratios were calculated by dividing PA by NA.   Participants reported less positive affect and lower positivity ratios when sleep deprived, relative to when rested. Evening chronotypes reported less positive affect and lower positivity ratios than morning chronotypes in both rested and sleep deprivation conditions.   These findings extend previous research by suggesting that adolescents are adversely impacted by sleep deprivation, and that an evening chronotype might serve as a useful marker of emotional vulnerability. Early intervention and prevention strategies can focus on improving sleep and on using chronotherapy principles to reduce eveningness. © 2011 The Authors. Journal of Child Psychology and Psychiatry © 2011 Association for Child and Adolescent Mental Health.

  17. Tired and misconnected: A breakdown of brain modularity following sleep deprivation.

    PubMed

    Ben Simon, Eti; Maron-Katz, Adi; Lahav, Nir; Shamir, Ron; Hendler, Talma

    2017-06-01

    Sleep deprivation (SD) critically affects a range of cognitive and affective functions, typically assessed during task performance. Whether such impairments stem from changes to the brain's intrinsic functional connectivity remain largely unknown. To examine this hypothesis, we applied graph theoretical analysis on resting-state fMRI data derived from 18 healthy participants, acquired during both sleep-rested and sleep-deprived states. We hypothesized that parameters indicative of graph connectivity, such as modularity, will be impaired by sleep deprivation and that these changes will correlate with behavioral outcomes elicited by sleep loss. As expected, our findings point to a profound reduction in network modularity without sleep, evident in the limbic, default-mode, salience and executive modules. These changes were further associated with behavioral impairments elicited by SD: a decrease in salience module density was associated with worse task performance, an increase in limbic module density was predictive of stronger amygdala activation in a subsequent emotional-distraction task and a shift in frontal hub lateralization (from left to right) was associated with increased negative mood. Altogether, these results portray a loss of functional segregation within the brain and a shift towards a more random-like network without sleep, already detected in the spontaneous activity of the sleep-deprived brain. Hum Brain Mapp 38:3300-3314, 2017. © 2017 Wiley Periodicals, Inc. © 2017 Wiley Periodicals, Inc.

  18. Neighborhood Economic Deprivation and Social Fragmentation: Associations With Children's Sleep.

    PubMed

    Bagley, Erika J; Fuller-Rowell, Thomas E; Saini, Ekjyot K; Philbrook, Lauren E; El-Sheikh, Mona

    2016-12-09

    A growing body of work indicates that experiences of neighborhood disadvantage place children at risk for poor sleep. This study aimed to examine how both neighborhood economic deprivation (a measure of poverty) and social fragmentation (an index of instability) are associated with objective measures of the length and quality of children's sleep. Participants were 210 children (54.3% boys) living predominantly in small towns and semirural communities in Alabama. On average children were 11.3 years old (SD = .63); 66.7% of the children were European American and 33.3% were African American. The sample was socioeconomically diverse with 67.9% of the participants living at or below the poverty line and 32.1% from lower-middle-class or middle-class families. Indicators of neighborhood characteristics were derived from the 2012 American Community Survey and composited to create two variables representing neighborhood economic deprivation and social fragmentation. Child sleep period, actual sleep minutes, and efficiency were examined using actigraphy. Higher levels of neighborhood economic deprivation were associated with fewer sleep minutes and poorer sleep efficiency. More neighborhood social fragmentation was also linked with poorer sleep efficiency. Analyses controlled for demographic characteristics, child health, and family socioeconomic status. Findings indicate that living in economically and socially disadvantaged neighborhoods predicts risk for shorter and lower-quality sleep in children. Examination of community context in addition to family and individual characteristics may provide a more comprehensive understanding of the factors shaping child sleep.

  19. The Effect of Acute Sleep Deprivation on Visual Evoked Potentials in Professional Drivers

    PubMed Central

    Jackson, Melinda L.; Croft, Rodney J.; Owens, Katherine; Pierce, Robert J.; Kennedy, Gerard A.; Crewther, David; Howard, Mark E.

    2008-01-01

    Study Objectives: Previous studies have demonstrated that as little as 18 hours of sleep deprivation can cause deleterious effects on performance. It has also been suggested that sleep deprivation can cause a “tunnel-vision” effect, in which attention is restricted to the center of the visual field. The current study aimed to replicate these behavioral effects and to examine the electrophysiological underpinnings of these changes. Design: Repeated-measures experimental study. Setting: University laboratory. Patients or Participants: Nineteen professional drivers (1 woman; mean age = 45.3 ± 9.1 years). Interventions: Two experimental sessions were performed; one following 27 hours of sleep deprivation and the other following a normal night of sleep, with control for circadian effects. Measurements & Results: A tunnel-vision task (central versus peripheral visual discrimination) and a standard checkerboard-viewing task were performed while 32-channel EEG was recorded. For the tunnel-vision task, sleep deprivation resulted in an overall slowing of reaction times and increased errors of omission for both peripheral and foveal stimuli (P < 0.05). These changes were related to reduced P300 amplitude (indexing cognitive processing) but not measures of early visual processing. No evidence was found for an interaction effect between sleep deprivation and visual-field position, either in terms of behavior or electrophysiological responses. Slower processing of the sustained parvocellular visual pathway was demonstrated. Conclusions: These findings suggest that performance deficits on visual tasks during sleep deprivation are due to higher cognitive processes rather than early visual processing. Sleep deprivation may differentially impair processing of more-detailed visual information. Features of the study design (eg, visual angle, duration of sleep deprivation) may influence whether peripheral visual-field neglect occurs. Citation: Jackson ML; Croft RJ; Owens K; Pierce

  20. The unrested resting brain: sleep deprivation alters activity within the default-mode network.

    PubMed

    Gujar, Ninad; Yoo, Seung-Schik; Hu, Peter; Walker, Matthew P

    2010-08-01

    The sleep-deprived brain has principally been characterized by examining dysfunction during cognitive task performance. However, far less attention has been afforded the possibility that sleep deprivation may be as, if not more, accurately characterized on the basis of abnormal resting-state brain activity. Here we report that one night of sleep deprivation significantly disrupts the canonical signature of task-related deactivation, resulting in a double dissociation within anterior as well as posterior midline regions of the default network. Indeed, deactivation within these regions alone discriminated sleep-deprived from sleep-control subjects with a 93% degree of sensitivity and 92% specificity. In addition, the relative balance of deactivation within these default nodes significantly correlated with the amount of prior sleep in the control group (and not extended time awake in the deprivation group). Therefore, the stability and the balance of task-related deactivation in key default-mode regions may be dependent on prior sleep, such that a lack thereof disrupts this signature pattern of brain activity, findings that may offer explanatory insights into conditions associated with sleep loss at both a clinical as well as societal level.

  1. Effects of total sleep deprivation on divided attention performance

    PubMed Central

    2017-01-01

    Dividing attention across two tasks performed simultaneously usually results in impaired performance on one or both tasks. Most studies have found no difference in the dual-task cost of dividing attention in rested and sleep-deprived states. We hypothesized that, for a divided attention task that is highly cognitively-demanding, performance would show greater impairment during exposure to sleep deprivation. A group of 30 healthy males aged 21–30 years was exposed to 40 h of continuous wakefulness in a laboratory setting. Every 2 h, subjects completed a divided attention task comprising 3 blocks in which an auditory Go/No-Go task was 1) performed alone (single task); 2) performed simultaneously with a visual Go/No-Go task (dual task); and 3) performed simultaneously with both a visual Go/No-Go task and a visually-guided motor tracking task (triple task). Performance on all tasks showed substantial deterioration during exposure to sleep deprivation. A significant interaction was observed between task load and time since wake on auditory Go/No-Go task performance, with greater impairment in response times and accuracy during extended wakefulness. Our results suggest that the ability to divide attention between multiple tasks is impaired during exposure to sleep deprivation. These findings have potential implications for occupations that require multi-tasking combined with long work hours and exposure to sleep loss. PMID:29166387

  2. Effects of total sleep deprivation on divided attention performance.

    PubMed

    Chua, Eric Chern-Pin; Fang, Eric; Gooley, Joshua J

    2017-01-01

    Dividing attention across two tasks performed simultaneously usually results in impaired performance on one or both tasks. Most studies have found no difference in the dual-task cost of dividing attention in rested and sleep-deprived states. We hypothesized that, for a divided attention task that is highly cognitively-demanding, performance would show greater impairment during exposure to sleep deprivation. A group of 30 healthy males aged 21-30 years was exposed to 40 h of continuous wakefulness in a laboratory setting. Every 2 h, subjects completed a divided attention task comprising 3 blocks in which an auditory Go/No-Go task was 1) performed alone (single task); 2) performed simultaneously with a visual Go/No-Go task (dual task); and 3) performed simultaneously with both a visual Go/No-Go task and a visually-guided motor tracking task (triple task). Performance on all tasks showed substantial deterioration during exposure to sleep deprivation. A significant interaction was observed between task load and time since wake on auditory Go/No-Go task performance, with greater impairment in response times and accuracy during extended wakefulness. Our results suggest that the ability to divide attention between multiple tasks is impaired during exposure to sleep deprivation. These findings have potential implications for occupations that require multi-tasking combined with long work hours and exposure to sleep loss.

  3. The effects of two types of sleep deprivation on visual working memory capacity and filtering efficiency.

    PubMed

    Drummond, Sean P A; Anderson, Dane E; Straus, Laura D; Vogel, Edward K; Perez, Veronica B

    2012-01-01

    Sleep deprivation has adverse consequences for a variety of cognitive functions. The exact effects of sleep deprivation, though, are dependent upon the cognitive process examined. Within working memory, for example, some component processes are more vulnerable to sleep deprivation than others. Additionally, the differential impacts on cognition of different types of sleep deprivation have not been well studied. The aim of this study was to examine the effects of one night of total sleep deprivation and 4 nights of partial sleep deprivation (4 hours in bed/night) on two components of visual working memory: capacity and filtering efficiency. Forty-four healthy young adults were randomly assigned to one of the two sleep deprivation conditions. All participants were studied: 1) in a well-rested condition (following 6 nights of 9 hours in bed/night); and 2) following sleep deprivation, in a counter-balanced order. Visual working memory testing consisted of two related tasks. The first measured visual working memory capacity and the second measured the ability to ignore distractor stimuli in a visual scene (filtering efficiency). Results showed neither type of sleep deprivation reduced visual working memory capacity. Partial sleep deprivation also generally did not change filtering efficiency. Total sleep deprivation, on the other hand, did impair performance in the filtering task. These results suggest components of visual working memory are differentially vulnerable to the effects of sleep deprivation, and different types of sleep deprivation impact visual working memory to different degrees. Such findings have implications for operational settings where individuals may need to perform with inadequate sleep and whose jobs involve receiving an array of visual information and discriminating the relevant from the irrelevant prior to making decisions or taking actions (e.g., baggage screeners, air traffic controllers, military personnel, health care providers).

  4. Assessing Individual Differences in Adaptation to Extreme Environments: A 36-Hour Sleep Deprivation Study

    NASA Technical Reports Server (NTRS)

    Martinez, Jacqueline; Cowings, Patricia S.; Toscano, William B.

    2012-01-01

    In space, astronauts may experience effects of cumulative sleep loss due to demanding work schedules that can result in cognitive performance impairments, mood state deteriorations, and sleep-wake cycle disruption. Individuals who experience sleep deprivation of six hours beyond normal sleep times experience detrimental changes in their mood and performance states. Hence, the potential for life threatening errors increases exponentially with sleep deprivation. We explored the effects of 36-hours of sleep deprivation on cognitive performance, mood states, and physiological responses to identify which metrics may best predict fatigue induced performance decrements of individuals.

  5. The effect of acute sleep deprivation on visual evoked potentials in professional drivers.

    PubMed

    Jackson, Melinda L; Croft, Rodney J; Owens, Katherine; Pierce, Robert J; Kennedy, Gerard A; Crewther, David; Howard, Mark E

    2008-09-01

    Previous studies have demonstrated that as little as 18 hours of sleep deprivation can cause deleterious effects on performance. It has also been suggested that sleep deprivation can cause a "tunnel-vision" effect, in which attention is restricted to the center of the visual field. The current study aimed to replicate these behavioral effects and to examine the electrophysiological underpinnings of these changes. Repeated-measures experimental study. University laboratory. Nineteen professional drivers (1 woman; mean age = 45.3 +/- 9.1 years). Two experimental sessions were performed; one following 27 hours of sleep deprivation and the other following a normal night of sleep, with control for circadian effects. A tunnel-vision task (central versus peripheral visual discrimination) and a standard checkerboard-viewing task were performed while 32-channel EEG was recorded. For the tunnel-vision task, sleep deprivation resulted in an overall slowing of reaction times and increased errors of omission for both peripheral and foveal stimuli (P < 0.05). These changes were related to reduced P300 amplitude (indexing cognitive processing) but not measures of early visual processing. No evidence was found for an interaction effect between sleep deprivation and visual-field position, either in terms of behavior or electrophysiological responses. Slower processing of the sustained parvocellular visual pathway was demonstrated. These findings suggest that performance deficits on visual tasks during sleep deprivation are due to higher cognitive processes rather than early visual processing. Sleep deprivation may differentially impair processing of more-detailed visual information. Features of the study design (eg, visual angle, duration of sleep deprivation) may influence whether peripheral visual-field neglect occurs.

  6. Evidence for cortical structural plasticity in humans after a day of waking and sleep deprivation.

    PubMed

    Elvsåshagen, Torbjørn; Zak, Nathalia; Norbom, Linn B; Pedersen, Per Ø; Quraishi, Sophia H; Bjørnerud, Atle; Alnæs, Dag; Doan, Nhat Trung; Malt, Ulrik F; Groote, Inge R; Westlye, Lars T

    2017-08-01

    Sleep is an evolutionarily conserved process required for human health and functioning. Insufficient sleep causes impairments across cognitive domains, and sleep deprivation can have rapid antidepressive effects in mood disorders. However, the neurobiological effects of waking and sleep are not well understood. Recently, animal studies indicated that waking and sleep are associated with substantial cortical structural plasticity. Here, we hypothesized that structural plasticity can be observed after a day of waking and sleep deprivation in the human cerebral cortex. To test this hypothesis, 61 healthy adult males underwent structural magnetic resonance imaging (MRI) at three time points: in the morning after a regular night's sleep, the evening of the same day, and the next morning, either after total sleep deprivation (N=41) or a night of sleep (N=20). We found significantly increased right prefrontal cortical thickness from morning to evening across all participants. In addition, pairwise comparisons in the deprived group between the two morning scans showed significant thinning of mainly bilateral medial parietal cortices after 23h of sleep deprivation, including the precuneus and posterior cingulate cortex. However, there were no significant group (sleep vs. sleep deprived group) by time interactions and we can therefore not rule out that other mechanisms than sleep deprivation per se underlie the bilateral medial parietal cortical thinning observed in the deprived group. Nonetheless, these cortices are thought to subserve wakefulness, are among the brain regions with highest metabolic rate during wake, and are considered some of the most sensitive cortical regions to a variety of insults. Furthermore, greater thinning within the left medial parietal cluster was associated with increased sleepiness after sleep deprivation. Together, these findings add to a growing body of data showing rapid structural plasticity within the human cerebral cortex detectable with

  7. Influence of sleep deprivation on learning among surgical house staff and medical students.

    PubMed

    Browne, B J; Van Susteren, T; Onsager, D R; Simpson, D; Salaymeh, B; Condon, R E

    1994-05-01

    Sleep deprivation as a result of in-house night call may alter capacity to learn. Surgical residents and medical students, in both sleep-deprived and rested states, read surgical journal articles and later answered questions regarding their content as a measure of ability to learn while participating in scheduled night call. Medical students (n = 35) and residents (n = 21) rotating on surgical services kept logs of hours slept during a 4-week study period. Subjects read six selected articles at separate early morning sittings during weeks 1 and 3. A multiple choice test was given 1 week after each session to assess short-term recall, and all tests were given again 3 months later to assess retention of information over the longer term. Scores were compared with the sleep data. Subjective measures of fatigue and motivation elicited from subjects also were evaluated. Sleep deprivation (4 hours or less uninterrupted sleep per night) resulted in increased fatigue and decreased motivation among medical students and residents (p < 0.05, t test). Objective scores on tests administered 1 week and 3 months after reading did not show an effect attributable to sleep deprivation (p > 0.05, t test). Sleep deprivation leads to subjective feelings of increased fatigue and decreased motivation. Residents and medical students, however, whether sleep deprived or not, obtain comparable scores on objective tests measuring both short-term and long-term retention of newly learned material. The ability to learn medically relevant information does not appear to be significantly altered by the degree of sleep deprivation associated with clinical rotations on surgical services.

  8. Blood-Gene Expression Reveals Reduced Circadian Rhythmicity in Individuals Resistant to Sleep Deprivation

    PubMed Central

    Arnardottir, Erna S.; Nikonova, Elena V.; Shockley, Keith R.; Podtelezhnikov, Alexei A.; Anafi, Ron C.; Tanis, Keith Q.; Maislin, Greg; Stone, David J.; Renger, John J.; Winrow, Christopher J.; Pack, Allan I.

    2014-01-01

    Study Objectives: To address whether changes in gene expression in blood cells with sleep loss are different in individuals resistant and sensitive to sleep deprivation. Design: Blood draws every 4 h during a 3-day study: 24-h normal baseline, 38 h of continuous wakefulness and subsequent recovery sleep, for a total of 19 time-points per subject, with every 2-h psychomotor vigilance task (PVT) assessment when awake. Setting: Sleep laboratory. Participants: Fourteen subjects who were previously identified as behaviorally resistant (n = 7) or sensitive (n = 7) to sleep deprivation by PVT. Intervention: Thirty-eight hours of continuous wakefulness. Measurements and Results: We found 4,481 unique genes with a significant 24-h diurnal rhythm during a normal sleep-wake cycle in blood (false discovery rate [FDR] < 5%). Biological pathways were enriched for biosynthetic processes during sleep. After accounting for circadian effects, two genes (SREBF1 and CPT1A, both involved in lipid metabolism) exhibited small, but significant, linear changes in expression with the duration of sleep deprivation (FDR < 5%). The main change with sleep deprivation was a reduction in the amplitude of the diurnal rhythm of expression of normally cycling probe sets. This reduction was noticeably higher in behaviorally resistant subjects than sensitive subjects, at any given P value. Furthermore, blood cell type enrichment analysis showed that the expression pattern difference between sensitive and resistant subjects is mainly found in cells of myeloid origin, such as monocytes. Conclusion: Individual differences in behavioral effects of sleep deprivation are associated with differences in diurnal amplitude of gene expression for genes that show circadian rhythmicity. Citation: Arnardottir ES, Nikonova EV, Shockley KR, Podtelezhnikov AA, Anafi RC, Tanis KQ, Maislin G, Stone DJ, Renger JJ, Winrow CJ, Pack AI. Blood-gene expression reveals reduced circadian rhythmicity in individuals resistant to

  9. Short-term sleep deprivation leads to decreased systemic redox metabolites and altered epigenetic status.

    PubMed

    Trivedi, Malav S; Holger, Dana; Bui, Anh Tuyet; Craddock, Travis J A; Tartar, Jaime L

    2017-01-01

    Sleep is critical for repair as well as the rejuvenation processes in the body and many of these functions are regulated via underlying cellular metabolic homeostasis. Changes in sleep pattern are reported to alter such metabolic function resulting in altered disease susceptibility or behavior. Here, we measured the extent to which overnight total sleep deprivation (SD) in young adult humans can influence systemic (plasma-derived) redox-metabolism including the major antioxidant, glutathione as well as DNA methylation levels. Nineteen participants (n = 19, μ age = 21, SD = 3.09) underwent morning testing before and after overnight total SD. Biochemical measures before and after SD revealed that glutathione, ATP, cysteine, and homocysteine levels were significantly reduced following one night of sleep deprivation (all p's < 0.01). Parallel to the well-recognized fact that sleep deprivation (maintaining wakefulness) uses up metabolic reserves, we observed that morning cortisol levels were blunted after sleep deprivation. There were no significant correlations between self-reported or actigraphy-measured sleep and the biochemical measurements, strongly indicating that prior sleep behavior did not have any direct influence on the biochemical measures taken at baseline or after sleep deprivation. Results from the current investigation supports the previous literature implicating the induction of oxidative stress and ATP depletion with sleep deprivation. Furthermore, such altered antioxidant status can also induce downstream epigenetic changes. Although we did not measure the specific genes that were altered under the influence of such sleep deprivation, such epigenetic changes could potentially contribute towards disease predisposition.

  10. Sleep deprivation during a specific 3-hour time window post-training impairs hippocampal synaptic plasticity and memory

    PubMed Central

    Prince, Toni-Moi; Wimmer, Mathieu; Choi, Jennifer; Havekes, Robbert; Aton, Sara; Abel, Ted

    2014-01-01

    Sleep deprivation disrupts hippocampal function and plasticity. In particular, long-term memory consolidation is impaired by sleep deprivation, suggesting that a specific critical period exists following learning during which sleep is necessary. To elucidate the impact of sleep deprivation on long-term memory consolidation and synaptic plasticity, long-term memory was assessed when mice were sleep deprived following training in the hippocampus-dependent object place recognition task. We found that 3 hours of sleep deprivation significantly impaired memory when deprivation began 1 hour after training. In contrast, 3 hours of deprivation beginning immediately post-training did not impair spatial memory. Furthermore, a 3-hour sleep deprivation beginning 1 hour after training impaired hippocampal long-term potentiation (LTP), whereas sleep deprivation immediately after training did not affect LTP. Together, our findings define a specific 3-hour critical period, extending from 1 to 4 hours after training, during which sleep deprivation impairs hippocampal function. PMID:24380868

  11. Effect of Sleep Deprivation on the Male Reproductive System in Rats.

    PubMed

    Choi, Ji Ho; Lee, Seung Hoon; Bae, Jae Hyun; Shim, Ji Sung; Park, Hong Seok; Kim, Young Sik; Shin, Chol

    2016-10-01

    There has been no study reporting on the influence of sleep deprivation on the male reproductive system including sperm quality. In this study, we hypothesized that sleep deprivation could lead to adverse effect on the male reproductive system. The rats were divided into three groups: 1) control (home-cage, n = 10); 2) SD4 (sleep deprivation for 4 days, n = 10); and 3) SD7 (sleep deprivation for 7 days, n = 10). Sleep deprivation was performed by a modified multiple platform method. Sperm quality (sperm motion parameters and counts), hormone levels (corticosterone and testosterone), and the histopathology of testis were evaluated and compared between the three groups. A statistically significant reduction (P = 0.018) was observed in sperm motility in the SD7 group compared to those of the control group. However, there were no significant differences in other sperm motion parameters, or in sperm counts of the testis and cauda epididymis between three groups. Compared with the control group, the SD4 (P = 0.033) and SD7 (P = 0.002) groups exhibited significant increases of corticosterone levels, but significant decreases of testosterone levels were found in the SD4 (P = 0.001) and SD7 (P < 0.001) groups. Seminiferous tubular atrophy and/or spermatid retention was partially observed in the SD4 and SD7 groups, compared with the normal histopathology of the control group. Sleep deprivation may have an adverse effect on the male reproductive system in rats.

  12. Switch-Task Performance in Rats Is Disturbed by 12 h of Sleep Deprivation But Not by 12 h of Sleep Fragmentation

    PubMed Central

    Leenaars, Cathalijn H.C.; Joosten, Ruud N.J.M.A.; Zwart, Allard; Sandberg, Hans; Ruimschotel, Emma; Hanegraaf, Maaike A.J.; Dematteis, Maurice; Feenstra, Matthijs G.P.; van Someren, Eus J.W.

    2012-01-01

    Study Objectives: Task-switching is an executive function involving the prefrontal cortex. Switching temporarily attenuates the speed and/or accuracy of performance, phenomena referred to as switch costs. In accordance with the idea that prefrontal function is particularly sensitive to sleep loss, switch-costs increase during prolonged waking in humans. It has been difficult to investigate the underlying neurobiological mechanisms because of the lack of a suitable animal model. Here, we introduce the first switch-task for rats and report the effects of sleep deprivation and inactivation of the medial prefrontal cortex. Design: Rats were trained to repeatedly switch between 2 stimulus-response associations, indicated by the presentation of a visual or an auditory stimulus. These stimulus-response associations were offered in blocks, and performance was compared for the first and fifth trials of each block. Performance was tested after exposure to 12 h of total sleep deprivation, sleep fragmentation, and their respective movement control conditions. Finally, it was tested after pharmacological inactivation of the medial prefrontal cortex. Settings: Controlled laboratory settings. Participants: 15 male Wistar rats. Measurements & Results: Both accuracy and latency showed switch-costs at baseline. Twelve hours of total sleep deprivation, but not sleep fragmentation, impaired accuracy selectively on the switch-trials. Inactivation of the medial prefrontal cortex by local neuronal inactivation resulted in an overall decrease in accuracy. Conclusions: We developed and validated a switch-task that is sensitive to sleep deprivation. This introduces the possibility for in-depth investigations on the neurobiological mechanisms underlying executive impairments after sleep disturbance in a rat model. Citation: Leenaars CHC; Joosten RNJMA; Zwart A; Sandberg H; Ruimschotel E; Hanegraaf MAJ; Dematteis M; Feenstra MGP; van Someren EJW. Switch-task performance in rats is disturbed

  13. The effects of extended work under sleep deprivation conditions on team-based performance.

    PubMed

    Pilcher, June J; Vander Wood, Melissa A; O'Connell, Kristina L

    2011-07-01

    Teamwork is becoming increasingly common in today's workplaces; however, little research has examined how well teams perform under sleep deprivation conditions. The purpose of the current study was to examine the effect of extended work under sleep deprivation conditions on team performance. A total of 24 participants were sleep deprived for 30 h and completed 16 h of sustained operations during the last portion of the sleep deprivation period. The participants completed the Wombat, a complex task including vigilance and cognitive components, with a partner in four 24-min testing sessions during the sustained operations period. The results indicated that team performance increased during the work period while, within each testing session, team performance on vigilance tasks remained stable and overall performance decreased. The current results suggest that performance on two-person teams results in improved performance but does not fully counteract the decreases in performance within each work period. Performance in two-person teams increased across an extended work shift under sleep deprivation conditions. However, vigilance performance remained stable while overall performance decreased when examining performance in 8-min segments. These results suggest that averaging team-based performance over a longer testing period may mask the negative effects of sleep deprivation. STATEMENT OF RELEVANCE: Performance in two-person teams increased across an extended work shift under sleep deprivation conditions. However, vigilance performance remained stable while overall performance decreased when examining performance in 8-min segments. These results suggest that averaging team-based performance over a longer testing period may mask the negative effects of sleep deprivation.

  14. Evidence that Sleep Deprivation Downregulates Dopamine D2R in Ventral Striatum in the Human Brain

    PubMed Central

    Volkow, Nora D.; Tomasi, Dardo; Wang, Gene-Jack; Telang, Frank; Fowler, Joanna S.; Logan, Jean; Benveniste, Helene; Kim, Ron; Thanos, Panayotis K.; Ferré, Sergi

    2012-01-01

    Dopamine D2 receptors are involved with wakefulness but their role in the decreased alertness associated with sleep deprivation is unclear. We had shown that sleep deprivation reduced dopamine D2/D3 receptor availability (measured with PET and [11C]raclopride in controls) in striatum, but could not determine if this reflected dopamine increases ([11C]raclopride competes with dopamine for D2/D3 receptor binding) or receptor downregulation. To clarify this, we compared the dopamine increases induced by methylphenidate (drug that increases dopamine by blocking dopamine transporters), during sleep deprivation versus rested-sleep with the assumption that methylphenidate’s effects would be greater, if indeed, dopamine release was increased during sleep deprivation. We scanned 20 controls with [11C]raclopride after rested-sleep and after one night of sleep deprivation; both after placebo and after methylphenidate. We corroborated a decrease in D2/D3 receptor availability in the ventral striatum with sleep deprivation (compared to rested-sleep) that was associated with reduced alertness and increased sleepiness. However, the dopamine increases induced by methylphenidate (measured as decreases in D2/D3 receptor availability compared to placebo) did not differ between rested-sleep and sleep deprivation and were associated with the increased alertness and reduced sleepiness when methylphenidate was administered after sleep deprivation. Similar findings were obtained by microdialysis in rodents subjected to one night of paradoxical sleep deprivation. These findings are consistent with a downregulation of D2/D3 receptors in ventral striatum with sleep deprivation that may contribute to the associated decreased wakefulness and also corroborate an enhancement of D2 receptor signaling in the arousing effects of methylphenidate in humans. PMID:22573693

  15. The effects of sleep deprivation on item and associative recognition memory.

    PubMed

    Ratcliff, Roger; Van Dongen, Hans P A

    2018-02-01

    Sleep deprivation adversely affects the ability to perform cognitive tasks, but theories range from predicting an overall decline in cognitive functioning because of reduced stability in attentional networks to specific deficits in various cognitive domains or processes. We measured the effects of sleep deprivation on two memory tasks, item recognition ("was this word in the list studied") and associative recognition ("were these two words studied in the same pair"). These tasks test memory for information encoded a few minutes earlier and so do not address effects of sleep deprivation on working memory or consolidation after sleep. A diffusion model was used to decompose accuracy and response time distributions to produce parameter estimates of components of cognitive processing. The model assumes that over time, noisy evidence from the task stimulus is accumulated to one of two decision criteria, and parameters governing this process are extracted and interpreted in terms of distinct cognitive processes. Results showed that sleep deprivation reduces drift rate (evidence used in the decision process), with little effect on the other components of the decision process. These results contrast with the effects of aging, which show little decline in item recognition but large declines in associative recognition. The results suggest that sleep deprivation degrades the quality of information stored in memory and that this may occur through degraded attentional processes. (PsycINFO Database Record (c) 2018 APA, all rights reserved).

  16. The effect of sleep deprivation on BOLD activity elicited by a divided attention task.

    PubMed

    Jackson, Melinda L; Hughes, Matthew E; Croft, Rodney J; Howard, Mark E; Crewther, David; Kennedy, Gerard A; Owens, Katherine; Pierce, Rob J; O'Donoghue, Fergal J; Johnston, Patrick

    2011-06-01

    Sleep loss, widespread in today's society and associated with a number of clinical conditions, has a detrimental effect on a variety of cognitive domains including attention. This study examined the sequelae of sleep deprivation upon BOLD fMRI activation during divided attention. Twelve healthy males completed two randomized sessions; one after 27 h of sleep deprivation and one after a normal night of sleep. During each session, BOLD fMRI was measured while subjects completed a cross-modal divided attention task (visual and auditory). After normal sleep, increased BOLD activation was observed bilaterally in the superior frontal gyrus and the inferior parietal lobe during divided attention performance. Subjects reported feeling significantly more sleepy in the sleep deprivation session, and there was a trend towards poorer divided attention task performance. Sleep deprivation led to a down regulation of activation in the left superior frontal gyrus, possibly reflecting an attenuation of top-down control mechanisms on the attentional system. These findings have implications for understanding the neural correlates of divided attention and the neurofunctional changes that occur in individuals who are sleep deprived.

  17. Blood-gene expression reveals reduced circadian rhythmicity in individuals resistant to sleep deprivation.

    PubMed

    Arnardottir, Erna S; Nikonova, Elena V; Shockley, Keith R; Podtelezhnikov, Alexei A; Anafi, Ron C; Tanis, Keith Q; Maislin, Greg; Stone, David J; Renger, John J; Winrow, Christopher J; Pack, Allan I

    2014-10-01

    To address whether changes in gene expression in blood cells with sleep loss are different in individuals resistant and sensitive to sleep deprivation. Blood draws every 4 h during a 3-day study: 24-h normal baseline, 38 h of continuous wakefulness and subsequent recovery sleep, for a total of 19 time-points per subject, with every 2-h psychomotor vigilance task (PVT) assessment when awake. Sleep laboratory. Fourteen subjects who were previously identified as behaviorally resistant (n = 7) or sensitive (n = 7) to sleep deprivation by PVT. Thirty-eight hours of continuous wakefulness. We found 4,481 unique genes with a significant 24-h diurnal rhythm during a normal sleep-wake cycle in blood (false discovery rate [FDR] < 5%). Biological pathways were enriched for biosynthetic processes during sleep. After accounting for circadian effects, two genes (SREBF1 and CPT1A, both involved in lipid metabolism) exhibited small, but significant, linear changes in expression with the duration of sleep deprivation (FDR < 5%). The main change with sleep deprivation was a reduction in the amplitude of the diurnal rhythm of expression of normally cycling probe sets. This reduction was noticeably higher in behaviorally resistant subjects than sensitive subjects, at any given P value. Furthermore, blood cell type enrichment analysis showed that the expression pattern difference between sensitive and resistant subjects is mainly found in cells of myeloid origin, such as monocytes. Individual differences in behavioral effects of sleep deprivation are associated with differences in diurnal amplitude of gene expression for genes that show circadian rhythmicity. © 2014 Associated Professional Sleep Societies, LLC.

  18. Acute Versus Chronic Partial Sleep Deprivation in Middle-Aged People: Differential Effect on Performance and Sleepiness

    PubMed Central

    Philip, Pierre; Sagaspe, Patricia; Prague, Mélanie; Tassi, Patricia; Capelli, Aurore; Bioulac, Bernard; Commenges, Daniel; Taillard, Jacques

    2012-01-01

    Study Objective: To evaluate the effects of acute sleep deprivation and chronic sleep restriction on vigilance, performance, and self-perception of sleepiness. Design: Habitual night followed by 1 night of total sleep loss (acute sleep deprivation) or 5 consecutive nights of 4 hr of sleep (chronic sleep restriction) and recovery night. Participants: Eighteen healthy middle-aged male participants (age [(± standard deviation] = 49.7 ± 2.6 yr, range 46-55 yr). Measurements: Multiple sleep latency test trials, Karolinska Sleepiness Scale scores, simple reaction time test (lapses and 10% fastest reaction times), and nocturnal polysomnography data were recorded. Results: Objective and subjective sleepiness increased immediately in response to sleep restriction. Sleep latencies after the second and third nights of sleep restriction reached levels equivalent to those observed after acute sleep deprivation, whereas Karolinska Sleepiness Scale scores did not reach these levels. Lapse occurrence increased after the second day of sleep restriction and reached levels equivalent to those observed after acute sleep deprivation. A statistical model revealed that sleepiness and lapses did not progressively worsen across days of sleep restriction. Ten percent fastest reaction times (i.e., optimal alertness) were not affected by acute or chronic sleep deprivation. Recovery to baseline levels of alertness and performance occurred after 8-hr recovery night. Conclusions: In middle-aged study participants, sleep restriction induced a high increase in sleep propensity but adaptation to chronic sleep restriction occurred beyond day 3 of restriction. This sleepiness attenuation was underestimated by the participants. One recovery night restores daytime sleepiness and cognitive performance deficits induced by acute or chronic sleep deprivation. Citation: Philip P; Sagaspe P; Prague M; Tassi P; Capelli A; Bioulac B; Commenges D; Taillard J. Acute versus chronic partial sleep deprivation in

  19. Acute versus chronic partial sleep deprivation in middle-aged people: differential effect on performance and sleepiness.

    PubMed

    Philip, Pierre; Sagaspe, Patricia; Prague, Mélanie; Tassi, Patricia; Capelli, Aurore; Bioulac, Bernard; Commenges, Daniel; Taillard, Jacques

    2012-07-01

    To evaluate the effects of acute sleep deprivation and chronic sleep restriction on vigilance, performance, and self-perception of sleepiness. Habitual night followed by 1 night of total sleep loss (acute sleep deprivation) or 5 consecutive nights of 4 hr of sleep (chronic sleep restriction) and recovery night. Eighteen healthy middle-aged male participants (age [(± standard deviation] = 49.7 ± 2.6 yr, range 46-55 yr). Multiple sleep latency test trials, Karolinska Sleepiness Scale scores, simple reaction time test (lapses and 10% fastest reaction times), and nocturnal polysomnography data were recorded. Objective and subjective sleepiness increased immediately in response to sleep restriction. Sleep latencies after the second and third nights of sleep restriction reached levels equivalent to those observed after acute sleep deprivation, whereas Karolinska Sleepiness Scale scores did not reach these levels. Lapse occurrence increased after the second day of sleep restriction and reached levels equivalent to those observed after acute sleep deprivation. A statistical model revealed that sleepiness and lapses did not progressively worsen across days of sleep restriction. Ten percent fastest reaction times (i.e., optimal alertness) were not affected by acute or chronic sleep deprivation. Recovery to baseline levels of alertness and performance occurred after 8-hr recovery night. In middle-aged study participants, sleep restriction induced a high increase in sleep propensity but adaptation to chronic sleep restriction occurred beyond day 3 of restriction. This sleepiness attenuation was underestimated by the participants. One recovery night restores daytime sleepiness and cognitive performance deficits induced by acute or chronic sleep deprivation. Philip P; Sagaspe P; Prague M; Tassi P; Capelli A; Bioulac B; Commenges D; Taillard J. Acute versus chronic partial sleep deprivation in middle-aged people: differential effect on performance and sleepiness. SLEEP 2012;35(7):997-1002.

  20. Sleep deprivation impairs inhibitory control during wakefulness in adult sleepwalkers.

    PubMed

    Labelle, Marc-Antoine; Dang-Vu, Thien Thanh; Petit, Dominique; Desautels, Alex; Montplaisir, Jacques; Zadra, Antonio

    2015-12-01

    Sleepwalkers often complain of excessive daytime somnolence. Although excessive daytime somnolence has been associated with cognitive impairment in several sleep disorders, very few data exist concerning sleepwalking. This study aimed to investigate daytime cognitive functioning in adults diagnosed with idiopathic sleepwalking. Fifteen sleepwalkers and 15 matched controls were administered the Continuous Performance Test and Stroop Colour-Word Test in the morning after an overnight polysomnographic assessment. Participants were tested a week later on the same neuropsychological battery, but after 25 h of sleep deprivation, a procedure known to precipitate sleepwalking episodes during subsequent recovery sleep. There were no significant differences between sleepwalkers and controls on any of the cognitive tests administered under normal waking conditions. Testing following sleep deprivation revealed significant impairment in sleepwalkers' executive functions related to inhibitory control, as they made more errors than controls on the Stroop Colour-Word Test and more commission errors on the Continuous Performance Test. Sleepwalkers' scores on measures of executive functions were not associated with self-reported sleepiness or indices of sleep fragmentation from baseline polysomnographic recordings. The results support the idea that sleepwalking involves daytime consequences and suggest that these may also include cognitive impairments in the form of disrupted inhibitory control following sleep deprivation. These disruptions may represent a daytime expression of sleepwalking's pathophysiological mechanisms. © 2015 European Sleep Research Society.

  1. Residency Training: The King-Devick test and sleep deprivation

    PubMed Central

    Davies, Emma C.; Henderson, Sam; Galetta, Steven L.

    2012-01-01

    Objective: The current study investigates the effect of sleep deprivation on the speed and accuracy of eye movements as measured by the King-Devick (K-D) test, a <1-minute test that involves rapid number naming. Methods: In this cohort study, neurology residents and staff from the University of Pennsylvania Health System underwent baseline followed by postcall K-D testing (n = 25); those not taking call (n = 10) also completed baseline and follow-up K-D testing. Differences in the times and errors between baseline and follow-up K-D scores were compared between the 2 groups. Results: Residents taking call had less improvement from baseline K-D times when compared to participants not taking call (p < 0.0001, Wilcoxon rank sum test). For both groups, the change in K-D time from baseline was correlated to amount of sleep obtained (rs = −0.50, p = 0.002) and subjective evaluation of level of alertness (rs = 0.33, p = 0.05) but had no correlation to time since last caffeine consumption (rs = −0.13, p = 0.52). For those residents on their actual call night, the duration of sleep obtained did not correlate with change in K-D scores from baseline (rs = 0.13, p = 0.54). Conclusions: The K-D test is sensitive to the effects of sleep deprivation on cognitive functioning, including rapid eye movements, concentration, and language function. As with other measures of sleep deprivation, K-D performance demonstrated significant interindividual variability in vulnerability to sleep deprivation. Severe fatigue appears to reduce the degree of improvement typically observed in K-D testing. PMID:22529208

  2. High-Intensity Interval Training Attenuates Insulin Resistance Induced by Sleep Deprivation in Healthy Males.

    PubMed

    de Souza, Jorge F T; Dáttilo, Murilo; de Mello, Marco T; Tufik, Sergio; Antunes, Hanna K M

    2017-01-01

    Introduction: Sleep deprivation can impair several physiological systems and recently, new evidence has pointed to the relationship between a lack of sleep and carbohydrate metabolism, consequently resulting in insulin resistance. To minimize this effect, High-Intensity Interval Training (HIIT) is emerging as a potential strategy. Objective: The aim of this study was to investigate the effects of HIIT on insulin resistance induced by sleep deprivation. Method: Eleven healthy male volunteers were recruited, aged 18-35 years, who declared taking 7-8 h sleep per night. All volunteers were submitted to four different conditions: a single night of regular sleep (RS condition), 24 h of total sleep deprivation ( SD condition), HIIT training followed by regular sleep (HIIT+RS condition), and HIIT training followed by 24 h of total sleep deprivation (HIIT+ SD condition). They performed six training sessions over 2 weeks and each session consisted of 8-12 × 60 s intervals at 100% of peak power output. In each experimental condition, tests for glucose, insulin, cortisol, free fatty acids, and insulin sensitivity, measured by oral glucose tolerance test (OGTT), were performed. Results: Sleep deprivation increased glycaemia and insulin levels, as well as the area under the curve. Furthermore, an increase in free fatty acids concentrations and basal metabolism was observed. There were no differences in the concentrations of cortisol. However, HIIT before 24 h of sleep deprivation attenuated the increase of glucose, insulin, and free fatty acids. Conclusion: Twenty-four hours of sleep deprivation resulted in acute insulin resistance. However, HIIT is an effective strategy to minimize the deleterious effects promoted by this condition.

  3. High-Intensity Interval Training Attenuates Insulin Resistance Induced by Sleep Deprivation in Healthy Males

    PubMed Central

    de Souza, Jorge F. T.; Dáttilo, Murilo; de Mello, Marco T.; Tufik, Sergio; Antunes, Hanna K. M.

    2017-01-01

    Introduction: Sleep deprivation can impair several physiological systems and recently, new evidence has pointed to the relationship between a lack of sleep and carbohydrate metabolism, consequently resulting in insulin resistance. To minimize this effect, High-Intensity Interval Training (HIIT) is emerging as a potential strategy. Objective: The aim of this study was to investigate the effects of HIIT on insulin resistance induced by sleep deprivation. Method: Eleven healthy male volunteers were recruited, aged 18–35 years, who declared taking 7–8 h sleep per night. All volunteers were submitted to four different conditions: a single night of regular sleep (RS condition), 24 h of total sleep deprivation (SD condition), HIIT training followed by regular sleep (HIIT+RS condition), and HIIT training followed by 24 h of total sleep deprivation (HIIT+SD condition). They performed six training sessions over 2 weeks and each session consisted of 8–12 × 60 s intervals at 100% of peak power output. In each experimental condition, tests for glucose, insulin, cortisol, free fatty acids, and insulin sensitivity, measured by oral glucose tolerance test (OGTT), were performed. Results: Sleep deprivation increased glycaemia and insulin levels, as well as the area under the curve. Furthermore, an increase in free fatty acids concentrations and basal metabolism was observed. There were no differences in the concentrations of cortisol. However, HIIT before 24 h of sleep deprivation attenuated the increase of glucose, insulin, and free fatty acids. Conclusion: Twenty-four hours of sleep deprivation resulted in acute insulin resistance. However, HIIT is an effective strategy to minimize the deleterious effects promoted by this condition. PMID:29270126

  4. Migraine, arousal and sleep deprivation: comment on: "sleep quality, arousal and pain thresholds in migraineurs: a blinded controlled polysomnographic study".

    PubMed

    Vollono, Catello; Testani, Elisa; Losurdo, Anna; Mazza, Salvatore; Della Marca, Giacomo

    2013-06-10

    We discuss the hypothesis proposed by Engstrom and coworkers that Migraineurs have a relative sleep deprivation, which lowers the pain threshold and predispose to attacks. Previous data indicate that Migraineurs have a reduction of Cyclic Alternating Pattern (CAP), an essential mechanism of NREM sleep regulation which allows to dump the effect of incoming disruptive stimuli, and to protect sleep. The modifications of CAP observed in Migraineurs are similar to those observed in patients with impaired arousal (narcolepsy) and after sleep deprivation. The impairment of this mechanism makes Migraineurs more vulnerable to stimuli triggering attacks during sleep, and represents part of a more general vulnerability to incoming stimuli.

  5. Evidence That Sleep Deprivation Downregulates Dopamine D2R in Ventral Striatum in the Human Brain

    DOE Office of Scientific and Technical Information (OSTI.GOV)

    Volkow N. D.; Fowler J.; Volkow, N.D.

    Dopamine D2 receptors are involved with wakefulness, but their role in the decreased alertness associated with sleep deprivation is unclear. We had shown that sleep deprivation reduced dopamine D2/D3 receptor availability (measured with PET and [{sup 11}C]raclopride in controls) in striatum, but could not determine whether this reflected dopamine increases ([{sup 11}C]raclopride competes with dopamine for D2/D3 receptor binding) or receptor downregulation. To clarify this, we compared the dopamine increases induced by methylphenidate (a drug that increases dopamine by blocking dopamine transporters) during sleep deprivation versus rested sleep, with the assumption that methylphenidate's effects would be greater if, indeed, dopaminemore » release was increased during sleep deprivation. We scanned 20 controls with [{sup 11}C]raclopride after rested sleep and after 1 night of sleep deprivation; both after placebo and after methylphenidate. We corroborated a decrease in D2/D3 receptor availability in the ventral striatum with sleep deprivation (compared with rested sleep) that was associated with reduced alertness and increased sleepiness. However, the dopamine increases induced by methylphenidate (measured as decreases in D2/D3 receptor availability compared with placebo) did not differ between rested sleep and sleep deprivation, and were associated with the increased alertness and reduced sleepiness when methylphenidate was administered after sleep deprivation. Similar findings were obtained by microdialysis in rodents subjected to 1 night of paradoxical sleep deprivation. These findings are consistent with a downregulation of D2/D3 receptors in ventral striatum with sleep deprivation that may contribute to the associated decreased wakefulness and also corroborate an enhancement of D2 receptor signaling in the arousing effects of methylphenidate in humans.« less

  6. Sleep and nutritional deprivation and performance of house officers.

    PubMed

    Hawkins, M R; Vichick, D A; Silsby, H D; Kruzich, D J; Butler, R

    1985-07-01

    A study was conducted by the authors to compare cognitive functioning in acutely and chronically sleep-deprived house officers. A multivariate analysis of variance revealed significant deficits in primary mental tasks involving basic rote memory, language, and numeric skills as well as in tasks requiring high-order cognitive functioning and traditional intellective abilities. These deficits existed only for the acutely sleep-deprived group. The finding of deficits in individuals who reported five hours or less of sleep in a 24-hour period suggests that the minimum standard of four hours that has been considered by some to be adequate for satisfactory performance may be insufficient for more complex cognitive functioning.

  7. Does hormone therapy affect attention and memory in sleep-deprived women?

    PubMed

    Alhola, P; Kylmälä, M; Urrila, A Sofia; Karakorpi, M; Portin, R; Kalleinen, N; Polo-Kantola, P

    2008-06-01

    To evaluate whether hormone therapy (HT) modifies cognitive performance during sleep deprivation in postmenopausal women. Comparison was made with a group of young women. Participants included 26 postmenopausal women (age 58-72 years, 16 HT users, 10 non-users), 11 young women (age 20-26 years). They spent four consecutive nights in the sleep laboratory. Cognitive tests of attention, working memory, and verbal episodic memory were carried out after the baseline night, 25-h sleep deprivation, and recovery night. Sleep deprivation impaired performance in all groups. It was manifested either as delayed practice effect or deteriorated performance (p < 0.05). In simple reaction time and 10-choice reaction time, non-users and young maintained their performance, whereas HT users suffered a minor impairment (p < 0.01). In other measurements, there was no interaction of group and condition. In 10-choice reaction time and vigilance, postmenopausal women made fewer errors and omissions than the young (p < 0.05). For most tasks, all groups showed improvement after one recovery night. HT had a minor adverse effect on cognitive performance during sleep deprivation. Attention and memory deteriorated similarly in postmenopausal and young women, despite the lower initial performance level of postmenopausal women. One night of sleep ensured recovery in most tasks.

  8. The influence of sleep deprivation and obesity on DNA damage in female Zucker rats.

    PubMed

    Tenorio, Neuli M; Ribeiro, Daniel A; Alvarenga, Tathiana A; Fracalossi, Ana Carolina C; Carlin, Viviane; Hirotsu, Camila; Tufik, Sergio; Andersen, Monica L

    2013-01-01

    The aim of this study was to evaluate overall genetic damage induced by total sleep deprivation in obese, female Zucker rats of differing ages. Lean and obese Zucker rats at 3, 6, and 15 months old were randomly distributed into two groups for each age group: home-cage control and sleep-deprived (N = 5/group). The sleep-deprived groups were deprived sleep by gentle handling for 6 hours, whereas the home-cage control group was allowed to remain undisturbed in their home-cage. At the end of the sleep deprivation period, or after an equivalent amount of time for the home-cage control groups, the rats were brought to an adjacent room and decapitated. The blood, brain, and liver tissue were collected and stored individually to evaluate DNA damage. Significant genetic damage was observed only in 15-month-old rats. Genetic damage was present in the liver cells from sleep-deprived obese rats compared with lean rats in the same condition. Sleep deprivation was associated with genetic damage in brain cells regardless of obesity status. DNA damage was observed in the peripheral blood cells regardless of sleep condition or obesity status. Taken together, these results suggest that obesity was associated with genetic damage in liver cells, whereas sleep deprivation was associated with DNA damage in brain cells. These results also indicate that there is no synergistic effect of these noxious conditions on the overall level of genetic damage. In addition, the level of DNA damage was significantly higher in 15-month-old rats compared to younger rats.

  9. Effects of acute sleep deprivation on state anxiety levels: a systematic review and meta-analysis.

    PubMed

    Pires, Gabriel Natan; Bezerra, Andreia Gomes; Tufik, Sergio; Andersen, Monica Levy

    2016-08-01

    Increased anxiety levels have been widely recognized as one of the most important consequences of sleep deprivation. However, despite this general consensus, there are still aspects of this relationship, such as the extent of the anxiogenic potential and the specific effects of different types of sleep deprivation, which remain unclear. As no broad review has been undertaken to evaluate this relationship, we performed a systematic review and meta-analysis regarding the effects of sleep deprivation on state anxiety. Our search strategy encompassed two databases - Pubmed/Medline and Scopus - through which we were able to identify 756 articles. After the selection process, 18 articles, encompassing 34 experiments, composed our final sample. Our analyses indicate that sleep deprivation, whether total or not, leads to a significant increase in state anxiety levels, but sleep restriction does not. Regarding the effect of the length of the period of sleep deprivation, no significant results were observed, but there was a notable tendency for an increase in anxiety in longer sleep deprivations. With regard to tools, the State-Trait Anxiety Inventory (STAI) seems to be the best one to measure sleep-induced anxiogenesis, while the Profile of Mood States (POMS) presented inconclusive results. In conclusion, it can be affirmed that sleep deprivation induces a state of increased anxiety, with similar results also in the case of total sleep deprivation; however, results in more specific experimental conditions are not definitive. Copyright © 2016 Elsevier B.V. All rights reserved.

  10. Changes in attention to an emotional task after sleep deprivation: neurophysiological and behavioral findings.

    PubMed

    Alfarra, Ramey; Fins, Ana I; Chayo, Isaac; Tartar, Jaime L

    2015-01-01

    While sleep loss is shown to have widespread effects on cognitive processes, little is known about the impact of sleep loss on emotion processes. In order to expand on previous behavioral and physiological findings on how sleep loss influences emotion processing, we administered positive, negative, and neutral affective visual stimuli to individuals after one night of sleep deprivation while simultaneously acquiring EEG event related potential (ERP) data and recording affective behavioral responses. We compared these responses to a baseline testing session. We specifically looked at the late positive potential (LPP) component of the visual ERP as an established sensitive measure of attention to emotionally-charged visual stimuli. Our results show that after sleep deprivation, the LPP no longer discriminates between emotional and non-emotional pictures; after sleep deprivation the LPP amplitude was of similar amplitude for neutral, positive, and negative pictures. This effect was driven by an increase in the LPP to neutral pictures. Our behavioral measures show that, relative to baseline testing, emotional pictures are rated as less emotional following sleep deprivation with a concomitant reduction in emotional picture-induced anxiety. We did not observe any change in cortisol concentrations after sleep deprivation before or after emotional picture exposure, suggesting that the observed changes in emotion processing are independent of potential stress effects of sleep deprivation. Combined, our findings suggest that sleep loss interferes with proper allocation of attention resources during an emotional task. Copyright © 2014 Elsevier B.V. All rights reserved.

  11. Cognitive Performance, Sleepiness, and Mood in Partially Sleep Deprived Adolescents: The Need for Sleep Study

    PubMed Central

    Lo, June C.; Ong, Ju Lynn; Leong, Ruth L.F.; Gooley, Joshua J.; Chee, Michael W.L.

    2016-01-01

    Study Objectives: To investigate the effects of sleep restriction (7 nights of 5 h time in bed [TIB]) on cognitive performance, subjective sleepiness, and mood in adolescents. Methods: A parallel-group design was adopted in the Need for Sleep Study. Fifty-six healthy adolescents (25 males, age = 15–19 y) who studied in top high schools and were not habitual short sleepers were randomly assigned to Sleep Restriction (SR) or Control groups. Participants underwent a 2-w protocol consisting of 3 baseline nights (TIB = 9 h), 7 nights of sleep opportunity manipulation (TIB = 5 h for the SR and 9 h for the control groups), and 3 nights of recovery sleep (TIB = 9 h) at a boarding school. A cognitive test battery was administered three times each day. Results: During the manipulation period, the SR group demonstrated incremental deterioration in sustained attention, working memory and executive function, increase in subjective sleepiness, and decrease in positive mood. Subjective sleepiness and sustained attention did not return to baseline levels even after 2 recovery nights. In contrast, the control group maintained baseline levels of cognitive performance, subjective sleepiness, and mood throughout the study. Incremental improvement in speed of processing, as a result of repeated testing and learning, was observed in the control group but was attenuated in the sleep-restricted participants, who, despite two recovery sleep episodes, continued to perform worse than the control participants. Conclusions: A week of partial sleep deprivation impairs a wide range of cognitive functions, subjective alertness, and mood even in high-performing high school adolescents. Some measures do not recover fully even after 2 nights of recovery sleep. Commentary: A commentary on this article appears in this issue on page 497. Citation: Lo JC, Ong JL, Leong RL, Gooley JJ, Chee MW. Cognitive performance, sleepiness, and mood in partially sleep deprived adolescents: the need for sleep study

  12. The effects of acute sleep deprivation during residency training.

    PubMed

    Bartle, E J; Sun, J H; Thompson, L; Light, A I; McCool, C; Heaton, S

    1988-08-01

    Verbal and symbol concentration, learning, problem solving, clear thinking, manual skills, and memory were tested in 42 surgical residents to assess the effects of acute sleep deprivation on specific neuropsychological parameters. A series of eight neuropsychological tests--digit symbols, digit vigilance, story memory, trail making, PASAT, Raven matrices, delayed story, and pegboard--and a questionnaire on mood states were completed by the residents both when fatigued (less than 4 hours of sleep: mean, 2.0 +/- 1.5 hours) and when rested (more than 4 hours of sleep: mean, 6.5 +/- 1.0 hours), with at least 7 days between tests. In order to eliminate the effects of learning from the first test series, randomization of residents was performed so that one half were first evaluated when rested and one half when fatigued. ANOVA, multiple regression analysis, and the Student t test were used to assess differences. In the acute sleep-deprived state, residents were less vigorous and more fatigued, depressed, tense, confused, and angry (p less than 0.05) than they were in rested state. Despite these changes in mood, however, the responses on all of the functional tests were no different statistically in those who were rested and those who were fatigued (even in those with less than 2 hours' sleep). We conclude that acute sleep deprivation of less than 4 hours alters mood state but does not change performance in test situations in which concentration, clear thinking, and problem solving are important.

  13. Sleep Deprivation Aggravates Median Nerve Injury-Induced Neuropathic Pain and Enhances Microglial Activation by Suppressing Melatonin Secretion

    PubMed Central

    Huang, Chun-Ta; Chiang, Rayleigh Ping-Ying; Chen, Chih-Li; Tsai, Yi-Ju

    2014-01-01

    Study Objectives: Sleep deprivation is common in patients with neuropathic pain, but the effect of sleep deprivation on pathological pain remains uncertain. This study investigated whether sleep deprivation aggravates neuropathic symptoms and enhances microglial activation in the cuneate nucleus (CN) in a median nerve chronic constriction injury (CCI) model. Also, we assessed if melatonin supplements during the sleep deprived period attenuates these effects. Design: Rats were subjected to sleep deprivation for 3 days by the disc-on-water method either before or after CCI. In the melatonin treatment group, CCI rats received melatonin supplements at doses of 37.5, 75, 150, or 300 mg/kg during sleep deprivation. Melatonin was administered at 23:00 once a day. Participants: Male Sprague-Dawley rats, weighing 180-250 g (n = 190), were used. Measurements: Seven days after CCI, behavioral testing was conducted, and immunohistochemistry, immunoblotting, and enzyme-linked immunosorbent assay were used for qualitative and quantitative analyses of microglial activation and measurements of proinflammatory cytokines. Results: In rats who underwent post-CCI sleep deprivation, microglia were more profoundly activated and neuropathic pain was worse than those receiving pre-CCI sleep deprivation. During the sleep deprived period, serum melatonin levels were low over the 24-h period. Administration of melatonin to CCI rats with sleep deprivation significantly attenuated activation of microglia and development of neuropathic pain, and markedly decreased concentrations of proinflammatory cytokines. Conclusions: Sleep deprivation makes rats more vulnerable to nerve injury-induced neuropathic pain, probably because of associated lower melatonin levels. Melatonin supplements to restore a circadian variation in melatonin concentrations during the sleep deprived period could alleviate nerve injury-induced behavioral hypersensitivity. Citation: Huang CT, Chiang RP, Chen CL, Tsai YJ. Sleep

  14. Partial Sleep Deprivation Reduces the Efficacy of Orexin-A to Stimulate Physical Activity and Energy Expenditure.

    PubMed

    DePorter, Danielle P; Coborn, Jamie E; Teske, Jennifer A

    2017-10-01

    Sufficient sleep is required for weight maintenance. Sleep deprivation due to noise exposure stimulates weight gain by increasing hyperphagia and reducing energy expenditure (EE). Yet the mechanistic basis underlying the weight gain response is unclear. Orexin-A promotes arousal and negative energy balance, and orexin terminals project to the ventrolateral preoptic area (VLPO), which is involved in sleep-to-wake transitions. To determine whether sleep deprivation reduces orexin function in VLPO and to test the hypothesis that sleep deprivation would attenuate the orexin-A-stimulated increase in arousal, physical activity (PA), and EE. Electroencephalogram, electromyogram, distance traveled, and EE were determined in male Sprague-Dawley rats following orexin-A injections into VLPO both before and after acute (12-h) and chronic (8 h/d, 9 d) sleep deprivation by noise exposure. Orexin-A in the VLPO significantly increased arousal, PA, total EE, and PA-related EE and reduced sleep and respiratory quotient before sleep deprivation. In contrast to after acute sleep deprivation in which orexin-A failed to stimulate EE during PA only, orexin-A failed to significantly increase arousal, PA, fat oxidation, total EE, and PA-related EE after chronic sleep deprivation. Sleep deprivation may reduce sensitivity to endogenous stimuli that enhance EE due to PA and thus stimulate weight gain. © 2017 The Obesity Society.

  15. Short-term total sleep deprivation alters delay-conditioned memory in the rat.

    PubMed

    Tripathi, Shweta; Jha, Sushil K

    2016-06-01

    Short-term sleep deprivation soon after training may impair memory consolidation. Also, a particular sleep stage or its components increase after learning some tasks, such as negative and positive reinforcement tasks, avoidance tasks, and spatial learning tasks, and so forth. It suggests that discrete memory types may require specific sleep stage or its components for their optimal processing. The classical conditioning paradigms are widely used to study learning and memory but the role of sleep in a complex conditioned learning is unclear. Here, we have investigated the effects of short-term sleep deprivation on the consolidation of delay-conditioned memory and the changes in sleep architecture after conditioning. Rats were trained for the delay-conditioned task (for conditioning, house-light [conditioned stimulus] was paired with fruit juice [unconditioned stimulus]). Animals were divided into 3 groups: (a) sleep deprived (SD); (b) nonsleep deprived (NSD); and (c) stress control (SC) groups. Two-way ANOVA revealed a significant interaction between groups and days (training and testing) during the conditioned stimulus-unconditioned stimulus presentation. Further, Tukey post hoc comparison revealed that the NSD and SC animals exhibited significant increase in performances during testing. The SD animals, however, performed significantly less during testing. Further, we observed that wakefulness and NREM sleep did not change after training and testing. Interestingly, REM sleep increased significantly on both days compared to baseline more specifically during the initial 4-hr time window after conditioning. Our results suggest that the consolidation of delay-conditioned memory is sleep-dependent and requires augmented REM sleep during an explicit time window soon after training. (PsycINFO Database Record (c) 2016 APA, all rights reserved).

  16. Circadian Rhythms, Sleep Deprivation, and Human Performance

    PubMed Central

    Goel, Namni; Basner, Mathias; Rao, Hengyi; Dinges, David F.

    2014-01-01

    Much of the current science on, and mathematical modeling of, dynamic changes in human performance within and between days is dominated by the two-process model of sleep–wake regulation, which posits a neurobiological drive for sleep that varies homeostatically (increasing as a saturating exponential during wakefulness and decreasing in a like manner during sleep), and a circadian process that neurobiologically modulates both the homeostatic drive for sleep and waking alertness and performance. Endogenous circadian rhythms in neurobehavioral functions, including physiological alertness and cognitive performance, have been demonstrated using special laboratory protocols that reveal the interaction of the biological clock with the sleep homeostatic drive. Individual differences in circadian rhythms and genetic and other components underlying such differences also influence waking neurobehavioral functions. Both acute total sleep deprivation and chronic sleep restriction increase homeostatic sleep drive and degrade waking neurobehavioral functions as reflected in sleepiness, attention, cognitive speed, and memory. Recent evidence indicating a high degree of stability in neurobehavioral responses to sleep loss suggests that these trait-like individual differences are phenotypic and likely involve genetic components, including circadian genes. Recent experiments have revealed both sleep homeostatic and circadian effects on brain metabolism and neural activation. Investigation of the neural and genetic mechanisms underlying the dynamically complex interaction between sleep homeostasis and circadian systems is beginning. A key goal of this work is to identify biomarkers that accurately predict human performance in situations in which the circadian and sleep homeostatic systems are perturbed. PMID:23899598

  17. The effects of low-intensity cycling on cognitive performance following sleep deprivation.

    PubMed

    Slutsky, Alexis B; Diekfuss, Jed A; Janssen, James A; Berry, Nate T; Shih, Chia-Hao; Raisbeck, Louisa D; Wideman, Laurie; Etnier, Jennifer L

    2017-10-15

    This study examined the effect of 24h of sleep deprivation on cognitive performance and assessed the effect of acute exercise on cognitive performance following sleep deprivation. Young, active, healthy adults (n=24, 14 males) were randomized to control (age=24.7±3.7years, BMI=27.2±7.0) or exercise (age=25.3±3.3years, BMI=25.6±5.1) groups. Cognitive testing included a 5-min psychomotor vigilance task (PVT), three memory tasks with increasing cognitive load, and performance of the PVT a second time. On morning one, cognitive testing followed a typical night's sleep. Following 24-h of sustained wakefulness, cognitive testing was conducted again prior to and after the acute intervention. Participants in the exercise condition performed low-intensity cycling (∼40%HRR) for 15-min and those in the control condition sat quietly on the bike for 15-min. t-Tests revealed sleep deprivation negatively affected performance on the PVT, but did not affect memory performance. Following the acute intervention, there were no cognitive performance differences between the exercise and rested conditions. We provide support for previous literature suggesting that during simple tasks, sleep deprivation has negative effects on cognitive performance. Importantly, in contrast to previous literature which has shown multiple bouts of exercise adding to cognitive detriment when combined with sleep deprivation, our results did not reveal any further detriments to cognitive performance from a single-bout of exercise following sleep deprivation. Copyright © 2017 Elsevier Inc. All rights reserved.

  18. Effect of 24 Hours of Sleep Deprivation on Auditory and Linguistic Perception: A Comparison among Young Controls, Sleep-Deprived Participants, Dyslexic Readers, and Aging Adults

    ERIC Educational Resources Information Center

    Fostick, Leah; Babkoff, Harvey; Zukerman, Gil

    2014-01-01

    Purpose: To test the effects of 24 hr of sleep deprivation on auditory and linguistic perception and to assess the magnitude of this effect by comparing such performance with that of aging adults on speech perception and with that of dyslexic readers on phonological awareness. Method: Fifty-five sleep-deprived young adults were compared with 29…

  19. Sleep deprivation aggravates median nerve injury-induced neuropathic pain and enhances microglial activation by suppressing melatonin secretion.

    PubMed

    Huang, Chun-Ta; Chiang, Rayleigh Ping-Ying; Chen, Chih-Li; Tsai, Yi-Ju

    2014-09-01

    Sleep deprivation is common in patients with neuropathic pain, but the effect of sleep deprivation on pathological pain remains uncertain. This study investigated whether sleep deprivation aggravates neuropathic symptoms and enhances microglial activation in the cuneate nucleus (CN) in a median nerve chronic constriction injury (CCI) model. Also, we assessed if melatonin supplements during the sleep deprived period attenuates these effects. Rats were subjected to sleep deprivation for 3 days by the disc-on-water method either before or after CCI. In the melatonin treatment group, CCI rats received melatonin supplements at doses of 37.5, 75, 150, or 300 mg/kg during sleep deprivation. Melatonin was administered at 23:00 once a day. Male Sprague-Dawley rats, weighing 180-250 g (n = 190), were used. Seven days after CCI, behavioral testing was conducted, and immunohistochemistry, immunoblotting, and enzyme-linked immunosorbent assay were used for qualitative and quantitative analyses of microglial activation and measurements of proinflammatory cytokines. In rats who underwent post-CCI sleep deprivation, microglia were more profoundly activated and neuropathic pain was worse than those receiving pre-CCI sleep deprivation. During the sleep deprived period, serum melatonin levels were low over the 24-h period. Administration of melatonin to CCI rats with sleep deprivation significantly attenuated activation of microglia and development of neuropathic pain, and markedly decreased concentrations of proinflammatory cytokines. Sleep deprivation makes rats more vulnerable to nerve injury-induced neuropathic pain, probably because of associated lower melatonin levels. Melatonin supplements to restore a circadian variation in melatonin concentrations during the sleep deprived period could alleviate nerve injury-induced behavioral hypersensitivity. © 2014 Associated Professional Sleep Societies, LLC.

  20. Human Hippocampal Structure: A Novel Biomarker Predicting Mnemonic Vulnerability to, and Recovery from, Sleep Deprivation

    PubMed Central

    Goldstein-Piekarski, Andrea N.; Greer, Stephanie M.; Stark, Shauna; Stark, Craig E.

    2016-01-01

    Sleep deprivation impairs the formation of new memories. However, marked interindividual variability exists in the degree to which sleep loss compromises learning, the mechanistic reasons for which are unclear. Furthermore, which physiological sleep processes restore learning ability following sleep deprivation are similarly unknown. Here, we demonstrate that the structural morphology of human hippocampal subfields represents one factor determining vulnerability (and conversely, resilience) to the impact of sleep deprivation on memory formation. Moreover, this same measure of brain morphology was further associated with the quality of nonrapid eye movement slow wave oscillations during recovery sleep, and by way of such activity, determined the success of memory restoration. Such findings provide a novel human biomarker of cognitive susceptibility to, and recovery from, sleep deprivation. Moreover, this metric may be of special predictive utility for professions in which memory function is paramount yet insufficient sleep is pervasive (e.g., aviation, military, and medicine). SIGNIFICANCE STATEMENT Sleep deprivation does not impact all people equally. Some individuals show cognitive resilience to the effects of sleep loss, whereas others express striking vulnerability, the reasons for which remain largely unknown. Here, we demonstrate that structural features of the human brain, specifically those within the hippocampus, accurately predict which individuals are susceptible (or conversely, resilient) to memory impairments caused by sleep deprivation. Moreover, this same structural feature determines the success of memory restoration following subsequent recovery sleep. Therefore, structural properties of the human brain represent a novel biomarker predicting individual vulnerability to (and recovery from) the effects of sleep loss, one with occupational relevance in professions where insufficient sleep is pervasive yet memory function is paramount. PMID:26911684

  1. Sleep deprivation: Impact on cognitive performance

    PubMed Central

    Alhola, Paula; Polo-Kantola, Päivi

    2007-01-01

    Today, prolonged wakefulness is a widespread phenomenon. Nevertheless, in the field of sleep and wakefulness, several unanswered questions remain. Prolonged wakefulness can be due to acute total sleep deprivation (SD) or to chronic partial sleep restriction. Although the latter is more common in everyday life, the effects of total SD have been examined more thoroughly. Both total and partial SD induce adverse changes in cognitive performance. First and foremost, total SD impairs attention and working memory, but it also affects other functions, such as long-term memory and decision-making. Partial SD is found to influence attention, especially vigilance. Studies on its effects on more demanding cognitive functions are lacking. Coping with SD depends on several factors, especially aging and gender. Also interindividual differences in responses are substantial. In addition to coping with SD, recovering from it also deserves attention. Cognitive recovery processes, although insufficiently studied, seem to be more demanding in partial sleep restriction than in total SD. PMID:19300585

  2. The effects of sleep restriction and sleep deprivation in producing false memories.

    PubMed

    Chatburn, Alex; Kohler, Mark J; Payne, Jessica D; Drummond, Sean P A

    2017-01-01

    False memory has been claimed to be the result of an associative process of generalisation, as well as to be representative of memory errors. These can occur at any stage of memory encoding, consolidation, or retrieval, albeit through varied mechanisms. The aim of this paper is to experimentally determine: (i) if cognitive dysfunction brought about by sleep loss at the time of stimulus encoding can influence false memory production; and (ii) whether this relationship holds across sensory modalities. Subjects undertook both the Deese-Roedigger-McDermott (DRM) false memory task and a visual task designed to produce false memories. Performance was measured while subjects were well-rested (9h Time in Bed or TIB), and then again when subjects were either sleep restricted (4h TIB for 4 nights) or sleep deprived (30h total SD). Results indicate (1) that partial and total sleep loss produced equivalent effects in terms of false and veridical verbal memory, (2) that subjects performed worse after sleep loss (regardless of whether this was partial or total sleep loss) on cued recognition-based false and veridical verbal memory tasks, and that sleep loss interfered with subjects' ability to recall veridical, but not false memories under free recall conditions, and (3) that there were no effects of sleep loss on a visual false memory task. This is argued to represent the dysfunction and slow repair of an online verbal associative process in the brain following inadequate sleep. Copyright © 2016 Elsevier Inc. All rights reserved.

  3. The Effects of Sleep Deprivation on Item and Associative Recognition Memory

    ERIC Educational Resources Information Center

    Ratcliff, Roger; Van Dongen, Hans P. A.

    2018-01-01

    Sleep deprivation adversely affects the ability to perform cognitive tasks, but theories range from predicting an overall decline in cognitive functioning because of reduced stability in attentional networks to specific deficits in various cognitive domains or processes. We measured the effects of sleep deprivation on two memory tasks, item…

  4. Sleep deprivation affects sensorimotor coupling in postural control of young adults.

    PubMed

    Aguiar, Stefane A; Barela, José A

    2014-06-27

    Although impairments in postural control have been reported due to sleep deprivation, the mechanisms underlying such performance decrements still need to be uncovered. The purpose of this study was to investigate the effects of sleep deprivation on the relationship between visual information and body sway in young adults' postural control. Thirty adults who remained awake during one night and 30 adults who slept normally the night before the experiment participated in this study. The moving room paradigm was utilized, manipulating visual information through the movement of a room while the floor remained motionless. Subjects stood upright inside of a moving room during four 60-s trials. In the first trial the room was kept stationary and in the following trials the room moved with a frequency of 0.2Hz, peak velocity of 0.6cm/s and 0.9cm peak-to-peak amplitude. Body sway and room displacement were measured through infrared markers. Results showed larger and faster body sway in sleep deprived subjects with and without visual manipulation. The magnitude with which visual stimulus influenced body sway and its temporal relationship were unaltered in sleep deprived individuals, but they became less coherent and more variable as they had to maintain upright stance during trials. These results indicate that after sleep deprivation adults become less stable and accurate in relating visual information to motor action, and this effect is observed after only a brief period performing postural tasks. The low cognitive load employed in this task suggests that attentional difficulties are not the only factor leading to sensorimotor coupling impairments observed following sleep deprivation. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

  5. Sleep Deprivation Attack Detection in Wireless Sensor Network

    NASA Astrophysics Data System (ADS)

    Bhattasali, Tapalina; Chaki, Rituparna; Sanyal, Sugata

    2012-02-01

    Deployment of sensor network in hostile environment makes it mainly vulnerable to battery drainage attacks because it is impossible to recharge or replace the battery power of sensor nodes. Among different types of security threats, low power sensor nodes are immensely affected by the attacks which cause random drainage of the energy level of sensors, leading to death of the nodes. The most dangerous type of attack in this category is sleep deprivation, where target of the intruder is to maximize the power consumption of sensor nodes, so that their lifetime is minimized. Most of the existing works on sleep deprivation attack detection involve a lot of overhead, leading to poor throughput. The need of the day is to design a model for detecting intrusions accurately in an energy efficient manner. This paper proposes a hierarchical framework based on distributed collaborative mechanism for detecting sleep deprivation torture in wireless sensor network efficiently. Proposed model uses anomaly detection technique in two steps to reduce the probability of false intrusion.

  6. Migraine, arousal and sleep deprivation: comment on: “sleep quality, arousal and pain thresholds in migraineurs: a blinded controlled polysomnographic study”

    PubMed Central

    2013-01-01

    We discuss the hypothesis proposed by Engstrom and coworkers that Migraineurs have a relative sleep deprivation, which lowers the pain threshold and predispose to attacks. Previous data indicate that Migraineurs have a reduction of Cyclic Alternating Pattern (CAP), an essential mechanism of NREM sleep regulation which allows to dump the effect of incoming disruptive stimuli, and to protect sleep. The modifications of CAP observed in Migraineurs are similar to those observed in patients with impaired arousal (narcolepsy) and after sleep deprivation. The impairment of this mechanism makes Migraineurs more vulnerable to stimuli triggering attacks during sleep, and represents part of a more general vulnerability to incoming stimuli. PMID:23758606

  7. Donepezil Improves Episodic Memory in Young Individuals Vulnerable to the Effects of Sleep Deprivation

    PubMed Central

    Chuah, Lisa Y.M.; Chong, Delise L.; Chen, Annette K.; Rekshan, William R.; Tan, Jiat-Chow; Zheng, Hui; Chee, Michael W.L.

    2009-01-01

    Study Objectives: We investigated if donepezil, a long-acting orally administered cholinesterase inhibitor, would reduce episodic memory deficits associated with 24 h of sleep deprivation. Design: Double-blind, placebo-controlled, crossover study involving 7 laboratory visits over 2 months. Participants underwent 4 functional MRI scans; 2 sessions (donepezil or placebo) followed a normal night's sleep, and 2 sessions followed a night of sleep deprivation. Setting: The study took place in a research laboratory. Participants: 26 young, healthy volunteers with no history of any sleep, psychiatric, or neurologic disorders. Interventions: 5 mg of donepezil was taken once daily for approximately 17 days. Measurements and Results: Subjects were scanned while performing a semantic judgment task and tested for word recognition outside the scanner 45 minutes later. Sleep deprivation increased the frequency of non-responses at encoding and impaired delayed recognition. No benefit of donepezil was evident when participants were well rested. When sleep deprived, individuals who showed greater performance decline improved with donepezil, whereas more resistant individuals did not benefit. Accompanying these behavioral effects, there was corresponding modulation of task-related activation in functionally relevant brain regions. Brain regions identified in relation to donepezil-induced alteration in non-response rates could be distinguished from regions relating to improved recognition memory. This suggests that donepezil can improve delayed recognition in sleep-deprived persons by improving attention as well as enhancing memory encoding. Conclusions: Donepezil reduced decline in recognition performance in individuals vulnerable to the effects of sleep deprivation. Additionally, our findings demonstrate the utility of combined fMRI–behavior evaluation in psychopharmacological studies. Citation: Chuah LYM; Chong DL; Chen AK; Rekshan WR; Tan JC; Zheng H; Chee MWL. Donepezil

  8. Sleep deprivation and adverse health effects in United States Coast Guard responders to Hurricanes Katrina and Rita.

    PubMed

    Bergan, Timothy; Thomas, Dana; Schwartz, Erica; McKibben, Jodi; Rusiecki, Jennifer

    2015-12-01

    Disaster responders are increasingly called upon to assist in various natural and manmade disasters. A critical safety concern for this population is sleep deprivation; however, there are limited published data regarding sleep deprivation and disaster responder safety. We expanded upon a cross-sectional study of 2695 United States Coast Guard personnel who responded to Hurricanes Katrina and Rita. Data were collected via survey on self-reported timing and location of deployment, missions performed, health effects, medical treatment sought, average nightly sleep, and other lifestyle variables. We created a 4-level sleep deprivation metric based on both average nightly reported sleep (d5hours; >5hours) and length of deployment (d2weeks; >2weeks) to examine the association between sustained sleep deprivation and illnesses, injuries, and symptoms using logistic regression to calculate odds ratios (ORs) and 95% confidence intervals. The strongest, statistically significant positive ORs for the highest sleep deprivation category compared with the least sleep-deprived category were for mental health and neurologic effects, specifically depression (OR=6.76), difficulty concentrating (OR=8.33), and confusion (OR=11.34), and for dehydration (OR=9.0). Injuries most strongly associated with sleep deprivation were twists, sprains, and strains (OR=6.20). Most health outcomes evaluated had monotonically increasing ORs with increasing sleep deprivation, and P tests for trend were statistically significant. Agencies deploying disaster responders should understand the risks incurred to their personnel by sustained sleep deprivation. Improved planning of response efforts to disasters can reduce the potential for sleep deprivation and lead to decreased morbidity in disaster responders. Published by Elsevier Inc.

  9. Selective REM-sleep deprivation does not diminish emotional memory consolidation in young healthy subjects.

    PubMed

    Morgenthaler, Jarste; Wiesner, Christian D; Hinze, Karoline; Abels, Lena C; Prehn-Kristensen, Alexander; Göder, Robert

    2014-01-01

    Sleep enhances memory consolidation and it has been hypothesized that rapid eye movement (REM) sleep in particular facilitates the consolidation of emotional memory. The aim of this study was to investigate this hypothesis using selective REM-sleep deprivation. We used a recognition memory task in which participants were shown negative and neutral pictures. Participants (N=29 healthy medical students) were separated into two groups (undisturbed sleep and selective REM-sleep deprived). Both groups also worked on the memory task in a wake condition. Recognition accuracy was significantly better for negative than for neutral stimuli and better after the sleep than the wake condition. There was, however, no difference in the recognition accuracy (neutral and emotional) between the groups. In summary, our data suggest that REM-sleep deprivation was successful and that the resulting reduction of REM-sleep had no influence on memory consolidation whatsoever.

  10. Performance Trends During Sleep Deprivation on a Tilt-Based Control Task.

    PubMed

    Bolkhovsky, Jeffrey B; Ritter, Frank E; Chon, Ki H; Qin, Michael

    2018-07-01

    Understanding human behavior under the effects of sleep deprivation allows for the mitigation of risk due to reduced performance. To further this goal, this study investigated the effects of short-term sleep deprivation using a tilt-based control device and examined whether existing user models accurately predict targeting performance. A task in which the user tilts a surface to roll a ball into a target was developed to examine motor performance. A model was built to predict human performance for this task under various levels of sleep deprivation. Every 2 h, 10 subjects completed the task until they reached 24 h of wakefulness. Performance measurements of this task, which were based on Fitts' law, included movement time, task throughput, and time intercept. The model predicted significant performance decrements over the 24-h period with an increase in movement time (R2 = 0.61), a decrease in throughput (R2 = 0.57), and an increase in time intercept (R2 = 0.60). However, it was found that in experimental trials there was no significant change in movement time (R2 = 0.11), throughput (R2 = 0.15), or time intercept (R2 = 0.27). The results found were unexpected as performance decrement is frequently reported during sleep deprivation. These findings suggest a reexamination of the initial thought of sleep loss leading to a decrement in all aspects of performance.Bolkovsky JB, Ritter FE, Chon KH, Qin M. Performance trends during sleep deprivation on a tilt-based control task. Aerosp Med Hum Perform. 2018; 89(7):626-633.

  11. Effects of daytime food intake on memory consolidation during sleep or sleep deprivation.

    PubMed

    Herzog, Nina; Friedrich, Alexia; Fujita, Naoko; Gais, Steffen; Jauch-Chara, Kamila; Oltmanns, Kerstin M; Benedict, Christian

    2012-01-01

    Sleep enhances memory consolidation. Bearing in mind that food intake produces many metabolic signals that can influence memory processing in humans (e.g., insulin), the present study addressed the question as to whether the enhancing effect of sleep on memory consolidation is affected by the amount of energy consumed during the preceding daytime. Compared to sleep, nocturnal wakefulness has been shown to impair memory consolidation in humans. Thus, a second question was to examine whether the impaired memory consolidation associated with sleep deprivation (SD) could be compensated by increased daytime energy consumption. To these aims, 14 healthy normal-weight men learned a finger tapping sequence (procedural memory) and a list of semantically associated word pairs (declarative memory). After the learning period, standardized meals were administered, equaling either ∼50% or ∼150% of the estimated daily energy expenditure. In the morning, after sleep or wakefulness, memory consolidation was tested. Plasma glucose was measured both before learning and retrieval. Polysomnographic sleep recordings were performed by electroencephalography (EEG). Independent of energy intake, subjects recalled significantly more word pairs after sleep than they did after SD. When subjects stayed awake and received an energy oversupply, the number of correctly recalled finger sequences was equal to those seen after sleep. Plasma glucose did not differ among conditions, and sleep time in the sleep conditions was not influenced by the energy intake interventions. These data indicate that the daytime energy intake level affects neither sleep's capacity to boost the consolidation of declarative and procedural memories, nor sleep's quality. However, high energy intake was followed by an improved procedural but not declarative memory consolidation under conditions of SD. This suggests that the formation of procedural memory is not only triggered by sleep but is also sensitive to the

  12. Melatonin modulates adiponectin expression on murine colitis with sleep deprivation.

    PubMed

    Kim, Tae Kyun; Park, Young Sook; Baik, Haing-Woon; Jun, Jin Hyun; Kim, Eun Kyung; Sull, Jae Woong; Sung, Ho Joong; Choi, Jin Woo; Chung, Sook Hee; Gye, Myung Chan; Lim, Ju Yeon; Kim, Jun Bong; Kim, Seong Hwan

    2016-09-07

    To determine adiponectin expression in colonic tissue of murine colitis and systemic cytokine expression after melatonin treatments and sleep deprivation. The following five groups of C57BL/6 mice were used in this study: (1) group I, control; (2) group II, 2% DSS induced colitis for 7 d; (3) group III, 2% DSS induced colitis and melatonin treatment; (4) group IV, 2% DSS induced colitis with sleep deprivation (SD) using specially designed and modified multiple platform water baths; and (5) group V, 2% DSS induced colitis with SD and melatonin treatment. Melatonin (10 mg/kg) or saline was intraperitoneally injected daily to mice for 4 d. The body weight was monitored daily. The degree of colitis was evaluated histologically after sacrificing the mice. Immunohistochemical staining and Western blot analysis was performed using anti-adiponectin antibody. After sampling by intracardiac punctures, levels of serum cytokines were measured by ELISA. Sleep deprivation in water bath exacerbated DSS induced colitis and worsened weight loss. Melatonin injection not only alleviated the severity of mucosal injury, but also helped survival during stressful condition. The expression level of adiponectin in mucosa was decreased in colitis, with the lowest level observed in colitis combined with sleep deprivation. Melatonin injection significantly (P < 0.05) recovered the expression of adiponectin. The expression levels of IL-6 and IL-17 were increased in the serum of mice with DSS colitis but decreased after melatonin injection. This study suggested that melatonin modulated adiponectin expression in colonic tissue and melatonin and adiponectin synergistically potentiated anti-inflammatory effects on colitis with sleep deprivation.

  13. Electrodermal lability as an indicator for subjective sleepiness during total sleep deprivation.

    PubMed

    Michael, Lars; Passmann, Sven; Becker, Ruth

    2012-08-01

    The present study addresses the suitability of electrodermal lability as an indicator of individual vulnerability to the effects of total sleep deprivation. During two complete circadian cycles, the effects of 48h of total sleep deprivation on physiological measures (electrodermal activity and body temperature), subjective sleepiness (measured by visual analogue scale and tiredness symptom scale) and task performance (reaction time and errors in a go/no go task) were investigated. Analyses of variance with repeated measures revealed substantial decreases of the number of skin conductance responses, body temperature, and increases for subjective sleepiness, reaction time and error rates. For all changes, strong circadian oscillations could be observed as well. The electrodermal more labile subgroup reported higher subjective sleepiness compared with electrodermal more stable participants, but showed no differences in the time courses of body temperature and task performance. Therefore, electrodermal lability seems to be a specific indicator for the changes in subjective sleepiness due to total sleep deprivation and circadian oscillations, but not a suitable indicator for vulnerability to the effects of sleep deprivation per se. © 2011 European Sleep Research Society.

  14. Human Hippocampal Structure: A Novel Biomarker Predicting Mnemonic Vulnerability to, and Recovery from, Sleep Deprivation.

    PubMed

    Saletin, Jared M; Goldstein-Piekarski, Andrea N; Greer, Stephanie M; Stark, Shauna; Stark, Craig E; Walker, Matthew P

    2016-02-24

    Sleep deprivation impairs the formation of new memories. However, marked interindividual variability exists in the degree to which sleep loss compromises learning, the mechanistic reasons for which are unclear. Furthermore, which physiological sleep processes restore learning ability following sleep deprivation are similarly unknown. Here, we demonstrate that the structural morphology of human hippocampal subfields represents one factor determining vulnerability (and conversely, resilience) to the impact of sleep deprivation on memory formation. Moreover, this same measure of brain morphology was further associated with the quality of nonrapid eye movement slow wave oscillations during recovery sleep, and by way of such activity, determined the success of memory restoration. Such findings provide a novel human biomarker of cognitive susceptibility to, and recovery from, sleep deprivation. Moreover, this metric may be of special predictive utility for professions in which memory function is paramount yet insufficient sleep is pervasive (e.g., aviation, military, and medicine). Copyright © 2016 the authors 0270-6474/16/362355-09$15.00/0.

  15. Effects of experimental sleep deprivation on anxiety-like behavior in animal research: Systematic review and meta-analysis.

    PubMed

    Pires, Gabriel Natan; Bezerra, Andréia Gomes; Tufik, Sergio; Andersen, Monica Levy

    2016-09-01

    Increased acute anxiety is a commonly reported behavioral consequence of sleep deprivation in humans. However, rodent studies conducted so far produced inconsistent results, failing to reproduce the same sleep deprivation induced-anxiety observed in clinical experiments. While some presented anxiogenesis as result of sleep deprivation, others reported anxiolysis. In face of such inconsistencies, this article explores the effects of experimental sleep deprivation on anxiety-like behavior in animal research through a systematic review and a series of meta-analyses. A total of 50 of articles met our inclusion criteria, 30 on mice, 19 on rats and one on Zebrafish. Our review shows that sleep deprivation induces a decrease in anxiety-like behavior in preclinical models, which is opposite to results observed in human settings. These results were corroborated in stratified analyses according to species, sleep deprivation method and anxiety measurement technique. In conclusion, the use of animal models for the evaluation of the relationship between sleep deprivation lacks translational applicability and new experimental tools are needed to properly evaluate sleep deprivation-induced anxiogenesis in rodents. Copyright © 2016 Elsevier Ltd. All rights reserved.

  16. Chronic sleep deprivation markedly reduces coagulation factor VII expression

    PubMed Central

    Pinotti, Mirko; Bertolucci, Cristiano; Frigato, Elena; Branchini, Alessio; Cavallari, Nicola; Baba, Kenkichi; Contreras-Alcantara, Susana; Ehlen, J. Christopher; Bernardi, Francesco; Paul, Ketema N.; Tosini, Gianluca

    2010-01-01

    Chronic sleep loss, a common feature of human life in industrialized countries, is associated to cardiovascular disorders. Variations in functional parameters of coagulation might contribute to explain this relationship. By exploiting the mouse model and a specifically designed protocol, we demonstrated that seven days of partial sleep deprivation significantly decreases (−30.5%) the thrombin generation potential in plasma evaluated upon extrinsic (TF/FVIIa pathway) but not intrinsic activation of coagulation. This variation was consistent with a decrease (−49.8%) in the plasma activity levels of factor VII (FVII), the crucial physiologicalal trigger of coagulation, which was even more pronounced at the liver mRNA level (−85.7%). The recovery in normal sleep conditions for three days completely restored thrombin generation and FVII activity in plasma. For the first time, we demonstrate that chronic sleep deprivation on its own reduces, in a reversible manner, the FVII expression levels, thus influencing the TF/FVIIa activation pathway efficiency. PMID:20418241

  17. Total Sleep Deprivation and Recovery Sleep Affect the Diurnal Variation of Agility Performance: The Gender Differences.

    PubMed

    Romdhani, Mohamed; Hammouda, Omar; Smari, Khawla; Chaabouni, Yassine; Mahdouani, Kacem; Driss, Tarak; Souissi, Nizar

    2018-05-30

    Romdhani, M, Hammouda, O, Smari, K, Chaabouni, Y, Mahdouani, K, Driss, T, and Souissi, N. Total sleep deprivation and recovery sleep affect the diurnal variation of agility performance: The gender differences. J Strength Cond Res XX(X): 000-000, 2018-This study aimed to investigate the effects of time-of-day, 24 and 36 hours of total sleep deprivation (TSD), and recovery sleep (RS) on repeated-agility performances. Twenty-two physical education students (11 male and 11 female students) completed 5 repeated modified agility T-test (RMAT) sessions (i.e., 2 after normal sleep night [NSN] [at 07:00 and 17:00 hours], 2 after TSD [at 07:00 hours, i.e., 24-hour TSD and at 17:00 hours, i.e., 36-hour TSD], and 1 after RS at 17:00 hours). The RMAT index decreased from the morning to the afternoon after NSN (p < 0.05, d = 1.05; p < 0.01, d = 0.73) and after TSD (p < 0.001, d = 0.92; d = 1.08), respectively, for total time (TT) and peak time (PT). This finding indicates a diurnal variation in repeated agility, which persisted after TSD. However, the diurnal increase in PT was less marked in the female group after NSN (2.98 vs. 6.24%). Moreover, TT and PT increased, respectively, after 24-hour TSD (p < 0.001; d = 0.84, d = 0.87) and 36-hour TSD (p < 0.001, d = 1.12; p < 0.01, d = 0.65). Female participants' PT was less affected by 24-hour TSD (1.76 vs. 6.81%) compared with male participants' PT. After 36-hour TSD, the amount of decrease was not different between groups, which increased the diurnal amplitude of PT only for male participants. Total sleep deprivation suppressed the diurnal increase of PT and increased the diurnal amplitude of oral temperature only in women. Nevertheless, RS normalized the sleep-loss-induced performance disruption. Conclusively, sleep loss and RS differently affect repeated-agility performance of men and women during the day. Sleep extension postdeprivation could have potent restorative effect on repeated-agility performances, and female

  18. Persistent Short-Term Memory Defects Following Sleep Deprivation in a Drosophila Model of Parkinson Disease

    PubMed Central

    Seugnet, Laurent; Galvin, James E.; Suzuki, Yasuko; Gottschalk, Laura; Shaw, Paul J.

    2009-01-01

    Study Objectives: Parkinson disease (PD) is the second most common neurodegenerative disorder in the United States. It is associated with motor deficits, sleep disturbances, and cognitive impairment. The pathology associated with PD and the effects of sleep deprivation impinge, in part, upon common molecular pathways suggesting that sleep loss may be particularly deleterious to the degenerating brain. Thus we investigated the long-term consequences of sleep deprivation on short-term memory using a Drosophila model of Parkinson disease. Participants: Transgenic strains of Drosophila melanogaster. Design: Using the GAL4-UAS system, human α-synuclein was expressed throughout the nervous system of adult flies. α-Synuclein expressing flies (αS flies) and the corresponding genetic background controls were sleep deprived for 12 h at age 16 days and allowed to recover undisturbed for at least 3 days. Short-term memory was evaluated using aversive phototaxis suppression. Dopaminergic systems were assessed using mRNA profiling and immunohistochemistry. Measurments and Results: When sleep deprived at an intermediate stage of the pathology, αS flies showed persistent short-term memory deficits that lasted ≥ 3 days. Cognitive deficits were not observed in younger αS flies nor in genetic background controls. Long-term impairments were not associated with accelerated loss of dopaminergic neurons. However mRNA expression of the dopamine receptors dDA1 and DAMB were significantly increased in sleep deprived αS flies. Blocking D1-like receptors during sleep deprivation prevented persistent short-term memory deficits. Importantly, feeding flies the polyphenolic compound curcumin blocked long-term learning deficits. Conclusions: These data emphasize the importance of sleep in a degenerating/reorganizing brain and shows that pathological processes induced by sleep deprivation can be dissected at the molecular and cellular level using Drosophila genetics. Citation: Seugnet L

  19. The effect of sleep deprivation on leadership behaviour in military officers: an experimental study.

    PubMed

    Olsen, Olav Kjellevold; Pallesen, Ståle; Torsheim, Torbjørn; Espevik, Roar

    2016-12-01

    While several studies show that leaders frequently lack sleep, little is known about how this influences leadership behaviour. The present study encompasses an experiment that investigated how three main types of leadership behaviour: transformational (four sub-facets); transactional (two sub-facets); and passive-avoidant (two sub-facets) leadership differed across a rested and a long-term, partially sleep-deprived condition. A total of 16 military naval officers participated. In both conditions, the leaders managed a team of three subordinates in a navy navigation simulator, instructed to complete a specific mission (A or B). Both sleep state (rested or sleep deprived) and mission were counterbalanced. Leadership behaviour was video recorded and subsequently rated on the three leadership behaviours. Overall, the scores on transformational leadership (and on two of four sub-facets) and transactional leadership (on both sub-facets) decreased from the rested to sleep-deprived condition, whereas scores on passive-avoidant leadership overall (and on both sub-facets) increased from the rested to sleep-deprived condition. This study underscores the importance of including sleep as a potentially important determinant when assessing leadership effectiveness. © 2016 European Sleep Research Society.

  20. Is sleep deprivation a contributor to obesity in children?

    PubMed

    Chaput, Jean-Philippe

    2016-03-01

    Chronic lack of sleep (called "sleep deprivation") is common in modern societies with 24/7 availability of commodities. Accumulating evidence supports the role of reduced sleep as contributing to the current obesity epidemic in children and youth. Longitudinal studies have consistently shown that short sleep duration is associated with weight gain and the development of obesity. Recent experimental studies have reported that sleep restriction leads to weight gain in humans. Increased food intake appears to be the main mechanism by which insufficient sleep results in weight gain. Voluntary sleep restriction has been shown to increase snacking, the number of meals eaten per day, and the preference for energy-dense foods. Although the causes of sleep loss in the pediatric population are numerous, more research looking at screen exposure before bedtime and its effects on sleep is needed given the pervasiveness of electronic media devices in today's environment. Health professionals should routinely ask questions about sleep and promote a good night's sleep because insufficient sleep impacts activity and eating behaviors. Future research should examine the clinical benefits of increasing sleep duration on eating behaviors and body weight control and determine the importance of adequate sleep to improve the treatment of obesity.

  1. Global Prevalence of Sleep Deprivation in Students and Heavy Media Use

    ERIC Educational Resources Information Center

    Zhang, Meilan; Tillman, Daniel A.; An, Song A.

    2017-01-01

    The latest two international educational assessments found global prevalence of sleep deprivation in students, consistent with what has been reported in sleep research. However, despite the fundamental role of adequate sleep in cognitive and social functioning, this important issue has been largely overlooked by educational researchers. Drawing…

  2. Switch-task performance in rats is disturbed by 12 h of sleep deprivation but not by 12 h of sleep fragmentation.

    PubMed

    Leenaars, Cathalijn H C; Joosten, Ruud N J M A; Zwart, Allard; Sandberg, Hans; Ruimschotel, Emma; Hanegraaf, Maaike A J; Dematteis, Maurice; Feenstra, Matthijs G P; van Someren, Eus J W

    2012-02-01

    Task-switching is an executive function involving the prefrontal cortex. Switching temporarily attenuates the speed and/or accuracy of performance, phenomena referred to as switch costs. In accordance with the idea that prefrontal function is particularly sensitive to sleep loss, switch-costs increase during prolonged waking in humans. It has been difficult to investigate the underlying neurobiological mechanisms because of the lack of a suitable animal model. Here, we introduce the first switch-task for rats and report the effects of sleep deprivation and inactivation of the medial prefrontal cortex. Rats were trained to repeatedly switch between 2 stimulus-response associations, indicated by the presentation of a visual or an auditory stimulus. These stimulus-response associations were offered in blocks, and performance was compared for the first and fifth trials of each block. Performance was tested after exposure to 12 h of total sleep deprivation, sleep fragmentation, and their respective movement control conditions. Finally, it was tested after pharmacological inactivation of the medial prefrontal cortex. Controlled laboratory settings. 15 male Wistar rats. Both accuracy and latency showed switch-costs at baseline. Twelve hours of total sleep deprivation, but not sleep fragmentation, impaired accuracy selectively on the switch-trials. Inactivation of the medial prefrontal cortex by local neuronal inactivation resulted in an overall decrease in accuracy. We developed and validated a switch-task that is sensitive to sleep deprivation. This introduces the possibility for in-depth investigations on the neurobiological mechanisms underlying executive impairments after sleep disturbance in a rat model.

  3. Sleep deprivation and divergent toll-like receptor-4 activation of cellular inflammation in aging.

    PubMed

    Carroll, Judith E; Carrillo, Carmen; Olmstead, Richard; Witarama, Tuff; Breen, Elizabeth C; Yokomizo, Megumi; Seeman, Teresa; Irwin, Michael R

    2015-02-01

    Sleep disturbance and aging are associated with increases in inflammation, as well as increased risk of infectious disease. However, there is limited understanding of the role of sleep loss on age-related differences in immune responses. This study examines the effects of sleep deprivation on toll-like receptor activation of monocytic inflammation in younger compared to older adults. Community-dwelling adults (n = 70) who were categorized as younger (25-39 y old, n = 21) and older (60-84 y old, n = 49) participants, underwent a sleep laboratory-based experimental partial sleep deprivation (PSD) protocol including adaptation, an uninterrupted night of sleep, sleep deprivation (sleep restricted to 03:00-07:00), and recovery. Blood samples were obtained each morning to measure toll-like receptor-4 activation of monocyte intracellular production of the inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). Partial sleep deprivation induced a significant increase in the production of IL-6 and/or TNF-α that persisted after a night of recovery sleep (F(2,121.2) = 3.8, P < 0.05). Age moderated the effects of sleep loss, such that younger adults had an increase in inflammatory cytokine production that was not present in older adults (F(2,121.2) = 4.0, P < 0.05). Older adults exhibit reduced toll-like receptor 4 stimulated cellular inflammation that, unlike in younger adults, is not activated after a night of partial sleep loss. Whereas sleep loss increases cellular inflammation in younger adults and may contribute to inflammatory disorders, blunted toll-like receptor activation in older adults may increase the risk of infectious disease seen with aging. © 2015 Associated Professional Sleep Societies, LLC.

  4. The impact of sleep deprivation on surgeons' performance during night shifts.

    PubMed

    Amirian, Ilda

    2014-09-01

    The median incidence of adverse events that may result in patient injury is a total of 9% of all in-hospital admissions. In order to reduce this high incidence initiatives are continuously worked on that can reduce the risk of patient harm during admission by strengthening hospital systems. However, the influence of physicians' shift work on the risk on adverse events in patients remains controversial. In the studies included in this PhD thesis we wished to examine the impact of sleep deprivation and circadian rhythm disturbances on surgeons' during night shifts. Further we wished to examine the impact sleep deprivation had on surgeons' performance as a measure of how patient safety would be affected. We found that sleep deprivation subjectively had an impact on the surgeons and that they were aware of the effect fatigue had on their work performance. As a result they applied different mechanisms to cope with fatigue. Attending surgeons felt that they had a better overview now, due to more experience and better skills, than when they were residents, despite the fatigue on night shifts. We monitored surgeons' performance during night shifts by laparoscopic simulation and cognitive tests in order to assess their performance; no deterioration was found when pre call values were compared to on call values. The surgeons were monitored prospectively for 4 days across a night shift in order to assess the circadian rhythm and sleep. We found that surgeons' circadian rhythm was affected by working night shifts and their sleep pattern altered, resembling that of shift workers on the post call day. We assessed the quality of admission in medical records as a measure of surgeons' performance, during day, evening and night hours and found no deterioration in the quality of night time medical records. However, consistent high errors were found in several categories. These findings should be followed up in the future with respect of clarifying mechanism and consequences for

  5. Mood and metabolic consequences of sleep deprivation as a potential endophenotype' in bipolar disorder.

    PubMed

    Aydin, Adem; Selvi, Yavuz; Besiroglu, Lutfullah; Boysan, Murat; Atli, Abdullah; Ozdemir, Osman; Kilic, Sultan; Balaharoglu, Ragıp

    2013-09-05

    It has been commonly recognized that circadian rhythm and sleep/wake cycle are causally involved in bipolar disorder. There has been a paucity of systematic research considering the relations between sleep and mood states in bipolar disorder. The current study examines the possible influences of sleep deprivation on mood states and endocrine functions among first-degree relatives of patients with bipolar disorder and healthy controls. Blood samples were taken at two time points in the consecutive mornings at predeprivation and postdeprivation periods. Participants simultaneously completed the Profiles of Mood States at two time points after giving blood samples. Plasma T3 and TSH levels increased after total sleep deprivation in both groups. Sleep deprivation induced TSH levels were reversely associated with depression-dejection among healthy controls. A paradoxical effect was detected for only the first-degree relatives of the patients that changes in plasma cortisol levels negatively linked to depression-dejection and anger-hostility scores after total sleep deprivation. Plasma DHEA levels became correlated with vigor-activity scores after sleep deprivation among first-degree relatives of bipolar patients. On the contrary, significant associations of depression-dejection, anger-hostility, and confusion-bewilderment with the baseline plasma DHEA levels became statistically trivial in the postdeprivation period. Findings suggested that first-degree relatives of patients with bipolar disorder had completely distinct characteristics with respect to sleep deprivation induced responses in terms of associations between endocrine functions and mood states as compared to individuals whose relatives had no psychiatric problems. Considering the relationships between endocrine functions and mood states among relatives of the patients, it appears like sleep deprivation changes the receptor sensitivity which probably plays a pivotal role on mood outcomes among the first

  6. Sleep deprivation and the organization of the behavioral states.

    NASA Technical Reports Server (NTRS)

    Dement, W. C.

    1972-01-01

    Questions concerning the significance of sleep in the developing organism are investigated, together with the mechanisms that underlie the unique distribution of behavioral states at any particular age and during any particular experimental manipulation. It is attempted to define the states of sleep and wakefulness in terms of a temporal confluence of a number of more or less independent processes, taking also into account the functional consequences of these attributes. The results of a selective deprivation of rapid eye movement sleep are explored, giving attention to effects on sleep, behavioral changes, brain excitability, pharmacological changes, and biochemical changes.

  7. Effects of food or sleep deprivation during civilian survival training on clinical chemistry variables.

    PubMed

    Ståhle, Lars; Granström, Elisabeth; Ljungdahl Ståhle, Ewa; Isaksson, Sven; Samuelsson, Anders; Rudling, Mats; Sepp, Harry

    2013-06-01

    To describe clinical chemistry and weight changes after short-term food or sleep deprivation or multiple deprivations during civilian survival training. Data from one baseline-controlled two-period crossover study designed to compare sleep deprivation for up to 50 hours with food deprivation for up to 66 hours (n = 12) and data from regular multiple-deprivations survival training comparing participants (n = 33) with nondeprived instructors (n = 10). Food deprivation was associated with decreased body weight, blood glucose, serum triglycerides, sodium, chloride, and urine pH, and there were increases in blood and urine ketones and serum free fatty acids. Sleep deprivation was associated with a minor decrease in hemoglobin and erythrocyte particle count and volume fraction and an increase in leukocytes. The clinical chemistry and body weight changes associated with food deprivation were qualitatively similar to those observed in fasting obese patients but developed quicker in the survival training setting. Sleep deprivation had few effects on the clinical chemistry profile except for hematological variables. Physicians evaluating clinical chemistry data from patients subjected to short-term food or sleep deprivation should take the physiological state into account in their assessment. Copyright © 2013 Wilderness Medical Society. Published by Elsevier Inc. All rights reserved.

  8. Vitamin C Prevents Sleep Deprivation-induced Elevation in Cortisol and Lipid Peroxidation in the Rat Plasma.

    PubMed

    Olayaki, L A; Sulaiman, S O; Anoba, N B

    2015-12-20

    Sleep deprivation (SD) is biological stressor that alters metabolic parameters, induced oxidative stress and lipid peroxidation. Previous studies have shown that antioxidants substances such as melatonin, tryptophan, vitamin E and vitamin C improved stress tolerance in laboratory animals. In this study, we examined the potential protective effects of administration of vitamin C on acute and chronic sleep deprivation-induced metabolic derangement. In addition, possible processes involved in vitamin C effects on acute and chronic sleep deprivation-induced metabolic derangement were determined. Thirty-five rats (120-250g) were used. The rats were divided into 7 groups of 5 rats each as Control (CTRL), Acute sleep deprived untreated with vitamin C (AC), Acute sleep deprived treated with vitamin C (AWC), Chronic sleep deprived untreated with vitamin C (CC), Chronic sleep deprived treated with vitamin C (CWC), Chronic sleep deprived + Recovery untreated with vitamin C (RC), and Chronic sleep deprived + Recovery treated with vitamin C (RWC). The SD was carried out for 20h for 1 day on the acute groups, and for 20h/day for 5 days on the chronic group, using the Multiple Modified Platforms (MMP) after oral administration of 300mg/kg of vitamin C to all vitamin C-treated groups. The recovery groups were further observed for five days after SD. The control group were treated with vitamin C and without stress in their home cages. At the end of the experiment, the animals were sacrificed and blood was collected for estimation of plasma glucose, insulin, cortisol and malondialdehyde (MDA). The results showed that acute and chronic SDs significantly  increased MDA and cortisol levels, while significantly reduced the levels of insulin. Treatment with vitamin C reversed the changes in the MDA, cortisol and plasma insulin levels. Additionally, allowing the rats to recover for 5 days after sleep deprivation corrected the observed changes. Plasma glucose was significantly

  9. Sleep Deprivation and Time-on-Task Performance Decrement in the Rat Psychomotor Vigilance Task

    PubMed Central

    Oonk, Marcella; Davis, Christopher J.; Krueger, James M.; Wisor, Jonathan P.; Van Dongen, Hans P.A.

    2015-01-01

    Study Objectives: The rat psychomotor vigilance task (rPVT) was developed as a rodent analog of the human psychomotor vigilance task (hPVT). We examined whether rPVT performance displays time-on-task effects similar to those observed on the hPVT. Design: The rPVT requires rats to respond to a randomly presented light stimulus to obtain a water reward. Rats were water deprived for 22 h prior to each 30-min rPVT session to motivate performance. We analyzed rPVT performance over time on task and as a function of the response-stimulus interval, at baseline and after sleep deprivation. Setting: The study was conducted in an academic research vivarium. Participants: Male Long-Evans rats were trained to respond to a 0.5 sec stimulus light within 3 sec of stimulus onset. Complete data were available for n = 20 rats. Interventions: Rats performed the rPVT for 30 min at baseline and after 24 h total sleep deprivation by gentle handling. Measurements and Results: Compared to baseline, sleep deprived rats displayed increased performance lapses and premature responses, similar to hPVT lapses of attention and false starts. However, in contrast to hPVT performance, the time-on-task performance decrement was not significantly enhanced by sleep deprivation. Moreover, following sleep deprivation, rPVT response times were not consistently increased after short response-stimulus intervals. Conclusions: The rat psychomotor vigilance task manifests similarities to the human psychomotor vigilance task in global performance outcomes, but not in post-sleep deprivation effects of time on task and response-stimulus interval. Citation: Oonk M, Davis CJ, Krueger JM, Wisor JP, Van Dongen HPA. Sleep deprivation and time-on-task performance decrement in the rat psychomotor vigilance task. SLEEP 2015;38(3):445–451. PMID:25515099

  10. Effects of Daytime Food Intake on Memory Consolidation during Sleep or Sleep Deprivation

    PubMed Central

    Herzog, Nina; Friedrich, Alexia; Fujita, Naoko; Gais, Steffen; Jauch-Chara, Kamila; Oltmanns, Kerstin M.; Benedict, Christian

    2012-01-01

    Sleep enhances memory consolidation. Bearing in mind that food intake produces many metabolic signals that can influence memory processing in humans (e.g., insulin), the present study addressed the question as to whether the enhancing effect of sleep on memory consolidation is affected by the amount of energy consumed during the preceding daytime. Compared to sleep, nocturnal wakefulness has been shown to impair memory consolidation in humans. Thus, a second question was to examine whether the impaired memory consolidation associated with sleep deprivation (SD) could be compensated by increased daytime energy consumption. To these aims, 14 healthy normal-weight men learned a finger tapping sequence (procedural memory) and a list of semantically associated word pairs (declarative memory). After the learning period, standardized meals were administered, equaling either ∼50% or ∼150% of the estimated daily energy expenditure. In the morning, after sleep or wakefulness, memory consolidation was tested. Plasma glucose was measured both before learning and retrieval. Polysomnographic sleep recordings were performed by electroencephalography (EEG). Independent of energy intake, subjects recalled significantly more word pairs after sleep than they did after SD. When subjects stayed awake and received an energy oversupply, the number of correctly recalled finger sequences was equal to those seen after sleep. Plasma glucose did not differ among conditions, and sleep time in the sleep conditions was not influenced by the energy intake interventions. These data indicate that the daytime energy intake level affects neither sleep’s capacity to boost the consolidation of declarative and procedural memories, nor sleep’s quality. However, high energy intake was followed by an improved procedural but not declarative memory consolidation under conditions of SD. This suggests that the formation of procedural memory is not only triggered by sleep but is also sensitive to the

  11. Donepezil improves episodic memory in young individuals vulnerable to the effects of sleep deprivation.

    PubMed

    Chuah, Lisa Y M; Chong, Delise L; Chen, Annette K; Rekshan, William R; Tan, Jiat-Chow; Zheng, Hui; Chee, Michael W L

    2009-08-01

    We investigated if donepezil, a long-acting orally administered cholinesterase inhibitor, would reduce episodic memory deficits associated with 24 h of sleep deprivation. Double-blind, placebo-controlled, crossover study involving 7 laboratory visits over 2 months. Participants underwent 4 functional MRI scans; 2 sessions (donepezil or placebo) followed a normal night's sleep, and 2 sessions followed a night of sleep deprivation. The study took place in a research laboratory. 26 young, healthy volunteers with no history of any sleep, psychiatric, or neurologic disorders. 5 mg of donepezil was taken once daily for approximately 17 days. Subjects were scanned while performing a semantic judgment task and tested for word recognition outside the scanner 45 minutes later. Sleep deprivation increased the frequency of non-responses at encoding and impaired delayed recognition. No benefit of donepezil was evident when participants were well rested. When sleep deprived, individuals who showed greater performance decline improved with donepezil, whereas more resistant individuals did not benefit. Accompanying these behavioral effects, there was corresponding modulation of task-related activation in functionally relevant brain regions. Brain regions identified in relation to donepezil-induced alteration in non-response rates could be distinguished from regions relating to improved recognition memory. This suggests that donepezil can improve delayed recognition in sleep-deprived persons by improving attention as well as enhancing memory encoding. Donepezil reduced decline in recognition performance in individuals vulnerable to the effects of sleep deprivation. Additionally, our findings demonstrate the utility of combined fMRI-behavior evaluation in psychopharmacological studies.

  12. Sleep deprivation increases blood pressure in healthy normotensive elderly and attenuates the blood pressure response to orthostatic challenge.

    PubMed

    Robillard, Rébecca; Lanfranchi, Paola A; Prince, François; Filipini, Daniel; Carrier, Julie

    2011-03-01

    To determine how aging affects the impact of sleep deprivation on blood pressure at rest and under orthostatic challenge. Subjects underwent a night of sleep and 24.5 h of sleep deprivation in a crossover counterbalanced design. Sleep laboratory. Sixteen healthy normotensive men and women: 8 young adults (mean 24 years [SD 3.1], range 20-28 years) and 8 elderly adults (mean 64.1 years [SD 3.4], range 60-69 years). Sleep deprivation. Brachial cuff arterial blood pressure and heart rate were measured in semi-recumbent and upright positions. These measurements were compared across homeostatic sleep pressure conditions and age groups. Sleep deprivation induced a significant increase in systolic and diastolic blood pressure in elderly but not young adults. Moreover, sleep deprivation attenuated the systolic blood pressure orthostatic response in both age groups. Our results suggest that sleep deprivation alters the regulatory mechanisms of blood pressure and might increase the risk of hypertension in healthy normotensive elderly.

  13. Serum Amyloid A Production Is Triggered by Sleep Deprivation in Mice and Humans: Is That the Link between Sleep Loss and Associated Comorbidities?

    PubMed Central

    de Oliveira, Edson M.; Visniauskas, Bruna; Tufik, Sergio; Andersen, Monica L.; Chagas, Jair R.; Campa, Ana

    2017-01-01

    Serum amyloid A (SAA) was recently associated with metabolic endotoxemia, obesity and insulin resistance. Concurrently, insufficient sleep adversely affects metabolic health and is an independent predisposing factor for obesity and insulin resistance. In this study we investigated whether sleep loss modulates SAA production. The serum SAA concentration increased in C57BL/6 mice subjected to sleep restriction (SR) for 15 days or to paradoxical sleep deprivation (PSD) for 72 h. Sleep restriction also induced the upregulation of Saa1.1/Saa2.1 mRNA levels in the liver and Saa3 mRNA levels in adipose tissue. SAA levels returned to the basal range after 24 h in paradoxical sleep rebound (PSR). Metabolic endotoxemia was also a finding in SR. Increased plasma levels of SAA were also observed in healthy human volunteers subjected to two nights of total sleep deprivation (Total SD), returning to basal levels after one night of recovery. The observed increase in SAA levels may be part of the initial biochemical alterations caused by sleep deprivation, with potential to drive deleterious conditions such as metabolic endotoxemia and weight gain. PMID:28335560

  14. An Overview of Sleep Deprivation and The Ameliorative Effects of Modafinil

    DTIC Science & Technology

    2002-11-01

    H., and Jouvet, M., Successful treatment of idiopathic hypersomnia and narcolepsy with modafinil. Progress in Neuro-Psychopharmacology and Biological...Laffont, F., Cathala, H.P., and Kohler, F. Effect of modafinil on narcolepsy and idiopathic hypersomnia . in the 5th European Congress of Sleep Research...amphetamine and modafinil on the sleep/wake cycle during experimental hypersomnia induced by sleep deprivation in the cat. Journal of Sleep Research, 2000. 9

  15. Persistent short-term memory defects following sleep deprivation in a drosophila model of Parkinson disease.

    PubMed

    Seugnet, Laurent; Galvin, James E; Suzuki, Yasuko; Gottschalk, Laura; Shaw, Paul J

    2009-08-01

    Parkinson disease (PD) is the second most common neurodegenerative disorder in the United States. It is associated with motor deficits, sleep disturbances, and cognitive impairment. The pathology associated with PD and the effects of sleep deprivation impinge, in part, upon common molecular pathways suggesting that sleep loss may be particularly deleterious to the degenerating brain. Thus we investigated the long-term consequences of sleep deprivation on shortterm memory using a Drosophila model of Parkinson disease. Transgenic strains of Drosophila melanogaster. Using the GAL4-UAS system, human alpha-synuclein was expressed throughout the nervous system of adult flies. Alpha-synuclein expressing flies (alpha S flies) and the corresponding genetic background controls were sleep deprived for 12 h at age 16 days and allowed to recover undisturbed for at least 3 days. Short-term memory was evaluated using aversive phototaxis suppression. Dopaminergic systems were assessed using mRNA profiling and immunohistochemistry. MEASURMENTS AND RESULTS: When sleep deprived at an intermediate stage of the pathology, alpha S flies showed persistent short-term memory deficits that lasted > or = 3 days. Cognitive deficits were not observed in younger alpha S flies nor in genetic background controls. Long-term impairments were not associated with accelerated loss of dopaminergic neurons. However mRNA expression of the dopamine receptors dDA1 and DAMB were significantly increased in sleep deprived alpha S flies. Blocking D1-like receptors during sleep deprivation prevented persistent shortterm memory deficits. Importantly, feeding flies the polyphenolic compound curcumin blocked long-term learning deficits. These data emphasize the importance of sleep in a degenerating/reorganizing brain and shows that pathological processes induced by sleep deprivation can be dissected at the molecular and cellular level using Drosophila genetics.

  16. Effects of Extreme Sleep Deprivation on Human Performance

    DOE Office of Scientific and Technical Information (OSTI.GOV)

    Tuan Tran; Kimberly R. Raddatz; Elizabeth T. Cady

    Sleep is a fundamental recuperative process for the nervous system. Disruption of this homeostatic drive can lead to severe impairments of the operator’s ability to perceive, recognize, and respond to emergencies and/or unanticipated events, putting the operator at risk. Therefore, establishing a comprehensive understanding of how sleep deprivation influences human performance is essential in order to counter fatigue or to develop mitigation strategies. The goal of the present study was to examine the psychological effects of prolonged sleep deprivation (approx. 75 hrs) over a four-day span on a general aviation pilot flying a fixed-based flight simulator. During the study, amore » series of tasks were employed every four hours in order to examine the pilot’s perceptual and higher level cognitive abilities. Overall, results suggest that the majority of cognitive and perceptual degradation occurs between 30-40 hours into the flight. Limitations and future research directions are also discussed.« less

  17. Sleep deprivation and time-on-task performance decrement in the rat psychomotor vigilance task.

    PubMed

    Oonk, Marcella; Davis, Christopher J; Krueger, James M; Wisor, Jonathan P; Van Dongen, Hans P A

    2015-03-01

    The rat psychomotor vigilance task (rPVT) was developed as a rodent analog of the human psychomotor vigilance task (hPVT). We examined whether rPVT performance displays time-on-task effects similar to those observed on the hPVT. The rPVT requires rats to respond to a randomly presented light stimulus to obtain a water reward. Rats were water deprived for 22 h prior to each 30-min rPVT session to motivate performance. We analyzed rPVT performance over time on task and as a function of the response-stimulus interval, at baseline and after sleep deprivation. The study was conducted in an academic research vivarium. Male Long-Evans rats were trained to respond to a 0.5 sec stimulus light within 3 sec of stimulus onset. Complete data were available for n = 20 rats. Rats performed the rPVT for 30 min at baseline and after 24 h total sleep deprivation by gentle handling. Compared to baseline, sleep deprived rats displayed increased performance lapses and premature responses, similar to hPVT lapses of attention and false starts. However, in contrast to hPVT performance, the time-on-task performance decrement was not significantly enhanced by sleep deprivation. Moreover, following sleep deprivation, rPVT response times were not consistently increased after short response-stimulus intervals. The rPVT manifests similarities to the hPVT in global performance outcomes, but not in post-sleep deprivation effects of time on task and response-stimulus interval. © 2015 Associated Professional Sleep Societies, LLC.

  18. Daily Acclimation Handling Does Not Affect Hippocampal Long-Term Potentiation or Cause Chronic Sleep Deprivation in Mice

    PubMed Central

    Vecsey, Christopher G.; Wimmer, Mathieu E. J.; Havekes, Robbert; Park, Alan J.; Perron, Isaac J.; Meerlo, Peter; Abel, Ted

    2013-01-01

    Study Objectives: Gentle handling is commonly used to perform brief sleep deprivation in rodents. It was recently reported that daily acclimation handling, which is often used before behavioral assays, causes alterations in sleep, stress, and levels of N-methyl-D-aspartate receptor subunits prior to the actual period of sleep deprivation. It was therefore suggested that acclimation handling could mediate some of the observed effects of subsequent sleep deprivation. Here, we examine whether acclimation handling, performed as in our sleep deprivation studies, alters sleep/wake behavior, stress, or forms of hippocampal synaptic plasticity that are impaired by sleep deprivation. Design: Adult C57BL/6J mice were either handled daily for 6 days or were left undisturbed in their home cages. On the day after the 6th day of handling, long-term potentiation (LTP) was induced in hippocampal slices with spaced four-train stimulation, which we previously demonstrated to be impaired by brief sleep deprivation. Basal synaptic properties were also assessed. In three other sets of animals, activity monitoring, polysomnography, and stress hormone measurements were performed during the 6 days of handling. Results: Daily gentle handling alone does not alter LTP, rest/activity patterns, or sleep/wake architecture. Handling initially induces a minimal stress response, but by the 6th day, stress hormone levels are unaltered by handling. Conclusion: It is possible to handle mice daily to accustom them to the researcher without causing alterations in sleep, stress, or synaptic plasticity in the hippocampus. Therefore, effects of acclimation handling cannot explain the impairments in signaling mechanisms, synaptic plasticity, and memory that result from brief sleep deprivation. Citation: Vecsey CG; Wimmer MEJ; Havekes R; Park AJ; Perron IJ; Meerlo P; Abel T. Daily acclimation handling does not affect hippocampal long-term potentiation or cause chronic sleep deprivation in mice. SLEEP 2013

  19. Sleep deprivation causes memory deficits by negatively impacting neuronal connectivity in hippocampal area CA1

    PubMed Central

    Havekes, Robbert; Park, Alan J; Tudor, Jennifer C; Luczak, Vincent G; Hansen, Rolf T; Ferri, Sarah L; Bruinenberg, Vibeke M; Poplawski, Shane G; Day, Jonathan P; Aton, Sara J; Radwańska, Kasia; Meerlo, Peter; Houslay, Miles D; Baillie, George S; Abel, Ted

    2016-01-01

    Brief periods of sleep loss have long-lasting consequences such as impaired memory consolidation. Structural changes in synaptic connectivity have been proposed as a substrate of memory storage. Here, we examine the impact of brief periods of sleep deprivation on dendritic structure. In mice, we find that five hours of sleep deprivation decreases dendritic spine numbers selectively in hippocampal area CA1 and increased activity of the filamentous actin severing protein cofilin. Recovery sleep normalizes these structural alterations. Suppression of cofilin function prevents spine loss, deficits in hippocampal synaptic plasticity, and impairments in long-term memory caused by sleep deprivation. The elevated cofilin activity is caused by cAMP-degrading phosphodiesterase-4A5 (PDE4A5), which hampers cAMP-PKA-LIMK signaling. Attenuating PDE4A5 function prevents changes in cAMP-PKA-LIMK-cofilin signaling and cognitive deficits associated with sleep deprivation. Our work demonstrates the necessity of an intact cAMP-PDE4-PKA-LIMK-cofilin activation-signaling pathway for sleep deprivation-induced memory disruption and reduction in hippocampal spine density. DOI: http://dx.doi.org/10.7554/eLife.13424.001 PMID:27549340

  20. Sleep deprivation as an experimental model system for psychosis: Effects on smooth pursuit, prosaccades, and antisaccades.

    PubMed

    Meyhöfer, Inga; Kumari, Veena; Hill, Antje; Petrovsky, Nadine; Ettinger, Ulrich

    2017-04-01

    Current antipsychotic medications fail to satisfactorily reduce negative and cognitive symptoms and produce many unwanted side effects, necessitating the development of new compounds. Cross-species, experimental behavioural model systems can be valuable to inform the development of such drugs. The aim of the current study was to further test the hypothesis that controlled sleep deprivation is a safe and effective model system for psychosis when combined with oculomotor biomarkers of schizophrenia. Using a randomized counterbalanced within-subjects design, we investigated the effects of 1 night of total sleep deprivation in 32 healthy participants on smooth pursuit eye movements (SPEM), prosaccades (PS), antisaccades (AS), and self-ratings of psychosis-like states. Compared with a normal sleep control night, sleep deprivation was associated with reduced SPEM velocity gain, higher saccadic frequency at 0.2 Hz, elevated PS spatial error, and an increase in AS direction errors. Sleep deprivation also increased intra-individual variability of SPEM, PS, and AS measures. In addition, sleep deprivation induced psychosis-like experiences mimicking hallucinations, cognitive disorganization, and negative symptoms, which in turn had moderate associations with AS direction errors. Taken together, sleep deprivation resulted in psychosis-like impairments in SPEM and AS performance. However, diverging somewhat from the schizophrenia literature, sleep deprivation additionally disrupted PS control. Sleep deprivation thus represents a promising but possibly unspecific experimental model that may be helpful to further improve our understanding of the underlying mechanisms in the pathophysiology of psychosis and aid the development of antipsychotic and pro-cognitive drugs.

  1. Sensitivity and validity of psychometric tests for assessing driving impairment: effects of sleep deprivation.

    PubMed

    Jongen, Stefan; Perrier, Joy; Vuurman, Eric F; Ramaekers, Johannes G; Vermeeren, Annemiek

    2015-01-01

    To assess drug induced driving impairment, initial screening is needed. However, no consensus has been reached about which initial screening tools have to be used. The present study aims to determine the ability of a battery of psychometric tests to detect performance impairing effects of clinically relevant levels of drowsiness as induced by one night of sleep deprivation. Twenty four healthy volunteers participated in a 2-period crossover study in which the highway driving test was conducted twice: once after normal sleep and once after one night of sleep deprivation. The psychometric tests were conducted on 4 occasions: once after normal sleep (at 11 am) and three times during a single night of sleep deprivation (at 1 am, 5 am, and 11 am). On-the-road driving performance was significantly impaired after sleep deprivation, as measured by an increase in Standard Deviation of Lateral Position (SDLP) of 3.1 cm compared to performance after a normal night of sleep. At 5 am, performance in most psychometric tests showed significant impairment. As expected, largest effect sizes were found on performance in the Psychomotor Vigilance Test (PVT). Large effects sizes were also found in the Divided Attention Test (DAT), the Attention Network Test (ANT), and the test for Useful Field of View (UFOV) at 5 and 11 am during sleep deprivation. Effects of sleep deprivation on SDLP correlated significantly with performance changes in the PVT and the DAT, but not with performance changes in the UFOV. From the psychometric tests used in this study, the PVT and DAT seem most promising for initial evaluation of drug impairment based on sensitivity and correlations with driving impairment. Further studies are needed to assess the sensitivity and validity of these psychometric tests after benchmark sedative drug use.

  2. Sensitivity and Validity of Psychometric Tests for Assessing Driving Impairment: Effects of Sleep Deprivation

    PubMed Central

    Jongen, Stefan; Perrier, Joy; Vuurman, Eric F.; Ramaekers, Johannes G.; Vermeeren, Annemiek

    2015-01-01

    Objective To assess drug induced driving impairment, initial screening is needed. However, no consensus has been reached about which initial screening tools have to be used. The present study aims to determine the ability of a battery of psychometric tests to detect performance impairing effects of clinically relevant levels of drowsiness as induced by one night of sleep deprivation. Methods Twenty four healthy volunteers participated in a 2-period crossover study in which the highway driving test was conducted twice: once after normal sleep and once after one night of sleep deprivation. The psychometric tests were conducted on 4 occasions: once after normal sleep (at 11 am) and three times during a single night of sleep deprivation (at 1 am, 5 am, and 11 am). Results On-the-road driving performance was significantly impaired after sleep deprivation, as measured by an increase in Standard Deviation of Lateral Position (SDLP) of 3.1 cm compared to performance after a normal night of sleep. At 5 am, performance in most psychometric tests showed significant impairment. As expected, largest effect sizes were found on performance in the Psychomotor Vigilance Test (PVT). Large effects sizes were also found in the Divided Attention Test (DAT), the Attention Network Test (ANT), and the test for Useful Field of View (UFOV) at 5 and 11 am during sleep deprivation. Effects of sleep deprivation on SDLP correlated significantly with performance changes in the PVT and the DAT, but not with performance changes in the UFOV. Conclusion From the psychometric tests used in this study, the PVT and DAT seem most promising for initial evaluation of drug impairment based on sensitivity and correlations with driving impairment. Further studies are needed to assess the sensitivity and validity of these psychometric tests after benchmark sedative drug use. PMID:25668292

  3. Auditory attention and multiattribute decision-making during a 33 h sleep-deprivation period: mean performance and between-subject dispersions.

    PubMed

    Linde, L; Edland, A; Bergström, M

    1999-05-01

    One purpose of this study was to compare attention in the evening (22:00 h), in the late night (04:00 h), in the morning (10:00 h) and in the afternoon (16:00 h) during a period of complete wakefulness beginning at 08:00 h with a mean daytime performance without sleep deprivation. Another purpose was to investigate sleep deprivation effects on a multi-attribute decision-making task with and without time pressure. Twelve sleep-deprived male students were compared with 12 male non-sleep-deprived students. Both groups were tested five times with an auditory attention and a symbol coding task. Significant declines (p < 0.05) in mean level of performance on the auditory attention task were found at 04:00, 10:00 and 16:00 h for subjects forced to the vigil. However, the effect of the sleep deprivation manifested itself even more in increased between-subject dispersions. There were no differences between time pressure and no time pressure on the decision-making task and no significant differences between sleep-deprived and non-sleep-deprived subjects in decision strategies. In fact, the pattern of decision strategies among the sleep-deprived subject was more similar to a pattern of decision strategies typical for non-stressful conditions than the pattern of decision strategies among the non-sleep-deprived subjects. This result may have been due to the fact that the sleep loss acted as a dearouser. Here too, however, the variances differed significantly among sleep-deprived and non-sleep-deprived subjects, indicating that the sleep-deprived subjects were more variable in their decision strategy pattern than the control group.

  4. Heritability of Performance Deficit Accumulation During Acute Sleep Deprivation in Twins

    PubMed Central

    Kuna, Samuel T.; Maislin, Greg; Pack, Frances M.; Staley, Bethany; Hachadoorian, Robert; Coccaro, Emil F.; Pack, Allan I.

    2012-01-01

    Study Objectives: To determine if the large and highly reproducible interindividual differences in rates of performance deficit accumulation during sleep deprivation, as determined by the number of lapses on a sustained reaction time test, the Psychomotor Vigilance Task (PVT), arise from a heritable trait. Design: Prospective, observational cohort study. Setting: Academic medical center. Participants: There were 59 monozygotic (mean age 29.2 ± 6.8 [SD] yr; 15 male and 44 female pairs) and 41 dizygotic (mean age 26.6 ± 7.6 yr; 15 male and 26 female pairs) same-sex twin pairs with a normal polysomnogram. Interventions: Thirty-eight hr of monitored, continuous sleep deprivation. Measurements and Results: Patients performed the 10-min PVT every 2 hr during the sleep deprivation protocol. The primary outcome was change from baseline in square root transformed total lapses (response time ≥ 500 ms) per trial. Patient-specific linear rates of performance deficit accumulation were separated from circadian effects using multiple linear regression. Using the classic approach to assess heritability, the intraclass correlation coefficients for accumulating deficits resulted in a broad sense heritability (h2) estimate of 0.834. The mean within-pair and among-pair heritability estimates determined by analysis of variance-based methods was 0.715. When variance components of mixed-effect multilevel models were estimated by maximum likelihood estimation and used to determine the proportions of phenotypic variance explained by genetic and nongenetic factors, 51.1% (standard error = 8.4%, P < 0.0001) of twin variance was attributed to combined additive and dominance genetic effects. Conclusion: Genetic factors explain a large fraction of interindividual variance among rates of performance deficit accumulations on PVT during sleep deprivation. Citation: Kuna ST; Maislin G; Pack FM; Staley B; Hachadoorian R; Coccaro EF; Pack AI. Heritability of performance deficit accumulation

  5. Disrupted directed connectivity along the cingulate cortex determines vigilance after sleep deprivation

    PubMed Central

    Piantoni, Giovanni; Cheung, Bing Leung P.; Van Veen, Barry D.; Romeijn, Nico; Riedner, Brady A.; Tononi, Giulio; Van Der Werf, Ysbrand D.; Van Someren, Eus J.W.

    2013-01-01

    The cingulate cortex is regarded as the backbone of structural and functional connectivity of the brain. While its functional connectivity has been intensively studied, little is known about its effective connectivity, its modulation by behavioral states, and its involvement in cognitive performance. Given their previously reported effects on cingulate functional connectivity, we investigated how eye-closure and sleep deprivation changed cingulate effective connectivity, estimated from resting-state high-density electroencephalography (EEG) using a novel method to calculate Granger Causality directly in source space. Effective connectivity along the cingulate cortex was dominant in the forward direction. Eyes-open connectivity in the forward direction was greater compared to eyes-closed, in well-rested participants. The difference between eyes-open and eyes-closed connectivity was attenuated and no longer significant after sleep deprivation. Individual variability in the forward connectivity after sleep deprivation predicted subsequent task performance, such that those subjects who showed a greater increase in forward connectivity between the eyes-open and the eyes-closed periods also performed better on a sustained attention task. Effective connectivity in the opposite, backward, direction was not affected by whether the eyes were open or closed or by sleep deprivation. These findings indicate that the effective connectivity from posterior to anterior cingulate regions is enhanced when a well-rested subject has his eyes open compared to when they are closed. Sleep deprivation impairs this directed information flow, proportional to its deleterious effect on vigilance. Therefore, sleep may play a role in the maintenance of waking effective connectivity. PMID:23643925

  6. EEG quantification of alertness: methods for early identification of individuals most susceptible to sleep deprivation

    NASA Astrophysics Data System (ADS)

    Berka, Chris; Levendowski, Daniel J.; Westbrook, Philip; Davis, Gene; Lumicao, Michelle N.; Olmstead, Richard E.; Popovic, Miodrag; Zivkovic, Vladimir T.; Ramsey, Caitlin K.

    2005-05-01

    Electroencephalographic (EEG) and neurocognitive measures were simultaneously acquired to quantify alertness from 24 participants during 44-hours of sleep deprivation. Performance on a three-choice vigilance task (3C-VT), paired-associate learning/memory task (PAL) and modified Maintenance of Wakefulness Test (MWT), and sleep technician-observed drowsiness (eye-closures, head-nods, EEG slowing) were quantified. The B-Alert system automatically classifies each second of EEG on an alertness/drowsiness continuum. B-Alert classifications were significantly correlated with technician-observations, visually scored EEG and performance measures. B-Alert classifications during 3C-VT, and technician observations and performance during the 3C-VT and PAL evidenced progressively increasing drowsiness as a result of sleep deprivation with a stabilizing effect observed at the batteries occurring between 0600 and 1100 suggesting a possible circadian effect similar to those reported in previous sleep deprivation studies. Participants were given an opportunity to take a 40-minute nap approximately 24-hours into the sleep deprivation portion of the study (i.e., 7 PM on Saturday). The nap was followed by a transient period of increased alertness. Approximately 8 hours after the nap, behavioral and physiological measures of drowsiness returned to levels prior to the nap. Cluster analysis was used to stratify individuals into three groups based on their level of impairment as a result of sleep deprivation. The combination of B-Alert and neuro-behavioral measures may identify individuals whose performance is most susceptible to sleep deprivation. These objective measures could be applied in an operational setting to provide a "biobehavioral assay" to determine vulnerability to sleep deprivation.

  7. Adenosine and sleep

    DOE Office of Scientific and Technical Information (OSTI.GOV)

    Yanik, G.M. Jr.

    Behavioral and biochemical approaches have been used to determine the relative contribution of endogenous adenosine and adenosine receptors to the sleep-wake cycle in the rat. Adenosine concentrations in specific areas of the rat brain were not affected by 24 hours of total sleep deprivation, or by 24 or 48 hours of REM sleep deprivation. In order to assess the effect of REM sleep deprivation on adenosine A/sub 1/ receptors, /sup 3/H-L-PIA binding was measured. The Bmax values for /sup 3/H-L-PIA binding to membrane preparations of the cortices and corpus striata from 48 hour REM sleep-deprived animals were increased 14.8% andmore » 23%, respectively. These increases were not maintained following the cessation of sleep deprivation and recovered within 2 hours. The results of a 96 hour REM deprivation experiment were similar to those of the 48 hour REM sleep deprivation experiment. However, these increases were not evident in similar structures taken from stress control animals, and conclusively demonstrated that the changes in /sup 3/H-L-PIA binding resulted from REM sleep deprivation and not from stress.« less

  8. Sleep deprivation treatment in depression: a review

    PubMed Central

    Roy, A.; Bhanji, S.

    1976-01-01

    Ten studies, including the authors' own, suggest that sleep deprivation may be a useful treatment in a third to a half of patients with endogenous depression. Caution and a controlled trial are suggested. PMID:1257175

  9. Cardiac autonomic modulation and sleepiness: physiological consequences of sleep deprivation due to 40 h of prolonged wakefulness.

    PubMed

    Glos, Martin; Fietze, Ingo; Blau, Alexander; Baumann, Gert; Penzel, Thomas

    2014-02-10

    The autonomic nervous system (ANS) is modulated by sleep and wakefulness. Noninvasive assessment of cardiac ANS with heart rate variability (HRV) analysis is a window for monitoring malfunctioning of cardiovascular autonomic modulation due to sleep deprivation. This study represents the first investigation of dynamic ANS effects and of electrophysiological and subjective sleepiness, in parallel, during 40 h of prolonged wakefulness under constant routine (CR) conditions. In eleven young male healthy subjects, ECG, EEG, EOG, and EMG chin recordings were performed during baseline sleep, during 40 h of sleep deprivation, and during recovery sleep. After sleep deprivation, slow-wave sleep and sleep efficiency increased, whereas HRV - global variability and HRV sympathovagal balance - was reduced (all p<0.05). Sleep-stage-dependent analysis revealed reductions in the sympathovagal balance only for NREM sleep stages (all p<0.05). Comparison of the daytime pattern of CR day one (CR baseline) with that of CR day two (CR sleep deprivation) disclosed an increase in subjective sleepiness, in the amount of unintended sleep, and in HRV sympathovagal balance, with accompaniment by increased EEG alpha attenuation (all p<0.05). Circadian rhythm analysis revealed the strongest influence on heart rate, with less influence on HRV sympathovagal balance. Hour-by-hour analysis disclosed the difference between CR sleep deprivation and CR baseline for subjective sleepiness at almost every single hour and for unintended sleep particularly in the morning and afternoon (both p<0.05). These findings indicate that 40 h of prolonged wakefulness lead in the following night to sleep-stage-dependent reduction in cardiac autonomic modulation. During daytime, an increased occurrence of behavioral and physiological signs of sleepiness was accompanied by diminished cardiac autonomic modulation. The observed changes are an indicator of autonomic stress due to sleep deprivation - which, if chronic

  10. Executive Functions are not Affected by 24 Hours of Sleep Deprivation: A Color-Word Stroop Task Study.

    PubMed

    Dixit, Abhinav; Mittal, Tushar

    2015-01-01

    Sleep is an important factor affecting cognitive performance. Sleep deprivation results in fatigue, lack of concentration, confusion and sleepiness along with anxiety, depression and irritability. Sleep deprivation can have serious consequences in professions like armed forces and medicine where quick decisions and actions need to be taken. Color-Word Stroop task is one of the reliable tests to assess attention and it analyzes the processing of information in two dimensions i.e., reading of words and naming of colour. The evidence regarding the effect of sleep deprivation on Stroop interference is conflicting. The present study evaluated the effect of 24 hours of sleep deprivation on reaction time and interference in Stroop task. The present study was done on 30 healthy male medical student volunteers in the age group of 18-25 years after taking their consent and clearance from Institute Ethics Committee. Recordings of Stroop task were at three times: baseline (between 7-9 am), after 12 hours (7-9 pm) and after 24 hours (7-9 am, next day). The subjects were allowed to perform normal daily activities. The study revealed a significant increase in reaction time after 24 hours of sleep deprivation in comparison to baseline and after 12 hours of sleep deprivation. There was no significant change in interference and facilitation after sleep deprivation in comparison to baseline. The number of errors also did not show any significant change after sleep deprivation. The study indicated that there was slowing of responses without change in executive functions after 24 hours of sleep deprivation. It is probable that 24 hours of sleep deprivation does not bring about change in areas of brain affecting executive functions in healthy individuals who have normal sleep cycle. The present study indicated that in professions like armed forces and medicine working 24 hours at a stretch can lead to decrease in motor responses without affecting information processing and judgment

  11. Effects of Partial and Acute Total Sleep Deprivation on Performance across Cognitive Domains, Individuals and Circadian Phase

    PubMed Central

    Lo, June C.; Groeger, John A.; Santhi, Nayantara; Arbon, Emma L.; Lazar, Alpar S.; Hasan, Sibah; von Schantz, Malcolm; Archer, Simon N.; Dijk, Derk-Jan

    2012-01-01

    Background Cognitive performance deteriorates during extended wakefulness and circadian phase misalignment, and some individuals are more affected than others. Whether performance is affected similarly across cognitive domains, or whether cognitive processes involving Executive Functions are more sensitive to sleep and circadian misalignment than Alertness and Sustained Attention, is a matter of debate. Methodology/Principal Findings We conducted a 2 × 12-day laboratory protocol to characterize the interaction of repeated partial and acute total sleep deprivation and circadian phase on performance across seven cognitive domains in 36 individuals (18 males; mean ± SD of age = 27.6±4.0 years). The sample was stratified for the rs57875989 polymorphism in PER3, which confers cognitive susceptibility to total sleep deprivation. We observed a deterioration of performance during both repeated partial and acute total sleep deprivation. Furthermore, prior partial sleep deprivation led to poorer cognitive performance in a subsequent total sleep deprivation period, but its effect was modulated by circadian phase such that it was virtually absent in the evening wake maintenance zone, and most prominent during early morning hours. A significant effect of PER3 genotype was observed for Subjective Alertness during partial sleep deprivation and on n-back tasks with a high executive load when assessed in the morning hours during total sleep deprivation after partial sleep loss. Overall, however, Subjective Alertness and Sustained Attention were more affected by both partial and total sleep deprivation than other cognitive domains and tasks including n-back tasks of Working Memory, even when implemented with a high executive load. Conclusions/Significance Sleep loss has a primary effect on Sleepiness and Sustained Attention with much smaller effects on challenging Working Memory tasks. These findings have implications for understanding how sleep debt and circadian rhythmicity

  12. Gender differences in sleep deprivation effects on risk and inequality aversion: evidence from an economic experiment.

    PubMed

    Ferrara, Michele; Bottasso, Anna; Tempesta, Daniela; Carrieri, Marika; De Gennaro, Luigi; Ponti, Giovanni

    2015-01-01

    Excessive working hours--even at night--are becoming increasingly common in our modern 24/7 society. The prefrontal cortex (PFC) is particularly vulnerable to the effects of sleep loss and, consequently, the specific behaviors subserved by the functional integrity of the PFC, such as risk-taking and pro-social behavior, may be affected significantly. This paper seeks to assess the effects of one night of sleep deprivation on subjects' risk and social preferences, which are probably the most explored behavioral domains in the tradition of Experimental Economics. This novel cross-over study employs thirty-two university students (gender-balanced) participating to 2 counterbalanced laboratory sessions in which they perform standard risk and social preference elicitation protocols. One session was after one night of undisturbed sleep at home, and the other was after one night of sleep deprivation in the laboratory. Sleep deprivation causes increased sleepiness and decreased alertness in all subjects. After sleep loss males make riskier decisions compared to the rested condition, while females do the opposite. Females likewise show decreased inequity aversion after sleep deprivation. As for the relationship between cognitive ability and economic decisions, sleep deprived individuals with higher cognitive reflection show lower risk aversion and more altruistic behavior. These results show that one night of sleep deprivation alters economic behavior in a gender-sensitive way. Females' reaction to sleep deprivation, characterized by reduced risky choices and increased egoism compared to males, may be related to intrinsic psychological gender differences, such as in the way men and women weigh up probabilities in their decision-making, and/or to the different neurofunctional substrate of their decision-making.

  13. Gender Differences in Sleep Deprivation Effects on Risk and Inequality Aversion: Evidence from an Economic Experiment

    PubMed Central

    Ferrara, Michele; Bottasso, Anna; Tempesta, Daniela; Carrieri, Marika; De Gennaro, Luigi; Ponti, Giovanni

    2015-01-01

    Excessive working hours—even at night—are becoming increasingly common in our modern 24/7 society. The prefrontal cortex (PFC) is particularly vulnerable to the effects of sleep loss and, consequently, the specific behaviors subserved by the functional integrity of the PFC, such as risk-taking and pro-social behavior, may be affected significantly. This paper seeks to assess the effects of one night of sleep deprivation on subjects’ risk and social preferences, which are probably the most explored behavioral domains in the tradition of Experimental Economics. This novel cross-over study employs thirty-two university students (gender-balanced) participating to 2 counterbalanced laboratory sessions in which they perform standard risk and social preference elicitation protocols. One session was after one night of undisturbed sleep at home, and the other was after one night of sleep deprivation in the laboratory. Sleep deprivation causes increased sleepiness and decreased alertness in all subjects. After sleep loss males make riskier decisions compared to the rested condition, while females do the opposite. Females likewise show decreased inequity aversion after sleep deprivation. As for the relationship between cognitive ability and economic decisions, sleep deprived individuals with higher cognitive reflection show lower risk aversion and more altruistic behavior. These results show that one night of sleep deprivation alters economic behavior in a gender-sensitive way. Females’ reaction to sleep deprivation, characterized by reduced risky choices and increased egoism compared to males, may be related to intrinsic psychological gender differences, such as in the way men and women weigh up probabilities in their decision-making, and/or to the different neurofunctional substrate of their decision-making. PMID:25793869

  14. Daily acclimation handling does not affect hippocampal long-term potentiation or cause chronic sleep deprivation in mice.

    PubMed

    Vecsey, Christopher G; Wimmer, Mathieu E J; Havekes, Robbert; Park, Alan J; Perron, Isaac J; Meerlo, Peter; Abel, Ted

    2013-04-01

    Gentle handling is commonly used to perform brief sleep deprivation in rodents. It was recently reported that daily acclimation handling, which is often used before behavioral assays, causes alterations in sleep, stress, and levels of N-methyl-D-aspartate receptor subunits prior to the actual period of sleep deprivation. It was therefore suggested that acclimation handling could mediate some of the observed effects of subsequent sleep deprivation. Here, we examine whether acclimation handling, performed as in our sleep deprivation studies, alters sleep/wake behavior, stress, or forms of hippocampal synaptic plasticity that are impaired by sleep deprivation. Adult C57BL/6J mice were either handled daily for 6 days or were left undisturbed in their home cages. On the day after the 6(th) day of handling, long-term potentiation (LTP) was induced in hippocampal slices with spaced four-train stimulation, which we previously demonstrated to be impaired by brief sleep deprivation. Basal synaptic properties were also assessed. In three other sets of animals, activity monitoring, polysomnography, and stress hormone measurements were performed during the 6 days of handling. Daily gentle handling alone does not alter LTP, rest/activity patterns, or sleep/wake architecture. Handling initially induces a minimal stress response, but by the 6(th) day, stress hormone levels are unaltered by handling. It is possible to handle mice daily to accustom them to the researcher without causing alterations in sleep, stress, or synaptic plasticity in the hippocampus. Therefore, effects of acclimation handling cannot explain the impairments in signaling mechanisms, synaptic plasticity, and memory that result from brief sleep deprivation.

  15. Exposure to bright light modifies HRV responses to mental tasks during nocturnal sleep deprivation.

    PubMed

    Yokoi, Mari; Aoki, Ken; Shimomura, Yoshihiro; Iwanaga, Koichi; Katsuura, Tetsuo

    2006-03-01

    This study was intended to determine the effects of continuous bright light exposure on cardiovascular responses, particularly heart rate variability (HRV), at rest and during performance of mental tasks with acute nocturnal sleep deprivation. Eight healthy male subjects stayed awake from 21.00 to 04.30 hours under bright (BL, 2800 lux) or dim (DL, 120 lux) light conditions. During sleep deprivation, mental tasks (Stroop color-word conflict test: CWT) were performed for 15 min each hour. Blood pressure, electrocardiogram, respiratory rate, urinary melatonin concentrations and rectal temperature were measured. During sleep deprivation, BL exposure depressed melatonin secretion in comparison to DL conditions. During sleep deprivation, exposure to BL delayed the decline in heart rate (HR) for 4 h in resting periods. A significant increment of HR induced by each CWT was detected, especially at 03.00 h and later, under DL conditions only. In addition, at 04.00 h, an index of sympathetic activity and sympatho-vagal balance on HRV during CWT increased significantly under DL conditions. In contrast, an index of parasympathetic activity during CWT decreased significantly under DL conditions. However, the indexes of HRV during CWT did not change throughout sleep deprivation under BL conditions. Our results suggest that BL exposure not only delays the nocturnal decrease in HR at rest but also maintains HR and balance of cardiac autonomic modulation to mental tasks during nocturnal sleep deprivation.

  16. Short-term sleep deprivation with exposure to nocturnal light alters mitochondrial bioenergetics in Drosophila.

    PubMed

    Rodrigues, Nathane Rosa; Macedo, Giulianna Echeverria; Martins, Illana Kemmerich; Gomes, Karen Kich; de Carvalho, Nélson Rodrigues; Posser, Thaís; Franco, Jeferson Luis

    2018-05-20

    Many studies have shown the effects of sleep deprivation in several aspects of health and disease. However, little is known about how mitochondrial bioenergetics function is affected under this condition. To clarify this, we developed a simple model of short-term sleep deprivation, in which fruit-flies were submitted to a nocturnal light condition and then mitochondrial parameters were assessed by high resolution respirometry (HRR). Exposure of flies to constant light was able to alter sleep patterns, causing locomotor deficits, increasing ROS production and lipid peroxidation, affecting mitochondrial activity, antioxidant defense enzymes and caspase activity. HRR analysis showed that sleep deprivation affected mitochondrial bioenergetics capacity, decreasing respiration at oxidative phosphorylation (OXPHOS) and electron transport system (ETS). In addition, the expression of genes involved in the response to oxidative stress and apoptosis were increased. Thus, our results suggest a connection between sleep deprivation and oxidative stress, pointing to mitochondria as a possible target of this relationship. Copyright © 2018 Elsevier Inc. All rights reserved.

  17. Partial sleep deprivation does not alter processes involved in semantic word priming: event-related potential evidence.

    PubMed

    Tavakoli, Paniz; Muller-Gass, Alexandra; Campbell, Kenneth

    2015-03-01

    Sleep deprivation has generally been observed to have a detrimental effect on tasks that require sustained attention for successful performance. It might however be possible to counter these effects by altering cognitive strategies. A recent semantic word priming study indicated that subjects used an effortful predictive-expectancy search of semantic memory following normal sleep, but changed to an automatic, effortless strategy following total sleep deprivation. Partial sleep deprivation occurs much more frequently than total sleep deprivation. The present study therefore employed a similar priming task following either 4h of sleep or following normal sleep. The purpose of the study was to determine whether partial sleep deprivation would also lead to a shift in cognitive strategy to compensate for an inability to sustain attention and effortful processing necessary for using the predicative expectancy strategy. Sixteen subjects were presented with word pairs, a prime and a target that were either strongly semantically associated (cat...dog), weakly associated (cow...barn) or not associated (apple...road). The subject's task was to determine if the target word was semantically associated to the prime. A strong priming effect was observed in both conditions. RTs were slower, accuracy lower, and N400 larger to unassociated targets, independent of the amount of sleep. The overall N400 did not differ as a function of sleep. The scalp distribution of the N400 was also similar following both normal sleep and sleep loss. There was thus little evidence of a difference in the processing of the target stimulus as a function of the amount sleep. Similarly, ERPs in the period between the onset of the prime and the subsequent target also did not differ between the normal sleep and sleep loss conditions. In contrast to total sleep deprivation, subjects therefore appeared to use a common predictive expectancy strategy in both conditions. This strategy does however require an

  18. In surgeons performing cardiothoracic surgery is sleep deprivation significant in its impact on morbidity or mortality?

    PubMed

    Asfour, Leila; Asfour, Victoria; McCormack, David; Attia, Rizwan

    2014-09-01

    A best evidence topic in cardiac surgery was written according to a structured protocol. The question addressed was: is there a difference in cardiothoracic surgery outcomes in terms of morbidity or mortality of patients operated on by a sleep-deprived surgeon compared with those operated by a non-sleep-deprived surgeon? Reported search criteria yielded 77 papers, of which 15 were deemed to represent the best evidence on the topic. Three studies directly related to cardiothoracic surgery and 12 studies related to non-cardiothoracic surgery. Recommendations are based on 18 121 cardiothoracic patients and 214 666 non-cardiothoracic surgical patients. Different definitions of sleep deprivation were used in the studies, either reviewing surgeon's sleeping hours or out-of-hours operating. Surgical outcomes reviewed included: mortality rate, neurological, renal, pulmonary, infectious complications, length of stay, length of intensive care stay, cardiopulmonary bypass times and aortic-cross-clamp times. There were no significant differences in mortality or intraoperative complications in the groups of patients operated on by sleep-deprived versus non-sleep-deprived surgeons in cardiothoracic studies. One study showed a significant increase in the rate of septicaemia in patients operated on by severely sleep-deprived surgeons (3.6%) compared with the moderately sleep-deprived (0.9%) and non-sleep-deprived groups (0.8%) (P = 0.03). In the non-cardiothoracic studies, 7 of the 12 studies demonstrated statistically significant higher reoperation rate in trauma cases (P <0.02) and kidney transplants (night = 16.8% vs day = 6.4%, P <0.01), as well as higher overall mortality (P = 0.028) and morbidity (P <0.0001). There is little direct evidence in the literature demonstrating the effect of sleep deprivation in cardiothoracic surgeons on morbidity or mortality. However, overall the non-cardiothoracic studies have demonstrated that operative time and sleep deprivation can have a

  19. Functional imaging correlates of impaired distractor suppression following sleep deprivation.

    PubMed

    Kong, Danyang; Soon, Chun Siong; Chee, Michael W L

    2012-05-15

    Sleep deprivation (SD) has been shown to affect selective attention but it is not known how two of its component processes: target enhancement and distractor suppression, are affected. To investigate, young volunteers either attended to houses or were obliged to ignore them (when attending to faces) while viewing superimposed face-house pictures. MR signal enhancement and suppression in the parahippocampal place area (PPA) were determined relative to a passive viewing control condition. Sleep deprivation was associated with lower PPA activation across conditions. Critically SD specifically impaired distractor suppression in selective attention, leaving target enhancement relatively preserved. These findings parallel some observations in cognitive aging. Additionally, following SD, attended houses were not significantly better recognized than ignored houses in a post-experiment test of recognition memory contrasting with the finding of superior recognition of attended houses in the well-rested state. These results provide evidence for co-encoding of distracting information with targets into memory when one is sleep deprived. Copyright © 2012 Elsevier Inc. All rights reserved.

  20. Sleep-deprivation effect on human performance: a meta-analysis approach

    DOE Office of Scientific and Technical Information (OSTI.GOV)

    Candice D. Griffith; Candice D. Griffith; Sankaran Mahadevan

    Human fatigue is hard to define since there is no direct measure of fatigue, much like stress. Instead fatigue must be inferred from measures that are affected by fatigue. One such measurable output affected by fatigue is reaction time. In this study the relationship of reaction time to sleep deprivation is studied. These variables were selected because reaction time and hours of sleep deprivation are straightforward characteristics of fatigue to begin the investigation of fatigue effects on performance. Meta-analysis, a widely used procedure in medical and psychological studies, is applied to the variety of fatigue literature collected from various fieldsmore » in this study. Meta-analysis establishes a procedure for coding and analyzing information from various studies to compute an effect size. In this research the effect size reported is the difference between standardized means, and is found to be -0.6341, implying a strong relationship between sleep deprivation and performance degradation.« less

  1. Odd one out: social ostracism affects self-reported needs in both sleep-deprived and well-rested persons.

    PubMed

    Liu, Jean C J; Mulick, Deepti; Chee, Michael W L

    2014-08-01

    Previous research suggests that sleep deprivation may heighten normal reactions to an aversive social encounter. In this study, we explored how 24 h of sleep deprivation may influence responses to ostracism. Ninety-six healthy young adults were randomly allocated to either the sleep-deprivation or well-rested condition, wherein they engaged in two rounds of a ball-tossing game (Cyberball) programmed so that they would be included or ostracized. As compared with being included, being ostracized reduced participants' fulfillment of four essential needs (to belong; to have control; to have self-esteem; and to have a meaningful existence); participants also showed poorer mood and had poorer perceptions of their co-players. These effects were not influenced by sleep deprivation. Taken together, our findings suggest that sleep deprivation does not influence immediate distress responses to ostracism. © 2014 European Sleep Research Society.

  2. Sleep homeostatic pressure and PER3 VNTR gene polymorphism influence antidepressant response to sleep deprivation in bipolar depression.

    PubMed

    Dallaspezia, Sara; Locatelli, Clara; Lorenzi, Cristina; Pirovano, Adele; Colombo, Cristina; Benedetti, Francesco

    2016-03-01

    Combined Total sleep deprivation (TSD) and light therapy (LT) cause a rapid improvement in bipolar depression which has been hypothesized to be paralleled by changes in sleep homeostasis. Recent studies showed that bipolar patients had lower changes of EEG theta power after sleep and responders to antidepressant TSD+LT slept less and showed a lower increase of EEG theta power then non-responders. A polymorphism in PER3 gene has been associated with diurnal preference, sleep structure and homeostatic response to sleep deprivation in healthy subjects. We hypothesized that the individual variability in the homeostatic response to TSD could be a correlate of antidepressant response and be influenced by genetic factors. We administered three TSD+LT cycles to bipolar depressed patients. Severity of depression was rated on Hamilton Depression Rating Scale. Actigraphic recordings were performed in a group of patients. PER3 polymorphism influenced changes in total sleep time (F=2.24; p=0.024): while PER3(4/4) and PER3(4/5) patients showed a reduction in it after treatment, PER3(5/5) subjects showed an increase of about 40min, suggesting a higher homeostatic pressure. The same polymorphism influenced the change of depressive symptomatology during treatment (F=3.72; p=0.028). Sleep information was recorded till the day after the end of treatment: a longer period of observation could give more information about the possible maintenance of allostatic adaptation. A higher sleep homeostatic pressure reduced the antidepressant response to TSD+LT, while an allostatic adaptation to sleep loss was associated with better response. This process seems to be under genetic control. Copyright © 2015 Elsevier B.V. All rights reserved.

  3. Bombesin administration impairs memory and does not reverse memory deficit caused by sleep deprivation.

    PubMed

    Ferreira, L B T; Oliveira, S L B; Raya, J; Esumi, L A; Hipolide, D C

    2017-07-28

    Sleep deprivation impairs performance in emotional memory tasks, however this effect on memory is not completely understood. Possible mechanisms may involve an alteration in neurotransmission systems, as shown by the fact that many drugs that modulate neural pathways can prevent memory impairment by sleep loss. Gastrin releasing peptide (GRP) is a neuropeptide that emerged as a regulatory molecule of emotional memory through the modulation of other neurotransmission systems. Thus, the present study addressed the effect of intraperitoneal (IP) administration of bombesin (BB) (2.5, 5.0 and 10.0μg/kg), a GRP agonist, on the performance of Wistar rats in a multiple trail inhibitory avoidance (MTIA) task, after sleep deprivation, using the modified multiple platforms method (MMPM). Sleep deprived animals exhibited acquisition and retention impairment that was not prevented by BB injection. In addition, non-sleep deprived animals treated with BB before and after the training session, but not before the test, have shown a retention deficit. In summary, BB did not improve the memory impairment by sleep loss and, under normal conditions, produced a memory consolidation deficit. Copyright © 2017 Elsevier B.V. All rights reserved.

  4. Protective effect of alprazolam against sleep deprivation-induced behavior alterations and oxidative damage in mice.

    PubMed

    Singh, Anant; Kumar, Anil

    2008-04-01

    Sleep deprivation is considered as a risk factor for various diseases. Sleep deprivation leads to behavioral, hormonal, neurochemical and biochemical alterations in the animals. The present study was designed to explore the possible involvement of GABAergic mechanism in protective effect of alprazolam against 72h sleep deprivation-induced behavior alterations and oxidative damage in mice. In the present study, sleep deprivation caused anxiety-like behavior, weight loss, impaired ambulatory movements and oxidative damage as indicated by increase in lipid peroxidation, nitrite level and depletion of reduced glutathione and catalase activity in sleep-deprived mice brain. Treatment with alprazolam (0.25 and 0.5 mg/kg, ip) significantly improved behavioral alterations. Biochemically, alprazolam treatment significantly restored depleted reduced glutathione, catalase activity, reversed raised lipid peroxidation and nitrite level. Combination of flumazenil (0.5 mg/kg) and picrotoxin (0.5 mg/kg) with lower dose of alprazolam (0.25mg/kg) significantly antagonized protective effect of alprazolam. However, combination of muscimol (0.05 mg/kg) with alprazolam (0.25 mg/kg, ip) potentiated protective effect of alprazolam. On the basis of these results, it might be suggested that alprazolam might produce protective effect by involving GABAergic system against sleep deprivation-induced behavior alterations and related oxidative damage.

  5. Functional Polymorphisms in Dopaminergic Genes Modulate Neurobehavioral and Neurophysiological Consequences of Sleep Deprivation.

    PubMed

    Holst, Sebastian C; Müller, Thomas; Valomon, Amandine; Seebauer, Britta; Berger, Wolfgang; Landolt, Hans-Peter

    2017-04-10

    Sleep deprivation impairs cognitive performance and reliably alters brain activation in wakefulness and sleep. Nevertheless, the molecular regulators of prolonged wakefulness remain poorly understood. Evidence from genetic, behavioral, pharmacologic and imaging studies suggest that dopaminergic signaling contributes to the behavioral and electroencephalographic (EEG) consequences of sleep loss, although direct human evidence thereof is missing. We tested whether dopamine neurotransmission regulate sustained attention and evolution of EEG power during prolonged wakefulness. Here, we studied the effects of functional genetic variation in the dopamine transporter (DAT1) and the dopamine D 2 receptor (DRD2) genes, on psychomotor performance and standardized waking EEG oscillations during 40 hours of wakefulness in 64 to 82 healthy volunteers. Sleep deprivation consistently enhanced sleepiness, lapses of attention and the theta-to-alpha power ratio (TAR) in the waking EEG. Importantly, DAT1 and DRD2 genotypes distinctly modulated sleep loss-induced changes in subjective sleepiness, PVT lapses and TAR, according to inverted U-shaped relationships. Together, the data suggest that genetically determined differences in DAT1 and DRD2 expression modulate functional consequences of sleep deprivation, supporting the hypothesis that striato-thalamo-cortical dopaminergic pathways modulate the neurobehavioral and neurophysiological consequences of sleep loss in humans.

  6. The impact of sleep deprivation on decision making: a review.

    PubMed

    Harrison, Y; Horne, J A

    2000-09-01

    Few sleep deprivation (SD) studies involve realism or high-level decision making, factors relevant to managers, military commanders, and so forth, who are undergoing prolonged work during crises. Instead, research has favored simple tasks sensitive to SD mostly because of their dull monotony. In contrast, complex rule-based, convergent, and logical tasks are unaffected by short-term SD, seemingly because of heightened participant interest and compensatory effort. However, recent findings show that despite this effort, SD still impairs decision making involving the unexpected, innovation, revising plans, competing distraction, and effective communication. Decision-making models developed outside SD provide useful perspectives on these latter effects, as does a neuropsychological explanation of sleep function. SD presents particular difficulties for sleep-deprived decision makers who require these latter skills during emergency situations.

  7. Sleep deprivation predisposes liver to oxidative stress and phospholipid damage: a quantitative molecular imaging study

    PubMed Central

    Chang, Hung-Ming; Mai, Fu-Der; Chen, Bo-Jung; Wu, Un-In; Huang, Yi-Lun; Lan, Chyn-Tair; Ling, Yong-Chien

    2008-01-01

    Sleep disorders are associated with an increased rate of various metabolic disturbances, which may be related to oxidative stress and consequent lipid peroxidation. Since hepatic phosphatidylcholine plays an important role in metabolic regulation, the aim of the present study was to determine phosphatidylcholine expression in the liver following total sleep deprivation. To determine the effects of total sleep deprivation, we used adult rats implanted for polygraphic recording. Phosphatidylcholine expression was examined molecularly by the use of time-of-flight secondary ion mass spectrometry, along with biochemical solid-phase extraction. The parameters of oxidative stress were investigated by evaluating the hepatic malondialdehyde levels as well as heat shock protein 25 immunoblotting and immunohistochemistry. In normal rats, the time-of-flight secondary ion mass spectrometry spectra revealed specific peaks (m/z 184 and 224) that could be identified as molecular ions for phosphatidylcholine. However, following total sleep deprivation, the signals for phosphatidylcholine were significantly reduced to nearly one-third of the normal values. The results of solid-phase extraction also revealed that the phosphatidylcholine concentration was noticeably decreased, from 15.7 µmol g–1 to 9.4 µmol g–1, after total sleep deprivation. By contrast, the biomarkers for oxidative stress were drastically up-regulated in the total sleep deprivation-treated rats as compared with the normal ones (4.03 vs. 1.58 nmol mg–1 for malondialdehyde levels, and 17.1 vs. 6.7 as well as 1.8 vs. 0.7 for heat shock protein 25 immunoblotting and immunoreactivity, respectively). Given that phosphatidylcholine is the most prominent component of all plasma lipoproteins, decreased expression of hepatic phosphatidylcholine following total sleep deprivation may be attributed to the enhanced oxidative stress and the subsequent lipid peroxidation, which would play an important role in the formation

  8. Sleep deprivation alters effort discounting but not delay discounting of monetary rewards.

    PubMed

    Libedinsky, Camilo; Massar, Stijn A A; Ling, Aiqing; Chee, Weiyan; Huettel, Scott A; Chee, Michael W L

    2013-06-01

    To determine whether sleep deprivation would affect the discounting of delayed rewards, of rewards entailing the expense of effort, or both. We measured rates of two types of reward discounting under conditions of rested wakefulness (RW) and sleep deprivation (SD). Delay discounting was defined as the willingness to accept smaller monetary rewards sooner rather than larger monetary rewards later. Effort discounting was defined as the willingness to accept smaller rewards that require less effort to obtain (e.g., typing a small number of letter strings backward) over larger but more effortful rewards (e.g., typing more letter strings to receive the reward). The first two experiments used a crossover design in which one session was conducted after a normal night of sleep (RW), and the other after a night without sleep (SD). The first experiment evaluated only temporal discounting whereas the second evaluated temporal and effort discounting. In the second experiment, the discounting tasks were repeatedly administered prior to the state comparisons to minimize the effects of order and/or repeated testing. In a third experiment, participants were studied only once in a between-subject evaluation of discounting across states. The study took place in a research laboratory. Seventy-seven healthy young adult participants: 20 in Experiment 1, 27 in Experiment 2, and 30 in Experiment 3. N/A. Sleep deprivation elicited increased effort discounting but did not affect delay discounting. The dissociable effects of sleep deprivation on two forms of discounting behavior suggest that they may have differing underlying neural mechanisms.

  9. Effects of stress upon psychophysiological responses and performance following sleep deprivation

    NASA Technical Reports Server (NTRS)

    Roessler, R.; Lester, J. W.

    1972-01-01

    The usefulness of psychological and physiological variables in predicting performance under stress of 48 hours of sleep deprivation was investigated. Performance tests, with subjects of different ego strength personalities, in concept acquisition, reading comprehension, word association, word memory, and anagrams were conducted, and physiological measurements of (1) the phasic and tonic electrodermal, (2) galvanic skin response, (3) thermal skin resistance, (4) heart rate, (5) respiration, and (6) plethysmographic finger pulse volumn were recorded. It was found that the changes in the pattern of performance were the result of testing subjects at times when they would normally be sleeping, and that sleep deprivation longer than 48 hours must be maintained to produce changes in simple or well learned tasks.

  10. Sleep Deprivation During Early-Adult Development Results in Long-Lasting Learning Deficits in Adult Drosophila

    PubMed Central

    Seugnet, Laurent; Suzuki, Yasuko; Donlea, Jeff M.; Gottschalk, Laura; Shaw, Paul J.

    2011-01-01

    Study Objectives: Multiple lines of evidence indicate that sleep is important for the developing brain, although little is known about which cellular and molecular pathways are affected. Thus, the aim of this study was to determine whether the early adult life of Drosophila, which is associated with high amounts of sleep and critical periods of brain plasticity, could be used as a model to identify developmental processes that require sleep. Subjects: Wild type Canton-S Drosophila melanogaster. Design; Intervention: Flies were sleep deprived on their first full day of adult life and allowed to recover undisturbed for at least 3 days. The animals were then tested for short-term memory and response-inhibition using aversive phototaxis suppression (APS). Components of dopamine signaling were further evaluated using mRNA profiling, immunohistochemistry, and pharmacological treatments. Measurements and Results: Flies exposed to acute sleep deprivation on their first day of life showed impairments in short-term memory and response inhibition that persisted for at least 6 days. These impairments in adult performance were reversed by dopamine agonists, suggesting that the deficits were a consequence of reduced dopamine signaling. However, sleep deprivation did not impact dopaminergic neurons as measured by their number or by the levels of dopamine, pale (tyrosine hydroxylase), dopadecarboxylase, and the Dopamine transporter. However, dopamine pathways were impacted as measured by increased transcript levels of the dopamine receptors D2R and dDA1. Importantly, blocking signaling through the dDA1 receptor in animals that were sleep deprived during their critical developmental window prevented subsequent adult learning impairments. Conclusions: These data indicate that sleep plays an important and phylogenetically conserved role in the developing brain. Citation: Seugnet L; Suzuki Y; Donlea JM; Gottschalk L; Shaw PJ. Sleep deprivation during early-adult development results in

  11. The effect of selective REM-sleep deprivation on the consolidation and affective evaluation of emotional memories.

    PubMed

    Wiesner, Christian D; Pulst, Julika; Krause, Fanny; Elsner, Marike; Baving, Lioba; Pedersen, Anya; Prehn-Kristensen, Alexander; Göder, Robert

    2015-07-01

    Emotion boosts the consolidation of events in the declarative memory system. Rapid eye movement (REM) sleep is believed to foster the memory consolidation of emotional events. On the other hand, REM sleep is assumed to reduce the emotional tone of the memory. Here, we investigated the effect of selective REM-sleep deprivation, SWS deprivation, or wake on the affective evaluation and consolidation of emotional and neutral pictures. Prior to an 9-h retention interval, sixty-two healthy participants (23.5 ± 2.5 years, 32 female, 30 male) learned and rated their affect to 80 neutral and 80 emotionally negative pictures. Despite rigorous deprivation of REM sleep or SWS, the residual sleep fostered the consolidation of neutral and negative pictures. Furthermore, emotional arousal helped to memorize the pictures. The better consolidation of negative pictures compared to neutral ones was most pronounced in the SWS-deprived group where a normal amount of REM sleep was present. This emotional memory bias correlated with REM sleep only in the SWS-deprived group. Furthermore, emotional arousal to the pictures decreased over time, but neither sleep nor wake had any differential effect. Neither the comparison of the affective ratings (arousal, valence) during encoding and recognition, nor the affective ratings of the recognized targets and rejected distractors supported the hypothesis that REM sleep dampens the emotional reaction to remembered stimuli. The data suggest that REM sleep fosters the consolidation of emotional memories but has no effect on the affective evaluation of the remembered contents. Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.

  12. The Effects of Sleep Deprivation on Dissociation and Profiles of Mood, and Its Association with Biochemical Changes

    PubMed Central

    SELVİ, Yavuz; KILIÇ, Sultan; AYDIN, Adem; GÜZEL ÖZDEMİR, Pınar

    2015-01-01

    Introduction Sleep deprivation is a method, which has being used in order to comprehend the functions of sleep both in healthy individuals and for the patients of depression with in treatment, for a long time. The objective of our present study is to examine the relation between hormonal values, which are known for being related to the effects of these said changes determined in the mood, dissociation and thought suppression in healthy individuals after one night of sleep deprivation implementation. Methods One night sleep deprivation was performed on a total of thirty-two healthy volunteers (16 males and 16 females) who were included in the study. Blood samples were taken from the individuals before and after sleep deprivation implementation in order to determine cortisol, dehydroepiandrosterone-sulfate (DHEA-S) and Thyroid Functions’ Levels tests. In order to evaluate the effects of the sleep deprivation on moods, “White Bear Suppression Inventory (WBSI)” has been conducted, with an aim of evaluating thought suppression, “Profile of Mood States (POMS)”, “Dissociative Experiences Scale (DES)” with a purpose of realizing any dissociation tendency. Results On the individuals who have been implemented for sleep deprivation, a decrease on depression and vigor-activity sub-scales values was detected, and an increase was determined on fatigue sub-scales values of “POMS”. While the values of DES were found to have been statistically increased after sleep deprivation, also a significant decrease was determined on WBSI values. Even if there hasn’t been any significant statistical change determined on cortisol levels after sleep deprivation, yet there had been some significant changes detected on Thyroid Stimulating Hormone (TSH), fT3, fT4, and DHEA-S levels. Decrease in “POMS” depression sub-scale values and increase on fatigue sub-scale values were determined on the individuals whose sT4 levels were found to be increased significantly in statistic

  13. Interleukin 1 receptor contributes to methamphetamine- and sleep deprivation-induced hypersomnolence

    PubMed Central

    Schmidt, Michelle A.; Wisor, Jonathan P.

    2014-01-01

    Methamphetamine-induced wakefulness is dependent on monoamine transporter blockade. Subsequent to methamphetamine-induced wakefulness, the amount of time spent asleep and the depth of sleep are increased relative to baseline sleep. The mechanisms that drive methamphetamine-induced hypersomnolence are not fully understood. We recently observed that methamphetamine exposure elevates the expression of the sleep-promoting cytokine, interleukin-1 β in CD11b-positive monocytes within the brain. Here, we sought to determine whether activation of the interleukin 1 receptor (IL1R) drives the increase in the depth and amount of sleep that occurs subsequent to methamphetamine-induced wakefulness. IL1R-deficient mice and wild type control mice were subjected to systemic methamphetamine (1 and 2mg/kg) and saline treatments. The wake-promoting effect of methamphetamine was modestly potentiated by IL1R-deficiency. Additionally, the increase in time spent in NREMS subsequent to methamphetamine-induced wakefulness in wild type mice was abolished in IL1R-deficient mice. The increase in time spent asleep after 3 h of behaviorally enforced wakefulness was also abolished in IL1R-deficient mice. Increases in EEG slow wave activity triggered by methamphetamine and sleep deprivation were of equal magnitude in IL1R-deficient and wild type mice. These data demonstrate that IL1R activation contributes to hypersomnolence that occurs after sleep loss, whether that sleep loss is triggered pharmacologically by methamphetamine or through behavioral sleep deprivation. PMID:22387068

  14. Partial sleep deprivation by environmental noise increases food intake and body weight in obesity resistant rats

    PubMed Central

    Mavanji, Vijayakumar; Teske, Jennifer A.; Billington, Charles J.; Kotz, Catherine M.

    2012-01-01

    Objective Sleep-restriction in humans increases risk for obesity, but previous rodent studies show weight loss following sleep deprivation, possibly due to stressful-methods used to prevent sleep. Obesity-resistant (OR) rats exhibit consolidated-sleep and resistance to weight-gain. We hypothesized that sleep disruption by a less-stressful method would increase body weight, and examined effect of partial sleep deprivation (PSD) on body weight in OR and Sprague-Dawley (SD) rats. Design and Methods OR and SD rats (n=12/group) were implanted with transmitters to record sleep/wake. After baseline recording, six SD and six OR rats underwent 8 h PSD during light-phase for 9 d. Sleep was reduced using recordings of random noise. Sleep/wake states were scored as wakefulness (W), slow-wave-sleep (SWS) and rapid-eye-movement-sleep (REMS). Total number of transitions between stages, SWS-delta-power, food intake and body weight were documented. Results Exposure to noise decreased SWS and REMS time, while increasing W time. Sleep-deprivation increased number of transitions between stages and SWS-delta-power. Further, PSD during the rest phase increased recovery-sleep during active phase. The PSD SD and OR rats had greater food intake and body weight compared to controls Conclusions PSD by less-stressful means increases body weight in rats. Also, PSD during rest phase increases active period sleep. PMID:23666828

  15. Partial sleep deprivation by environmental noise increases food intake and body weight in obesity-resistant rats.

    PubMed

    Mavanji, Vijayakumar; Teske, Jennifer A; Billington, Charles J; Kotz, Catherine M

    2013-07-01

    Sleep restriction in humans increases risk for obesity, but previous rodent studies show weight loss following sleep deprivation, possibly due to stressful methods used to prevent sleep. Obesity-resistant (OR) rats exhibit consolidated-sleep and resistance to weight gain. It was hypothesized that sleep disruption by a less-stressful method would increase body weight, and the effect of partial sleep deprivation (PSD) on body weight in OR and Sprague-Dawley (SD) rats was examined. OR and SD rats (n = 12/group) were implanted with transmitters to record sleep/wake. After baseline recording, six SD and six OR rats underwent 8 h PSD during light phase for 9 days. Sleep was reduced using recordings of random noise. Sleep/wake states were scored as wakefulness (W), slow-wave-sleep (SWS), and rapid-eye-movement-sleep (REMS). Total number of transitions between stages, SWS-delta-power, food intake, and body weight were documented. Exposure to noise decreased SWS and REMS time, while increasing W time. Sleep-deprivation increased the number of transitions between stages and SWS-delta-power. Further, PSD during the rest phase increased recovery sleep during the active phase. The PSD SD and OR rats had greater food intake and body weight compared to controls PSD by less-stressful means increases body weight in rats. Also, PSD during the rest phase increases active period sleep. Copyright © 2012 The Obesity Society.

  16. Linalool Ameliorates Memory Loss and Behavioral Impairment Induced by REM-Sleep Deprivation through the Serotonergic Pathway.

    PubMed

    Lee, Bo Kyung; Jung, An Na; Jung, Yi-Sook

    2018-07-01

    Rapid eye movement (REM) sleep has an essential role in the process of learning and memory in the hippocampus. It has been reported that linalool, a major component of Lavandula angustifolia , has antioxidant, anti-inflammatory, and neuroprotective effects, along with other effects. However, the effect of linalool on the cognitive impairment and behavioral alterations that are induced by REM-sleep deprivation has not yet been elucidated. Several studies have reported that REM-sleep deprivation-induced memory deficits provide a well-known model of behavioral alterations. In the present study, we examined whether linalool elicited an anti-stress effect, reversing the behavioral alterations observed following REM-sleep deprivation in mice. Furthermore, we investigated the underlying mechanism of the effect of linalool. Spatial memory and learning memory were assessed through Y maze and passive avoidance tests, respectively, and the forced swimming test was used to evaluate anti-stress activity. The mechanisms through which linalool improves memory loss and behavioral alterations in sleep-deprived mice appeared to be through an increase in the serotonin levels. Linalool significantly ameliorated the spatial and learning memory deficits, and stress activity observed in sleep-deprived animals. Moreover, linalool led to serotonin release, and cortisol level reduction. Our findings suggest that linalool has beneficial effects on the memory loss and behavioral alterations induced by REM-sleep deprivation through the regulation of serotonin levels.

  17. Epigenomics of Total Acute Sleep Deprivation in Relation to Genome-Wide DNA Methylation Profiles and RNA Expression.

    PubMed

    Nilsson, Emil K; Boström, Adrian E; Mwinyi, Jessica; Schiöth, Helgi B

    2016-06-01

    Despite an established link between sleep deprivation and epigenetic processes in humans, it remains unclear to what extent sleep deprivation modulates DNA methylation. We performed a within-subject randomized blinded study with 16 healthy subjects to examine the effect of one night of total sleep deprivation (TSD) on the genome-wide methylation profile in blood compared with that in normal sleep. Genome-wide differences in methylation between both conditions were assessed by applying a paired regression model that corrected for monocyte subpopulations. In addition, the correlations between the methylation of genes detected to be modulated by TSD and gene expression were examined in a separate, publicly available cohort of 10 healthy male donors (E-GEOD-49065). Sleep deprivation significantly affected the DNA methylation profile both independently and in dependency of shifts in monocyte composition. Our study detected differential methylation of 269 probes. Notably, one CpG site was located 69 bp upstream of ING5, which has been shown to be differentially expressed after sleep deprivation. Gene set enrichment analysis detected the Notch and Wnt signaling pathways to be enriched among the differentially methylated genes. These results provide evidence that total acute sleep deprivation alters the methylation profile in healthy human subjects. This is, to our knowledge, the first study that systematically investigated the impact of total acute sleep deprivation on genome-wide DNA methylation profiles in blood and related the epigenomic findings to the expression data.

  18. Changes in Body Water Caused by Sleep Deprivation in Taeeum and Soyang Types in Sasang Medicine: Prospective Intervention Study

    PubMed Central

    2017-01-01

    Background There is a negative relationship between sleep deprivation and health. However, no study has investigated the effect of sleep deprivation on individuals with different body composition. The aim of this study was to determine the differential effect of sleep deprivation in individuals with different body compositions (fluid) according to Soyang type (SY) and Taeeum type (TE). Methods Sixty-two cognitively normal, middle-aged people with normal sleep patterns were recruited from the local population. The duration of participants' sleep was restricted to 4 h/day during the intervention phase. To examine the physiological changes brought on by sleep deprivation and recovery, 10 ml of venous blood was obtained. Results Total Body Water (TBW) and Extracellular Water (ECW) were significantly different between the groups in the intervention phase. Physiological parameters also varied from the beginning of the resting phase to the end of the experiment. Potassium levels changed more in SY than TE individuals. Conclusion Participants responded differently to the same amount of sleep deprivation depending on their Sasang constitution types. This study indicated that SY individuals were more sensitive to sleep deprivation and were slower to recover from the effects of sleep deprivation than TE individuals. PMID:28676829

  19. Effect of sleep-wake reversal and sleep deprivation on the circadian rhythm of oxygen toxicity seizure susceptibility.

    NASA Technical Reports Server (NTRS)

    Dexter, J. D.; Hof, D. G.; Mengel, C. E.

    1972-01-01

    Albino Sprague-Dawley rats were exposed in a previously O2 flushed, CO2 free chamber. The exposure began with attainment of 60 psi (gauge) and the end point was the first generalized oxygen toxicity seizure. Animals were exposed to reversal diurnal conditions since weanlings until their sleep-wake cycles had completely reversed, and then divided into four groups of 20 based on the time of day exposed. The time of exposure to oxygen at high pressure prior to seizure was now significantly longer in the group exposed from 1900 to 2000 hr and a reversal of the circadian rhythm of oxygen toxicity seizure susceptibility was noted. Animals maintained on normal diurnal conditions were deprived of sleep on the day of exposure for the 12 hours prior to exposure at 1900 hr, while controls were allowed to sleep. There was no significant differences in the time prior to seizure between the deprived animals and the controls with an n = 40. Thus the inherent threshold in susceptibility to high-pressure oxygen seizures seems not to be a function of sleep itself, but of some biochemical/physiologic event which manifests a circadian rhythm.

  20. Sustained Attention Performance during Sleep Deprivation Associates with Instability in Behavior and Physiologic Measures at Baseline

    PubMed Central

    Chua, Eric Chern-Pin; Yeo, Sing-Chen; Lee, Ivan Tian-Guang; Tan, Luuan-Chin; Lau, Pauline; Cai, Shiwei; Zhang, Xiaodong; Puvanendran, Kathiravelu; Gooley, Joshua J.

    2014-01-01

    Study Objectives: To identify baseline behavioral and physiologic markers that associate with individual differences in sustained attention during sleep deprivation. Design: In a retrospective study, ocular, electrocardiogram, and electroencephalogram (EEG) measures were compared in subjects who were characterized as resilient (n = 15) or vulnerable (n = 15) to the effects of total sleep deprivation on sustained attention. Setting: Chronobiology and Sleep Laboratory, Duke-NUS Graduate Medical School Singapore. Participants: Healthy volunteers aged 22-32 years from the general population. Interventions: Subjects were kept awake for at least 26 hours under constant environmental conditions. Every 2 hours, sustained attention was assessed using a 10-minute psychomotor vigilance task (PVT). Measurements and Results: During baseline sleep and recovery sleep, EEG slow wave activity was similar in resilient versus vulnerable subjects, suggesting that individual differences in vulnerability to sleep loss were not related to differences in homeostatic sleep regulation. Rather, irrespective of time elapsed since wake, subjects who were vulnerable to sleep deprivation exhibited slower and more variable PVT response times, lower and more variable heart rate, and higher and more variable EEG spectral power in the theta frequency band (6.0-7.5 Hz). Conclusions: Performance decrements in sustained attention during sleep deprivation associate with instability in behavioral and physiologic measures at baseline. Small individual differences in sustained attention that are present at baseline are amplified during prolonged wakefulness, thus contributing to large between-subjects differences in performance and sleepiness. Citation: Chua EC; Yeo SC; Lee IT; Tan LC; Lau P; Cai S; Zhang X; Puvanendran K; Gooley JJ. Sustained attention performance during sleep deprivation associates with instability in behavior and physiologic measures at baseline. SLEEP 2014;37(1):27-39. PMID:24470693

  1. Behavioral and genetic effects promoted by sleep deprivation in rats submitted to pilocarpine-induced status epilepticus.

    PubMed

    Matos, Gabriela; Ribeiro, Daniel A; Alvarenga, Tathiana A; Hirotsu, Camila; Scorza, Fulvio A; Le Sueur-Maluf, Luciana; Noguti, Juliana; Cavalheiro, Esper A; Tufik, Sergio; Andersen, Monica L

    2012-05-02

    The interaction between sleep deprivation and epilepsy has been well described in electrophysiological studies, but the mechanisms underlying this association remain unclear. The present study evaluated the effects of sleep deprivation on locomotor activity and genetic damage in the brains of rats treated with saline or pilocarpine-induced status epilepticus (SE). After 50 days of pilocarpine or saline treatment, both groups were assigned randomly to total sleep deprivation (TSD) for 6 h, paradoxical sleep deprivation (PSD) for 24 h, or be kept in their home cages. Locomotor activity was assessed with the open field test followed by resection of brain for quantification of genetic damage by the single cell gel electrophoresis (comet) assay. Status epilepticus induced significant hyperactivity in the open field test and caused genetic damage in the brain. Sleep deprivation procedures (TSD and PSD) did not affect locomotor activity in epileptic or healthy rats, but resulted in significant DNA damage in brain cells. Although PSD had this effect in both vehicle and epileptic groups, TSD caused DNA damage only in epileptic rats. In conclusion, our results revealed that, despite a lack of behavioral effects of sleep deprivation, TSD and PSD induced genetic damage in rats submitted to pilocarpine-induced SE. Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.

  2. Sustained attention performance during sleep deprivation associates with instability in behavior and physiologic measures at baseline.

    PubMed

    Chua, Eric Chern-Pin; Yeo, Sing-Chen; Lee, Ivan Tian-Guang; Tan, Luuan-Chin; Lau, Pauline; Cai, Shiwei; Zhang, Xiaodong; Puvanendran, Kathiravelu; Gooley, Joshua J

    2014-01-01

    To identify baseline behavioral and physiologic markers that associate with individual differences in sustained attention during sleep deprivation. In a retrospective study, ocular, electrocardiogram, and electroencephalogram (EEG) measures were compared in subjects who were characterized as resilient (n = 15) or vulnerable (n = 15) to the effects of total sleep deprivation on sustained attention. Chronobiology and Sleep Laboratory, Duke-NUS Graduate Medical School Singapore. Healthy volunteers aged 22-32 years from the general population. Subjects were kept awake for at least 26 hours under constant environmental conditions. Every 2 hours, sustained attention was assessed using a 10-minute psychomotor vigilance task (PVT). During baseline sleep and recovery sleep, EEG slow wave activity was similar in resilient versus vulnerable subjects, suggesting that individual differences in vulnerability to sleep loss were not related to differences in homeostatic sleep regulation. Rather, irrespective of time elapsed since wake, subjects who were vulnerable to sleep deprivation exhibited slower and more variable PVT response times, lower and more variable heart rate, and higher and more variable EEG spectral power in the theta frequency band (6.0-7.5 Hz). Performance decrements in sustained attention during sleep deprivation associate with instability in behavioral and physiologic measures at baseline. Small individual differences in sustained attention that are present at baseline are amplified during prolonged wakefulness, thus contributing to large between-subjects differences in performance and sleepiness.

  3. Sleep Deprivation Impairs the Human Central and Peripheral Nervous System Discrimination of Social Threat

    PubMed Central

    Goldstein-Piekarski, Andrea N.; Greer, Stephanie M.; Saletin, Jared M.

    2015-01-01

    Facial expressions represent one of the most salient cues in our environment. They communicate the affective state and intent of an individual and, if interpreted correctly, adaptively influence the behavior of others in return. Processing of such affective stimuli is known to require reciprocal signaling between central viscerosensory brain regions and peripheral-autonomic body systems, culminating in accurate emotion discrimination. Despite emerging links between sleep and affective regulation, the impact of sleep loss on the discrimination of complex social emotions within and between the CNS and PNS remains unknown. Here, we demonstrate in humans that sleep deprivation impairs both viscerosensory brain (anterior insula, anterior cingulate cortex, amygdala) and autonomic-cardiac discrimination of threatening from affiliative facial cues. Moreover, sleep deprivation significantly degrades the normally reciprocal associations between these central and peripheral emotion-signaling systems, most prominent at the level of cardiac-amygdala coupling. In addition, REM sleep physiology across the sleep-rested night significantly predicts the next-day success of emotional discrimination within this viscerosensory network across individuals, suggesting a role for REM sleep in affective brain recalibration. Together, these findings establish that sleep deprivation compromises the faithful signaling of, and the “embodied” reciprocity between, viscerosensory brain and peripheral autonomic body processing of complex social signals. Such impairments hold ecological relevance in professional contexts in which the need for accurate interpretation of social cues is paramount yet insufficient sleep is pervasive. PMID:26180190

  4. Sleep Deprivation Impairs the Human Central and Peripheral Nervous System Discrimination of Social Threat.

    PubMed

    Goldstein-Piekarski, Andrea N; Greer, Stephanie M; Saletin, Jared M; Walker, Matthew P

    2015-07-15

    Facial expressions represent one of the most salient cues in our environment. They communicate the affective state and intent of an individual and, if interpreted correctly, adaptively influence the behavior of others in return. Processing of such affective stimuli is known to require reciprocal signaling between central viscerosensory brain regions and peripheral-autonomic body systems, culminating in accurate emotion discrimination. Despite emerging links between sleep and affective regulation, the impact of sleep loss on the discrimination of complex social emotions within and between the CNS and PNS remains unknown. Here, we demonstrate in humans that sleep deprivation impairs both viscerosensory brain (anterior insula, anterior cingulate cortex, amygdala) and autonomic-cardiac discrimination of threatening from affiliative facial cues. Moreover, sleep deprivation significantly degrades the normally reciprocal associations between these central and peripheral emotion-signaling systems, most prominent at the level of cardiac-amygdala coupling. In addition, REM sleep physiology across the sleep-rested night significantly predicts the next-day success of emotional discrimination within this viscerosensory network across individuals, suggesting a role for REM sleep in affective brain recalibration. Together, these findings establish that sleep deprivation compromises the faithful signaling of, and the "embodied" reciprocity between, viscerosensory brain and peripheral autonomic body processing of complex social signals. Such impairments hold ecological relevance in professional contexts in which the need for accurate interpretation of social cues is paramount yet insufficient sleep is pervasive. Copyright © 2015 the authors 0270-6474/15/3510135-11$15.00/0.

  5. Effects of 72hours total sleep deprivation on male astronauts' executive functions and emotion.

    PubMed

    Liu, Qing; Zhou, Renlai; Liu, Lei; Zhao, Xin

    2015-08-01

    To provide evidence for better understanding stressful situations, the present study was designed to investigate the specific physiological and psychological responses under stressful situations like social isolation and sleep deprivation. Twelve healthy male adults (age: 18-30years old) who participated in our study were randomized to the 72hours of social isolation and 72hours of sleep deprivation experimental conditions. Performances (event-related potentials and physiological activities) on the Go/Nogo task which reflected the executive functions were accessed at baseline (pretest) and after 72-hour of the experiment (posttest). The results showed that compared to the social isolation, the participants got strengthened heart rate (HR), weakened HR variability and smaller amplitude of the P300 under the sleep deprivation condition; moreover, they had lower positive emotion and higher negative mood in the posttest. The present study indicated that sleep deprivation specifically influenced the intensity of task-relevant information processing, mood and vagal tone. Copyright © 2015. Published by Elsevier Inc.

  6. Sleep deprivation decreases phase-shift responses of circadian rhythms to light in the mouse: role of serotonergic and metabolic signals.

    PubMed

    Challet, E; Turek, F W; Laute, M; Van Reeth, O

    2001-08-03

    The circadian pacemaker in the suprachiasmatic nuclei is primarily synchronized to the daily light-dark cycle. The phase-shifting and synchronizing effects of light can be modulated by non-photic factors, such as behavioral, metabolic or serotonergic cues. The present experiments examine the effects of sleep deprivation on the response of the circadian pacemaker to light and test the possible involvement of serotonergic and/or metabolic cues in mediating the effects of sleep deprivation. Photic phase-shifting of the locomotor activity rhythm was analyzed in mice transferred from a light-dark cycle to constant darkness, and sleep-deprived for 8 h from Zeitgeber Time 6 to Zeitgeber Time 14. Phase-delays in response to a 10-min light pulse at Zeitgeber Time 14 were reduced by 30% in sleep-deprived mice compared to control mice, while sleep deprivation without light exposure induced no significant phase-shifts. Stimulation of serotonin neurotransmission by fluoxetine (10 mg/kg), a serotonin reuptake inhibitor that decreases light-induced phase-delays in non-deprived mice, did not further reduce light-induced phase-delays in sleep-deprived mice. Impairment of serotonin neurotransmission with p-chloroamphetamine (three injections of 10 mg/kg), which did not increase light-induced phase-delays in non-deprived mice significantly, partially normalized light-induced phase-delays in sleep-deprived mice. Injections of glucose increased light-induced phase-delays in control and sleep-deprived mice. Chemical damage of the ventromedial hypothalamus by gold-thioglucose (600 mg/kg) prevented the reduction of light-induced phase-delays in sleep-deprived mice, without altering phase-delays in control mice. Taken together, the present results indicate that sleep deprivation can reduce the light-induced phase-shifts of the mouse suprachiasmatic pacemaker, due to serotonergic and metabolic changes associated with the loss of sleep.

  7. Procedural performance following sleep deprivation remains impaired despite extended practice and an afternoon nap

    PubMed Central

    Kurniawan, Irma Triasih; Cousins, James Nicholas; Chong, Pearlynne L. H.; Chee, Michael W. L.

    2016-01-01

    The negative impact of sleep loss on procedural memory is well established, yet it remains unclear how extended practice opportunities or daytime naps can modulate the effect of a night of sleep deprivation. Here, participants underwent three training and test conditions on a sequential finger tapping task (SFTT) separated by at least one week. In the first condition they were trained in the evening followed by a night of sleep. Two further conditions took place where evening training was followed by a night of total sleep deprivation (TSD). One of the TSD conditions included a one-hour nap opportunity (15:00). Compared to the condition in which sleep was permitted, a night of TSD resulted in poorer performance across 4 practices the following day (10:00–19:00). The deleterious effect of a single night of TSD on procedural performance, was neither clearly alleviated by an afternoon nap nor by multiple practice opportunities. Interestingly, significant gains in performance were observed in all conditions after a one-week delay. Recovery sleep on subsequent nights thus appeared to nullify the effect of a single night of sleep deprivation, underscoring the importance of offline consolidation on the acquisition of procedural skill. PMID:27782172

  8. The experience of sleep deprivation in intensive care patients: findings from a larger hermeneutic phenomenological study.

    PubMed

    Tembo, Agness C; Parker, Vicki; Higgins, Isabel

    2013-12-01

    Sleep deprivation in critically ill patients has been well documented for more than 30 years. Despite the large body of literature, sleep deprivation remains a significant concern in critically ill patients in intensive care unit (ICU). This paper discusses sleep deprivation in critically ill patients as one of the main findings from a study that explored the lived experiences of critically ill patients in ICU with daily sedation interruption (DSI). Twelve participants aged between 20 and 76 years with an ICU stay ranging from three to 36 days were recruited from a 16 bed ICU in a large regional referral hospital in New South Wales (NSW), Australia. Participants were intubated, mechanically ventilated and subjected to daily sedation interruption during their critical illness in ICU. In-depth face to face interviews with the participants were conducted at two weeks after discharge from ICU. A second interview was conducted with eight participants six to eleven months later. Interviews were audio taped and transcribed. Data were analysed thematically. "Longing for sleep" and "being tormented by nightmares" capture the experiences and concerns of some of the participants. The findings suggest a need for models of care that seek to support restful sleep and prevent or alleviate sleep deprivation and nightmares. These models of care need to promote both quality and quantity of sleep in and beyond ICU and identify patients suffering from sleep deprivation to make appropriate referrals for treatment and support. Copyright © 2013 Elsevier Ltd. All rights reserved.

  9. Distinct unfolded protein responses mitigate or mediate effects of nonlethal deprivation of C. elegans sleep in different tissues.

    PubMed

    Sanders, Jarred; Scholz, Monika; Merutka, Ilaria; Biron, David

    2017-08-28

    Disrupting sleep during development leads to lasting deficits in chordates and arthropods. To address lasting impacts of sleep deprivation in Caenorhabditis elegans, we established a nonlethal deprivation protocol. Deprivation triggered protective insulin-like signaling and two unfolded protein responses (UPRs): the mitochondrial (UPR mt ) and the endoplasmic reticulum (UPR ER ) responses. While the latter is known to be triggered by sleep deprivation in rodent and insect brains, the former was not strongly associated with sleep deprivation previously. We show that deprivation results in a feeding defect when the UPR mt is deficient and in UPR ER -dependent germ cell apoptosis. In addition, when the UPR ER is deficient, deprivation causes excess twitching in vulval muscles, mirroring a trend caused by loss of egg-laying command neurons. These data show that nonlethal deprivation of C. elegans sleep causes proteotoxic stress. Unless mitigated, distinct types of deprivation-induced proteotoxicity can lead to anatomically and genetically separable lasting defects. The relative importance of different UPRs post-deprivation likely reflects functional, developmental, and genetic differences between the respective tissues and circuits.

  10. Low levels of alcohol impair driving simulator performance and reduce perception of crash risk in partially sleep deprived subjects.

    PubMed

    Banks, Siobhan; Catcheside, Peter; Lack, Leon; Grunstein, Ron R; McEvoy, R Doug

    2004-09-15

    Partial sleep deprivation and alcohol consumption are a common combination, particularly among young drivers. We hypothesized that while low blood alcohol concentration (<0.05 g/dL) may not significantly increase crash risk, the combination of partial sleep deprivation and low blood alcohol concentration would cause significant performance impairment. Experimental Sleep Disorders Unit Laboratory 20 healthy volunteers (mean age 22.8 years; 9 men). Subjects underwent driving simulator testing at 1 am on 2 nights a week apart. On the night preceding simulator testing, subjects were partially sleep deprived (5 hours in bed). Alcohol consumption (2-3 standard alcohol drinks over 2 hours) was randomized to 1 of the 2 test nights, and blood alcohol concentrations were estimated using a calibrated Breathalyzer. During the driving task subjects were monitored continuously with electroencephalography for sleep episodes and were prompted every 4.5 minutes for answers to 2 perception scales-performance and crash risk. Mean blood alcohol concentration on the alcohol night was 0.035 +/- 0.015 g/dL. Compared with conditions during partial sleep deprivation alone, subjects had more microsleeps, impaired driving simulator performance, and poorer ability to predict crash risk in the combined partial sleep deprivation and alcohol condition. Women predicted crash risk more accurately than did men in the partial sleep deprivation condition, but neither men nor women predicted the risk accurately in the sleep deprivation plus alcohol condition. Alcohol at legal blood alcohol concentrations appears to increase sleepiness and impair performance and the detection of crash risk following partial sleep deprivation. When partially sleep deprived, women appear to be either more perceptive of increased crash risk or more willing to admit to their driving limitations than are men. Alcohol eliminated this behavioral difference.

  11. Failure to Find Executive Function Deficits Following One Night’s Total Sleep-Deprivation in University Students under Naturalistic Conditions

    PubMed Central

    Pace-Schott, Edward F.; Hutcherson, Cendri A.; Bemporad, Brenda; Morgan, Alexandra; Kumar, Arjun; Hobson, J. Allan; Stickgold, Robert

    2018-01-01

    Young adult male students participated in a naturalistic, group-design experiment to ascertain the effects of one night’s total sleep deprivation (TSD) on performance of diverse executive function tasks presented as an extended, multi-task battery. On the majority of component tasks in this battery, performance has been reported to be impaired following one night’s TSD when tasks are administered in isolation. However, subjects sleep deprived 35–39 hours showed few performance deficits among tests in this battery when compared with non sleep-deprived controls. Sleep-deprived subjects showed only poorer recognition memory and overconfidence in incorrect temporal judgments. Behavioral and physiological adaptation to chronically sleep-restricting lifestyles may confer resistance to the cognitive effects of sleep deprivation in high-functioning young adults. PMID:19568965

  12. Cognitive Performance, Sleepiness, and Mood in Partially Sleep Deprived Adolescents: The Need for Sleep Study.

    PubMed

    Lo, June C; Ong, Ju Lynn; Leong, Ruth L F; Gooley, Joshua J; Chee, Michael W L

    2016-03-01

    To investigate the effects of sleep restriction (7 nights of 5 h time in bed [TIB]) on cognitive performance, subjective sleepiness, and mood in adolescents. A parallel-group design was adopted in the Need for Sleep Study. Fifty-six healthy adolescents (25 males, age = 15-19 y) who studied in top high schools and were not habitual short sleepers were randomly assigned to Sleep Restriction (SR) or Control groups. Participants underwent a 2-w protocol consisting of 3 baseline nights (TIB = 9 h), 7 nights of sleep opportunity manipulation (TIB = 5 h for the SR and 9 h for the control groups), and 3 nights of recovery sleep (TIB = 9 h) at a boarding school. A cognitive test battery was administered three times each day. During the manipulation period, the SR group demonstrated incremental deterioration in sustained attention, working memory and executive function, increase in subjective sleepiness, and decrease in positive mood. Subjective sleepiness and sustained attention did not return to baseline levels even after 2 recovery nights. In contrast, the control group maintained baseline levels of cognitive performance, subjective sleepiness, and mood throughout the study. Incremental improvement in speed of processing, as a result of repeated testing and learning, was observed in the control group but was attenuated in the sleep-restricted participants, who, despite two recovery sleep episodes, continued to perform worse than the control participants. A week of partial sleep deprivation impairs a wide range of cognitive functions, subjective alertness, and mood even in high-performing high school adolescents. Some measures do not recover fully even after 2 nights of recovery sleep. A commentary on this article appears in this issue on page 497. © 2016 Associated Professional Sleep Societies, LLC.

  13. Replication and Pedagogy in the History of Psychology IV: Patrick and Gilbert (1896) on Sleep Deprivation

    ERIC Educational Resources Information Center

    Fuchs, Thomas; Burgdorf, Jeffrey

    2008-01-01

    We report an attempted replication of G. T. W. Patrick and J. A. Gilbert's pioneering sleep deprivation experiment "Studies from the psychological laboratory of the University of Iowa. On the effects of loss of sleep", conducted in 1895/96. Patrick and Gilbert's study was the first sleep deprivation experiment of its kind, performed by some of the…

  14. Combining two model systems of psychosis: The effects of schizotypy and sleep deprivation on oculomotor control and psychotomimetic states.

    PubMed

    Meyhöfer, Inga; Steffens, Maria; Faiola, Eliana; Kasparbauer, Anna-Maria; Kumari, Veena; Ettinger, Ulrich

    2017-11-01

    Model systems of psychosis, such as schizotypy or sleep deprivation, are valuable in informing our understanding of the etiology of the disorder and aiding the development of new treatments. Schizophrenia patients, high schizotypes, and sleep-deprived subjects are known to share deficits in oculomotor biomarkers. Here, we aimed to further validate the schizotypy and sleep deprivation models and investigated, for the first time, their interactive effects on smooth pursuit eye movements (SPEM), prosaccades, antisaccades, predictive saccades, and measures of psychotomimetic states, anxiety, depression, and stress. To do so, n = 19 controls and n = 17 high positive schizotypes were examined after both a normal sleep night and 24 h of sleep deprivation. Schizotypes displayed higher SPEM global position error, catch-up saccade amplitude, and increased psychotomimetic states. Sleep deprivation impaired SPEM, prosaccade, antisaccade, and predictive saccade performance and increased levels of psychotomimetic experiences. Additionally, sleep deprivation reduced SPEM gain in schizotypes but not controls. We conclude that oculomotor impairments are observed in relation to schizotypy and following sleep deprivation, supporting their utility as biomarkers in model systems of psychosis. The combination of these models with oculomotor biomarkers may be particularly fruitful in assisting the development of new antipsychotic or pro-cognitive drugs. © 2017 Society for Psychophysiological Research.

  15. Sleep Deprivation and Oxidative Stress in Animal Models: A Systematic Review

    PubMed Central

    Villafuerte, Gabriel; Miguel-Puga, Adán; Murillo Rodríguez, Eric; Machado, Sergio; Manjarrez, Elias; Arias-Carrión, Oscar

    2015-01-01

    Because the function and mechanisms of sleep are partially clear, here we applied a meta-analysis to address the issue whether sleep function includes antioxidative properties in mice and rats. Given the expansion of the knowledge in the sleep field, it is indeed ambitious to describe all mammals, or other animals, in which sleep shows an antioxidant function. However, in this paper we reviewed the current understanding from basic studies in two species to drive the hypothesis that sleep is a dynamic-resting state with antioxidative properties. We performed a systematic review of articles cited in Medline, Scopus, and Web of Science until March 2015 using the following search terms: Sleep or sleep deprivation and oxidative stress, lipid peroxidation, glutathione, nitric oxide, catalase or superoxide dismutase. We found a total of 266 studies. After inclusion and exclusion criteria, 44 articles were included, which are presented and discussed in this study. The complex relationship between sleep duration and oxidative stress is discussed. Further studies should consider molecular and genetic approaches to determine whether disrupted sleep promotes oxidative stress. PMID:25945148

  16. Differential effects of total and partial sleep deprivation on salivary factors in Wistar rats.

    PubMed

    Lasisi, Dr T J; Shittu, S T; Meludu, C C; Salami, A A

    2017-01-01

    Aim of this study was to investigate the effects of sleep deprivation on salivary factors in rats. Animals were randomly assigned into three groups of 6 animals each as control, total sleep deprivation (TSD) and partial sleep deprivation (PSD) groups. The multiple platform method was used to induce partial and total sleep deprivation for 7days. On the 8th day, stimulated saliva samples were collected for the analysis of salivary lag time, flow rate, salivary amylase activity, immunoglobulin A secretion rate and corticosterone levels using ELISA and standard kinetic enzyme assay. Data were analyzed using ANOVA with Dunnett T3 post hoc tests. Salivary flow rate reduced significantly in the TSD group compared with the PSD group as well as the control group (p=0.01). The secretion rate of salivary IgA was significantly reduced in the TSD group compared with the control group (p=0.04). Salivary amylase activity was significantly elevated in the TSD group compared with the PSD group as well as control group (p<0.001). However, there were no significant changes in the salivary lag time and levels of corticosterone among the groups. These findings suggest that total sleep deprivation is associated with reduced salivary flow rate and secretion rate of IgA as well as elevated levels of salivary amylase activity in rats. However, sleep recovery of four hours in the PSD group produced ameliorative effects on the impaired functions of salivary glands. Copyright © 2016 Elsevier Ltd. All rights reserved.

  17. Diurnal Rhythms in Blood Cell Populations and the Effect of Acute Sleep Deprivation in Healthy Young Men

    PubMed Central

    Ackermann, Katrin; Revell, Victoria L.; Lao, Oscar; Rombouts, Elwin J.; Skene, Debra J.; Kayser, Manfred

    2012-01-01

    Study Objectives: The sleep/wake cycle is accompanied by changes in circulating numbers of immune cells. The goal of this study was to provide an in-depth characterization of diurnal rhythms in different blood cell populations and to investigate the effect of acute sleep deprivation on the immune system, as an indicator of the body's acute stress response. Design: Observational within-subject design. Setting: Home environment and Clinical Research Centre. Participants: 15 healthy male participants aged 23.7 ± 5.4 (standard deviation) yr. Interventions: Total sleep deprivation. Measurements and Results: Diurnal rhythms of several blood cell populations were assessed under a normal sleep/wake cycle followed by 29 hr of extended wakefulness. The effect of condition (sleep versus sleep deprivation) on peak time and amplitude was investigated. Interindividual variation of, and the level of correlation between, the different cell populations was assessed. Comprehensive nonlinear curve fitting showed significant diurnal rhythms for all blood cell types investigated, with CD4 (naïve) cells exhibiting the most robust rhythms independent of condition. For those participants exhibiting significant diurnal rhythms in blood cell populations, only the amplitude of the granulocyte rhythm was significantly reduced by sleep deprivation. Granulocytes were the most diverse population, being most strongly affected by condition, and showed the lowest correlations with any other given cell type while exhibiting the largest interindividual variation in abundance. Conclusions: Granulocyte levels and diurnal rhythmicity are directly affected by acute sleep deprivation; these changes mirror the body's immediate immune response upon exposure to stress. Citation: Ackermann K; Revell VL; Lao O; Rombouts EJ; Skene DJ; Kayser M. Diurnal rhythms in blood cell populations and the effect of acute sleep deprivation in healthy young men. SLEEP 2012;35(7):933-940. PMID:22754039

  18. Paradoxical Sleep Deprivation Causes Cardiac Dysfunction and the Impairment Is Attenuated by Resistance Training.

    PubMed

    Giampá, Sara Quaglia de Campos; Mônico-Neto, Marcos; de Mello, Marco Tulio; Souza, Helton de Sá; Tufik, Sergio; Lee, Kil Sun; Koike, Marcia Kiyomi; Dos Santos, Alexandra Alberta; Antonio, Ednei Luiz; Serra, Andrey Jorge; Tucci, Paulo José Ferreira; Antunes, Hanna Karen Moreira

    2016-01-01

    Paradoxical sleep deprivation activates the sympathetic nervous system and the hypothalamus-pituitary-adrenal axis, subsequently interfering with the cardiovascular system. The beneficial effects of resistance training are related to hemodynamic, metabolic and hormonal homeostasis. We hypothesized that resistance training can prevent the cardiac remodeling and dysfunction caused by paradoxical sleep deprivation. Male Wistar rats were distributed into four groups: control (C), resistance training (RT), paradoxical sleep deprivation for 96 hours (PSD96) and both resistance training and sleep deprivation (RT/PSD96). Doppler echocardiograms, hemodynamics measurements, cardiac histomorphometry, hormonal profile and molecular analysis were evaluated. Compared to the C group, PSD96 group had a higher left ventricular systolic pressure, heart rate and left atrium index. In contrast, the left ventricle systolic area and the left ventricle cavity diameter were reduced in the PSD96 group. Hypertrophy and fibrosis were also observed. Along with these alterations, reduced levels of serum testosterone and insulin-like growth factor-1 (IGF-1), as well as increased corticosterone and angiotensin II, were observed in the PSD96 group. Prophylactic resistance training attenuated most of these changes, except angiotensin II, fibrosis, heart rate and concentric remodeling of left ventricle, confirmed by the increased of NFATc3 and GATA-4, proteins involved in the pathologic cardiac hypertrophy pathway. Resistance training effectively attenuates cardiac dysfunction and hormonal imbalance induced by paradoxical sleep deprivation.

  19. Metabolic Response of the Cerebral Cortex Following Gentle Sleep Deprivation and Modafinil Administration

    PubMed Central

    Petit, Jean-Marie; Tobler, Irene; Kopp, Caroline; Morgenthaler, Florence; Borbély, Alexander A.; Magistretti, Pierre J.

    2010-01-01

    Study Objectives: The main energy reserve of the brain is glycogen, which is almost exclusively localized in astrocytes. We previously reported that cerebral expression of certain genes related to glycogen metabolism changed following instrumental sleep deprivation in mice. Here, we extended our investigations to another set of genes related to glycogen and glucose metabolism. We also compared the effect of instrumentally and pharmacologically induced prolonged wakefulness, followed (or not) by 3 hours of sleep recovery, on the expression of genes related to brain energy metabolism. Design: Sleep deprivation for 6–7 hours. Setting: Animal sleep research laboratory. Participants: Adults OF1 mice. Interventions: Wakefulness was maintained by “gentle sleep deprivation” method (GSD) or by administration of the wakefulness-promoting drug modafinil (MOD) (200 mg/kg i.p.). Measurements and Results: Levels of mRNAs encoding proteins related to energy metabolism were measured by quantitative real-time PCR in the cerebral cortex. The mRNAs encoding protein targeting to glycogen (PTG) and the glial glucose transporter were significantly increased following both procedures used to prolong wakefulness. Glycogenin mRNA levels were increased only after GSD, while neuronal glucose transporter mRNA only after MOD. These effects were reversed after sleep recovery. A significant enhancement of glycogen synthase activity without any changes in glycogen levels was observed in both conditions. Conclusions: These results indicate the existence of a metabolic adaptation of astrocytes aimed at maintaining brain energy homeostasis during the sleep-wake cycle. Citation: Petit, JM; Tobler I; Kopp C; Morgenthaler F; Borbély AA; Magistretti PJ. Metabolic response of the cerebral cortex following gentle sleep deprivation and modafinil administration. SLEEP 2010;33(7):901–908. PMID:20614850

  20. Changes in Cardiac Variability after REM Sleep Deprivation in Recurrent Nightmares

    PubMed Central

    Nielsen, Tore; Paquette, Tyna; Solomonova, Elizaveta; Lara-Carrasco, Jessica; Colombo, Roberto; Lanfranchi, Paola

    2010-01-01

    Study Objectives: To assess whether dysfunctional autonomic regulation during REM sleep as indexed by heart rate variability (HRV) is a pathophysiological factor in frequent nightmares (NMs). Design: Monitoring with polysomnography (PSG) and electrocardiography (ECG) for 3 consecutive nights: Night 1 (N1), adaptation night; N2, administration of partial REM sleep deprivation; N3, recovery night. Differences between NM and control (CTL) groups assessed for ECG measures drawn from wakefulness, REM sleep, and Stage 2 sleep on both N1 and N3. Setting: Hospital-based sleep laboratory Participants: Sixteen subjects with frequent NMs ( ≥ 1 NM/week; mean age = 26.1 ± 8.7 years) but no other medical or psychiatric disorders and 11 healthy comparison subjects ( < 1 NM/month; mean age = 27.1±5.6 years). Results: NM and CTL groups differed on 2 REM sleep measures only on N1; the NM group had longer REM latencies and REM/NREM cycle durations than did the CTL group. No differences were found on time domain and absolute frequency domain ECG measures for either N1 or N3. However, altered HRV for the NM group was suggested by significantly higher LFnu, lower HFnu, and higher LF/HF ratio than for the CTL group. Conclusions: Results are consistent with a higher than normal sympathetic drive among NM subjects which is unmasked by high REM sleep propensity. Results also support a growing literature linking anxiety disorders of several types (panic disorder, posttraumatic stress disorder (PTSD), generalized anxiety disorder) to altered HR variability. Citation: Nielsen T; Paquette T; Solomonova E; Lara-Carrasco J; Colombo R; Lanfranchi P. Changes in cardiac variability after rem sleep deprivation in recurrent nightmares. SLEEP 2010;33(1):113-122. PMID:20120628

  1. Sleep Deprivation Decreases [11C]Raclopride’s Binding to Dopamine D2/D3 Receptors in the Human Brain

    PubMed Central

    Volkow, Nora D.; Wang, Gene-Jack; Telang, Frank; Fowler, Joanna S.; Logan, Jean; Wong, Christopher; Ma, Jim; Pradhan, Kith; Tomasi, Dardo; Thanos, Peter K.; Ferré, Sergi; Jayne, Millard

    2009-01-01

    Sleep deprivation can markedly impair human performance contributing to accidents and poor productivity. The mechanisms underlying this impairment are not well understood but brain dopamine systems have been implicated. Here we test whether one night of sleep deprivation changes dopamine brain activity. We studied fifteen healthy subjects using positron emission tomography and [11C]raclopride (dopamine D2/3 receptor radioligand) and [11C]cocaine (dopamine transporter radioligand). Subjects were tested twice; after one night of rested sleep and after on night of sleep deprivation. [11C]Raclopride’s specific binding in striatum and thalamus were significantly reduced after sleep deprivation and the magnitude of this reduction correlated with increases in fatigue (tiredness and sleepiness) and with deterioration in cognitive performance (visual attention and working memory). In contrast sleep deprivation did not affect the specific binding of [11C]cocaine in striatum. Since [11C]raclopride competes with endogenous dopamine for binding to D2/D3 receptors, we interpret the decreases in binding to reflect dopamine increases with sleep deprivation. However, we can not rule out the possibility that decreased [11C]raclopride binding reflects decreases in receptor levels or affinity. Sleep deprivation did not affect dopamine transporters (target for most wake-promoting medications) and thus dopamine increases are likely to reflect increases in dopamine cell firing and/or release rather than decreases in dopamine reuptake. Inasmuch as dopamine-enhancing drugs increase wakefulness we postulate that dopamine increases after sleep deprivation is a mechanism by which the brain maintains arousal as the drive to sleep increases but one that is insufficient to counteract behavioral and cognitive impairment. PMID:18716203

  2. Investigating systematic individual differences in sleep-deprived performance on a high-fidelity flight simulator.

    PubMed

    Van Dongen, Hans P A; Caldwell, John A; Caldwell, J Lynn

    2006-05-01

    Laboratory research has revealed considerable systematic variability in the degree to which individuals' alertness and performance are affected by sleep deprivation. However, little is known about whether or not different populations exhibit similar levels of individual variability. In the present study, we examined individual variability in performance impairment due to sleep loss in a highly select population of militaryjet pilots. Ten active-duty F-117 pilots were deprived of sleep for 38 h and studied repeatedly in a high-fidelity flight simulator. Data were analyzed with a mixed-model ANOVA to quantify individual variability. Statistically significant, systematic individual differences in the effects of sleep deprivation were observed, even when baseline differences were accounted for. The findings suggest that highly select populations may exhibit individual differences in vulnerability to performance impairment from sleep loss just as the general population does. Thus, the scientific and operational communities' reliance on group data as opposed to individual data may entail substantial misestimation of the impact of job-related stressors on safety and performance.

  3. Sleep Deprivation and Caffeine Treatment Potentiate Photic Resetting of the Master Circadian Clock in a Diurnal Rodent.

    PubMed

    Jha, Pawan Kumar; Bouâouda, Hanan; Gourmelen, Sylviane; Dumont, Stephanie; Fuchs, Fanny; Goumon, Yannick; Bourgin, Patrice; Kalsbeek, Andries; Challet, Etienne

    2017-04-19

    Circadian rhythms in nocturnal and diurnal mammals are primarily synchronized to local time by the light/dark cycle. However, nonphotic factors, such as behavioral arousal and metabolic cues, can also phase shift the master clock in the suprachiasmatic nuclei (SCNs) and/or reduce the synchronizing effects of light in nocturnal rodents. In diurnal rodents, the role of arousal or insufficient sleep in these functions is still poorly understood. In the present study, diurnal Sudanian grass rats, Arvicanthis ansorgei , were aroused at night by sleep deprivation (gentle handling) or caffeine treatment that both prevented sleep. Phase shifts of locomotor activity were analyzed in grass rats transferred from a light/dark cycle to constant darkness and aroused in early night or late night. Early night, but not late night, sleep deprivation induced a significant phase shift. Caffeine on its own induced no phase shifts. Both sleep deprivation and caffeine treatment potentiated light-induced phase delays and phase advances in response to a 30 min light pulse, respectively. Sleep deprivation in early night, but not late night, potentiated light-induced c-Fos expression in the ventral SCN. Caffeine treatment in midnight triggered c-Fos expression in dorsal SCN. Both sleep deprivation and caffeine treatment potentiated light-induced c-Fos expression in calbindin-containing cells of the ventral SCN in early and late night. These findings indicate that, in contrast to nocturnal rodents, behavioral arousal induced either by sleep deprivation or caffeine during the sleeping period potentiates light resetting of the master circadian clock in diurnal rodents, and activation of calbindin-containing suprachiasmatic cells may be involved in this effect. SIGNIFICANCE STATEMENT Arousing stimuli have the ability to regulate circadian rhythms in mammals. Behavioral arousal in the sleeping period phase shifts the master clock in the suprachiasmatic nuclei and/or slows down the photic

  4. EphA4 is Involved in Sleep Regulation but Not in the Electrophysiological Response to Sleep Deprivation

    PubMed Central

    Freyburger, Marlène; Pierre, Audrey; Paquette, Gabrielle; Bélanger-Nelson, Erika; Bedont, Joseph; Gaudreault, Pierre-Olivier; Drolet, Guy; Laforest, Sylvie; Blackshaw, Seth; Cermakian, Nicolas; Doucet, Guy; Mongrain, Valérie

    2016-01-01

    Study Objectives: Optimal sleep is ensured by the interaction of circadian and homeostatic processes. Although synaptic plasticity seems to contribute to both processes, the specific players involved are not well understood. The EphA4 tyrosine kinase receptor is a cell adhesion protein regulating synaptic plasticity. We investigated the role of EphA4 in sleep regulation using electrocorticography in mice lacking EphA4 and gene expression measurements. Methods: EphA4 knockout (KO) mice, ClockΔ19/Δ19 mutant mice and littermates, C57BL/6J and CD-1 mice, and Sprague-Dawley rats were studied under a 12 h light: 12 h dark cycle, under undisturbed conditions or 6 h sleep deprivation (SLD), and submitted to a 48 h electrophysiological recording and/or brain sampling at different time of day. Results: EphA4 KO mice showed less rapid eye movement sleep (REMS), enhanced duration of individual bouts of wakefulness and nonrapid eye movement sleep (NREMS) during the light period, and a blunted daily rhythm of NREMS sigma activity. The NREMS delta activity response to SLD was unchanged in EphA4 KO mice. However, SLD increased EphA4 expression in the thalamic/hypothalamic region in C57BL/6J mice. We further show the presence of E-boxes in the promoter region of EphA4, a lower expression of EphA4 in Clock mutant mice, a rhythmic expression of EphA4 ligands in several brain areas, expression of EphA4 in the suprachiasmatic nuclei of the hypothalamus (SCN), and finally an unchanged number of cells expressing Vip, Grp and Avp in the SCN of EphA4 KO mice. Conclusions: Our results suggest that EphA4 is involved in circadian sleep regulation. Citation: Freyburger M, Pierre A, Paquette G, Bélanger-Nelson E, Bedont J, Gaudreault PO, Drolet G, Laforest S, Blackshaw S, Cermakian N, Doucet G, Mongrain V. EphA4 is involved in sleep regulation but not in the electrophysiological response to sleep deprivation. SLEEP 2016;39(3):613–624. PMID:26612390

  5. Sleep Deprivation: A Cause of High Blood Pressure?

    MedlinePlus

    ... Is it true that sleep deprivation can cause high blood pressure? Answers from Sheldon G. Sheps, M.D. Possibly. It's thought ... night may be at higher risk of developing high blood pressure or worsening already high blood pressure. There's also ...

  6. Paradoxical (REM) sleep deprivation in mice using the small-platforms-over-water method: polysomnographic analyses and melanin-concentrating hormone and hypocretin/orexin neuronal activation before, during and after deprivation.

    PubMed

    Arthaud, Sebastien; Varin, Christophe; Gay, Nadine; Libourel, Paul-Antoine; Chauveau, Frederic; Fort, Patrice; Luppi, Pierre-Herve; Peyron, Christelle

    2015-06-01

    Studying paradoxical sleep homeostasis requires the specific and efficient deprivation of paradoxical sleep and the evaluation of the subsequent recovery period. With this aim, the small-platforms-over-water technique has been used extensively in rats, but only rare studies were conducted in mice, with no sleep data reported during deprivation. Mice are used increasingly with the emergence of transgenic mice and technologies such as optogenetics, raising the need for a reliable method to manipulate paradoxical sleep. To fulfil this need, we refined this deprivation method and analysed vigilance states thoroughly during the entire protocol. We also studied activation of hypocretin/orexin and melanin-concentrating hormone neurones using Fos immunohistochemistry to verify whether mechanisms regulating paradoxical sleep in mice are similar to those in rats. We showed that 48 h of deprivation was highly efficient, with a residual amount of paradoxical sleep of only 2.2%. Slow wave sleep and wake quantities were similar to baseline, except during the first 4 h of deprivation, where slow wave sleep was strongly reduced. After deprivation, we observed a 124% increase in paradoxical sleep quantities during the first hour of rebound. In addition, 34% of hypocretin/orexin neurones were activated during deprivation, whereas melanin-concentrated hormone neurones were activated only during paradoxical sleep rebound. Corticosterone level showed a twofold increase after deprivation and returned to baseline level after 4 h of recovery. In summary, a fairly selective deprivation and a significant rebound of paradoxical sleep can be obtained in mice using the small-platforms-over-water method. As in rats, rebound is accompanied by a selective activation of melanin-concentrating hormone neurones. © 2014 European Sleep Research Society.

  7. Effects of acute caffeine withdrawal on Short Category Test performance in sleep-deprived individuals.

    PubMed

    Killgore, William D S; Kahn-Greene, Ellen T; Killgore, Desiree B; Kamimori, Gary H; Balkin, Thomas J

    2007-12-01

    Caffeine is a popular stimulant often used to counter the effects of sleep loss and fatigue. Withdrawal from caffeine may produce mild declines in simple cognitive capacities such as attention and concentration, but it is unclear whether more complex cognitive functions, such as abstract reasoning or concept formation, may be similarly affected. To assess the effect of acute caffeine withdrawal on executive functioning during sleep deprivation, 26 healthy volunteers were administered in double-blind form either repeated doses of caffeine or placebo over two nights of continuous wakefulness. The 108-item Short Category Test was administered after 56 hr. of total sleep deprivation (9 hr. post-caffeine administration). The caffeine group scored significantly more poorly, making approximately 57% more errors on the test than the placebo group. These findings suggest that acute caffeine withdrawal during prolonged sleep deprivation has an adverse effect on abstract reasoning and concept formation.

  8. Cognitive flexibility: A distinct element of performance impairment due to sleep deprivation.

    PubMed

    Honn, K A; Hinson, J M; Whitney, P; Van Dongen, H P A

    2018-03-14

    In around-the-clock operations, reduced alertness due to circadian misalignment and sleep loss causes performance impairment, which can lead to catastrophic errors and accidents. There is mounting evidence that performance on different tasks is differentially affected, but the general principles underlying this differentiation are not well understood. One factor that may be particularly relevant is the degree to which tasks require executive control, that is, control over the initiation, monitoring, and termination of actions in order to achieve goals. A key aspect of this is cognitive flexibility, i.e., the deployment of cognitive control resources to adapt to changes in events. Loss of cognitive flexibility due to sleep deprivation has been attributed to "feedback blunting," meaning that feedback on behavioral outcomes has reduced salience - and that feedback is therefore less effective at driving behavior modification under changing circumstances. The cognitive mechanisms underlying feedback blunting are as yet unknown. Here we present data from an experiment that investigated the effects of sleep deprivation on performance after an unexpected reversal of stimulus-response mappings, requiring cognitive flexibility to maintain good performance. Nineteen healthy young adults completed a 4-day in-laboratory study. Subjects were randomized to either a total sleep deprivation condition (n = 11) or a control condition (n = 8). Athree-phase reversal learning decision task was administered at baseline, and again after 30.5 h of sleep deprivation, or matching well-rested control. The task was based on a go/no go task paradigm, in which stimuli were assigned to either a go (response) set or a no go (no response) set. Each phase of the task included four stimuli (two in the go set and two in the no go set). After each stimulus presentation, subjects could make a response within 750 ms or withhold their response. They were then shown feedback on the accuracy of

  9. Insufficient sleep: Enhanced risk-seeking relates to low local sleep intensity.

    PubMed

    Maric, Angelina; Montvai, Eszter; Werth, Esther; Storz, Matthias; Leemann, Janina; Weissengruber, Sebastian; Ruff, Christian C; Huber, Reto; Poryazova, Rositsa; Baumann, Christian R

    2017-09-01

    Chronic sleep restriction is highly prevalent in modern society and is, in its clinical form, insufficient sleep syndrome, one of the most prevalent diagnoses in clinical sleep laboratories, with substantial negative impact on health and community burden. It reflects every-day sleep loss better than acute sleep deprivation, but its effects and particularly the underlying mechanisms remain largely unknown for a variety of critical cognitive domains, as, for example, risky decision making. We assessed financial risk-taking behavior after 7 consecutive nights of sleep restriction and after 1 night of acute sleep deprivation compared to a regular sleep condition in a within-subject design. We further investigated potential underlying mechanisms of sleep-loss-induced changes in behavior by high-density electroencephalography recordings during restricted sleep. We show that chronic sleep restriction increases risk-seeking, whereas this was not observed after acute sleep deprivation. This increase was subjectively not noticed and was related to locally lower values of slow-wave energy during preceding sleep, an electrophysiological marker of sleep intensity and restoration, in electrodes over the right prefrontal cortex. This study provides, for the first time, evidence that insufficient sleep restoration over circumscribed cortical areas leads to aberrant behavior. In chronically sleep restricted subjects, low slow-wave sleep intensity over the right prefrontal cortex-which has been shown to be linked to risk behavior-may lead to increased and subjectively unnoticed risk-seeking. Ann Neurol 2017;82:409-418. © 2017 American Neurological Association.

  10. Cell Injury and Repair Resulting from Sleep Loss and Sleep Recovery in Laboratory Rats

    PubMed Central

    Everson, Carol A.; Henchen, Christopher J.; Szabo, Aniko; Hogg, Neil

    2014-01-01

    Study Objectives: Increased cell injury would provide the type of change in constitution that would underlie sleep disruption as a risk factor for multiple diseases. The current study was undertaken to investigate cell injury and altered cell fate as consequences of sleep deprivation, which were predicted from systemic clues. Design: Partial (35% sleep reduction) and total sleep deprivation were produced in rats for 10 days, which was tolerated and without overtly deteriorated health. Recovery rats were similarly sleep deprived for 10 days, then allowed undisturbed sleep for 2 days. The plasma, liver, lung, intestine, heart, and spleen were analyzed and compared to control values for damage to DNA, proteins, and lipids; apoptotic cell signaling and death; cell proliferation; and concentrations of glutathione peroxidase and catalase. Measurements and Results: Oxidative DNA damage in totally sleep deprived rats was 139% of control values, with organ-specific effects in the liver (247%), lung (166%), and small intestine (145%). Overall and organ-specific DNA damage was also increased in partially sleep deprived rats. In the intestinal epithelium, total sleep deprivation resulted in 5.3-fold increases in dying cells and 1.5-fold increases in proliferating cells, compared with control. Two days of recovery sleep restored the balance between DNA damage and repair, and resulted in normal or below-normal metabolic burdens and oxidative damage. Conclusions: These findings provide physical evidence that sleep loss causes cell damage, and in a manner expected to predispose to replication errors and metabolic abnormalities; thereby providing linkage between sleep loss and disease risk observed in epidemiological findings. Properties of recovery sleep include biochemical and molecular events that restore balance and decrease cell injury. Citation: Everson CA, Henchen CJ, Szabo A, Hogg N. Cell injury and repair resulting from sleep loss and sleep recovery in laboratory rats

  11. Aging induced ER stress alters sleep and sleep homeostasis

    PubMed Central

    Brown, Marishka K.; Chan, May T.; Zimmerman, John E.; Pack, Allan I.; Jackson, Nicholas E.; Naidoo, Nirinjini

    2014-01-01

    Alterations in the quality, quantity and architecture of baseline and recovery sleep have been shown to occur during aging. Sleep deprivation induces endoplasmic reticular (ER) stress and upregulates a protective signaling pathway termed the unfolded protein response (UPR). The effectiveness of the adaptive UPR is diminished by age. Previously, we showed that endogenous chaperone levels altered recovery sleep in Drosophila melanogaster. We now report that acute administration of the chemical chaperone sodium 4-phenylbutyrate (PBA) reduces ER stress and ameliorates age-associated sleep changes in Drosophila. PBA consolidates both baseline and recovery sleep in aging flies. The behavioral modifications of PBA are linked to its suppression of ER stress. PBA decreased splicing of x-box binding protein 1 (XBP1) and upregulation of phosphorylated elongation initiation factor 2 α (p-eIF2α), in flies that were subjected to sleep deprivation. We also demonstrate that directly activating ER stress in young flies fragments baseline sleep and alters recovery sleep. Alleviating prolonged/sustained ER stress during aging contributes to sleep consolidation and improves recovery sleep/ sleep debt discharge. PMID:24444805

  12. The effects of a single night of sleep deprivation on fluency and prefrontal cortex function during divergent thinking

    PubMed Central

    Vartanian, Oshin; Bouak, Fethi; Caldwell, J. L.; Cheung, Bob; Cupchik, Gerald; Jobidon, Marie-Eve; Lam, Quan; Nakashima, Ann; Paul, Michel; Peng, Henry; Silvia, Paul J.; Smith, Ingrid

    2014-01-01

    The dorsal and ventral aspects of the prefrontal cortex (PFC) are the two regions most consistently recruited in divergent thinking tasks. Given that frontal tasks have been shown to be vulnerable to sleep loss, we explored the impact of a single night of sleep deprivation on fluency (i.e., number of generated responses) and PFC function during divergent thinking. Participants underwent functional magnetic resonance imaging scanning twice while engaged in the Alternate Uses Task (AUT) – once following a single night of sleep deprivation and once following a night of normal sleep. They also wore wrist activity monitors, which enabled us to quantify daily sleep and model cognitive effectiveness. The intervention was effective, producing greater levels of fatigue and sleepiness. Modeled cognitive effectiveness and fluency were impaired following sleep deprivation, and sleep deprivation was associated with greater activation in the left inferior frontal gyrus (IFG) during AUT. The results suggest that an intervention known to temporarily compromise frontal function can impair fluency, and that this effect is instantiated in the form of an increased hemodynamic response in the left IFG. PMID:24795594

  13. Does caffeine change the effect of sleep deprivation on moderate to severe depressed patients?

    PubMed

    Schwartzhaupt, Alexandre W; Lara, Diogo R; Hirakata, Vânia N; Schuch, Alice; Almeida, Ellen; Silveira, Leonardo; Caldieraro, Marco A K; Fleck, Marcelo P

    2009-01-01

    Sleep deprivation (SD) has been used as an alternative approach to treat major depressive disorder (MDD). Caffeine, due to its stimulating effect, could be an alternative to promote sleep deprivation. However, there are no data about its potential influence on the antidepressive effect of SD. The objective of this study is to assess the effect of caffeine on SD in non-psychotic patients with moderate to severe unipolar depression. Randomized, double-blind, crossover clinical trial comparing caffeine and placebo in moderate to severe depressed patients who underwent total sleep deprivation (SD). The patients were assessed with items of the Bond-Lader scale, the 6-item Hamilton Depression Rating Scale (HAMD-6), and the Clinical Global Impression (CGI)-Severity/Improvement. Twenty patients participated in this study. The patients who consumed caffeine presented the same level of energy before and after sleep deprivation (lethargic-energetic item of the Bond-Lader scale), while the patients in the placebo group had a reduced level of energy after sleep deprivation (p=0.0045). There was no difference between the caffeine and placebo groups in the other items of the Bond-Lader scale. The combined use of caffeine and SD can be a useful strategy to keep the patient awake without impairing the effect of SD on depressed outpatients. However, further studies involving patients who have responded to SD are needed in order to verify if caffeine also does not interfere with the results in this group.

  14. Cell injury and repair resulting from sleep loss and sleep recovery in laboratory rats.

    PubMed

    Everson, Carol A; Henchen, Christopher J; Szabo, Aniko; Hogg, Neil

    2014-12-01

    Increased cell injury would provide the type of change in constitution that would underlie sleep disruption as a risk factor for multiple diseases. The current study was undertaken to investigate cell injury and altered cell fate as consequences of sleep deprivation, which were predicted from systemic clues. Partial (35% sleep reduction) and total sleep deprivation were produced in rats for 10 days, which was tolerated and without overtly deteriorated health. Recovery rats were similarly sleep deprived for 10 days, then allowed undisturbed sleep for 2 days. The plasma, liver, lung, intestine, heart, and spleen were analyzed and compared to control values for damage to DNA, proteins, and lipids; apoptotic cell signaling and death; cell proliferation; and concentrations of glutathione peroxidase and catalase. Oxidative DNA damage in totally sleep deprived rats was 139% of control values, with organ-specific effects in the liver (247%), lung (166%), and small intestine (145%). Overall and organ-specific DNA damage was also increased in partially sleep deprived rats. In the intestinal epithelium, total sleep deprivation resulted in 5.3-fold increases in dying cells and 1.5-fold increases in proliferating cells, compared with control. Recovery sleep restored the balance between DNA damage and repair, and resulted in normal or below-normal metabolic burdens and oxidative damage. These findings provide physical evidence that sleep loss causes cell damage, and in a manner expected to predispose to replication errors and metabolic abnormalities; thereby providing linkage between sleep loss and disease risk observed in epidemiological findings. Properties of recovery sleep include biochemical and molecular events that restore balance and decrease cell injury. © 2014 Associated Professional Sleep Societies, LLC.

  15. Nap polygraphic recordings after partial sleep deprivation in patients with suspected epileptic seizures.

    PubMed

    Peraita-Adrados, R; Gutierrez-Solana, L; Ruiz-Falcó, M L; García-Peñas, J J

    2001-02-01

    A review of the literature shows that nap recordings make a significant contribution to epilepsy studies, providing evidence of specific EEG findings in patients suspected of having epilepsy. In addition, sleep deprivation can cause paroxysmal EEG activity and clinical seizures. We studied retrospectively 686 patients, 51.8% males and 48.2% females, who had experienced at least one episode classified from the clinical point of view as epileptic in origin. They were divided into six age groups. Patients underwent a two-hour (1 P.M.-3 P.M.) nap-video-polygraphic recording (EEG 13 channels using the standard 10-20 system, EOG, ECG, EMG and respiration), following a partial sleep deprivation (1 to 3 h) the night before. A second recording was made in 40 patients. In 35.3% of patients, a complete sleep cycle was obtained; in 64.6% sufficient light and deep NREM sleep was obtained, but not REM stage; in 9.3%, we only observed drowsiness and stage 1 of sleep, and this group was excluded from the analysis. Interictal and/or ictal epileptic discharges were observed during the first nap recording in 245 patients (40.4% of the sample). In addition, in 40 patients (11%) with normal or inconclusive first nap EEG, a second recording was able to demonstrate epileptic abnormalities in 35% of cases. Because of its good cost/benefit ratio and availability in most western laboratories, we consider the 'nap plus partial sleep deprivation' method as advantageous over other activation procedures.

  16. Acute sleep deprivation increases portion size and affects food choice in young men.

    PubMed

    Hogenkamp, Pleunie S; Nilsson, Emil; Nilsson, Victor C; Chapman, Colin D; Vogel, Heike; Lundberg, Lina S; Zarei, Sanaz; Cedernaes, Jonathan; Rångtell, Frida H; Broman, Jan-Erik; Dickson, Suzanne L; Brunstrom, Jeffrey M; Benedict, Christian; Schiöth, Helgi B

    2013-09-01

    Acute sleep loss increases food intake in adults. However, little is known about the influence of acute sleep loss on portion size choice, and whether this depends on both hunger state and the type of food (snack or meal item) offered to an individual. The aim of the current study was to compare portion size choice after a night of sleep and a period of nocturnal wakefulness (a condition experienced by night-shift workers, e.g. physicians and nurses). Sixteen men (age: 23 ± 0.9 years, BMI: 23.6 ± 0.6 kg/m(2)) participated in a randomized within-subject design with two conditions, 8-h of sleep and total sleep deprivation (TSD). In the morning following sleep interventions, portion size, comprising meal and snack items, was measured using a computer-based task, in both fasted and sated state. In addition, hunger as well as plasma levels of ghrelin were measured. In the morning after TSD, subjects had increased plasma ghrelin levels (13%, p=0.04), and chose larger portions (14%, p=0.02), irrespective of the type of food, as compared to the sleep condition. Self-reported hunger was also enhanced (p<0.01). Following breakfast, sleep-deprived subjects chose larger portions of snacks (16%, p=0.02), whereas the selection of meal items did not differ between the sleep interventions (6%, p=0.13). Our results suggest that overeating in the morning after sleep loss is driven by both homeostatic and hedonic factors. Further, they show that portion size choice after sleep loss depend on both an individual's hunger status, and the type of food offered. Copyright © 2013 Elsevier Ltd. All rights reserved.

  17. Repeated Sleep Restriction in Adolescent Rats Altered Sleep Patterns and Impaired Spatial Learning/Memory Ability

    PubMed Central

    Yang, Su-Rong; Sun, Hui; Huang, Zhi-Li; Yao, Ming-Hui; Qu, Wei-Min

    2012-01-01

    Study Objectives: To investigate possible differences in the effect of repeated sleep restriction (RSR) during adolescence and adulthood on sleep homeostasis and spatial learning and memory ability. Design: The authors examined electroencephalograms of rats as they were subjected to 4-h daily sleep deprivation that continued for 7 consecutive days and assessed the spatial learning and memory by Morris water maze test (WMT). Participants: Adolescent and adult rats. Measurements and Results: Adolescent rats exhibited a similar amount of rapid eye movement (REM) and nonrapid eye movement (NREM) sleep with higher slow wave activity (SWA, 0.5-4 Hz) and fewer episodes and conversions with prolonged durations, indicating they have better sleep quality than adult rats. After RSR, adult rats showed strong rebound of REM sleep by 31% on sleep deprivation day 1; this value was 37% on sleep deprivation day 7 in adolescents compared with 20-h baseline level. On sleep deprivation day 7, SWA in adult and adolescent rats increased by 47% and 33%, and such elevation lasted for 5 h and 7 h, respectively. Furthermore, the authors investigated the effects of 4-h daily sleep deprivation immediately after the water maze training sessions on spatial cognitive performance. Adolescent rats sleep-restricted for 7 days traveled a longer distance to find the hidden platform during the acquisition training and had fewer numbers of platform crossings in the probe trial than those in the control group, something that did not occur in the sleep-deprived adult rats. Conclusions: Repeated sleep restriction (RSR) altered sleep profiles and mildly impaired spatial learning and memory capability in adolescent rats. Citation: Yang SR; Sun H; Huang ZL; Yao MH; Qu WM. Repeated sleep restriction in adolescent rats altered sleep patterns and impaired spatial learning/memory ability. SLEEP 2012;35(6):849-859. PMID:22654204

  18. Caffeine and sleep-deprivation mediated changes in open-field behaviours, stress response and antioxidant status in mice.

    PubMed

    Onaolapo, J Olakunle; Onaolapo, Y Adejoke; Akanmu, A Moses; Olayiwola, Gbola

    2016-01-01

    Effects of daily caffeine consumption on open-field behaviours, serum corticosterone and brain antioxidant levels were investigated after six hours of total sleep-deprivation in prepubertal mice. We tested the hypothesis that daily caffeine consumption may significantly alter behaviour, stress and antioxidative response of prepubertal mice to an acute episode of total sleep-deprivation. Prepubertal Swiss mice of both sexes were assigned to two main groups of 120 each (subdivided into 6 groups of 10 each, based on sex), and administered vehicle or graded oral doses of caffeine (10, 20, 40, 80 and 120 mg/kg/day) for 14 days. On day 14, a main group was subjected to 6 h of total sleep-deprivation by 'gentle-handling'. Open-field behaviours were then assessed in both groups, after which animals were euthanized, and levels of corticosterone, superoxide dismutase and glutathione peroxidase assayed. Horizontal locomotion, rearing and grooming increased significantly, compared to control, with sleep-deprived (SD) mice showing stronger caffeine-driven responses at higher doses; and SD female mice showing sustained response to caffeine, compared to respective males. Plasma corticosterone increased with increasing doses of caffeine in both non sleep-deprived (NSD) and SD mice; although SD mice had higher corticosterone levels. Sleep-deprivation and/or higher doses of caffeine were associated with derangements in brain antioxidant levels. Repeated caffeine consumption and/or acute sleep-deprivation led to significant changes in pattern of open-field behaviour and stress/antioxidant response in mice. Responses seen in the study are probably due to modulatory effects of caffeine on the total body response to stressful stimuli.

  19. What Are Some Myths About Sleep?

    MedlinePlus

    ... is REM sleep? What is the effect of sleep deprivation? What are sleep myths? What are sleep disorders? ... as it becomes larger. In addition, long-term sleep deprivation contributes to several conditions involving health, safety, and ...

  20. Spontaneous sleep-wake cycle and sleep deprivation differently induce Bdnf1, Bdnf4 and Bdnf9a DNA methylation and transcripts levels in the basal forebrain and frontal cortex in rats.

    PubMed

    Ventskovska, Olena; Porkka-Heiskanen, Tarja; Karpova, Nina N

    2015-04-01

    Brain-derived neurotrophic factor (Bdnf) regulates neuronal plasticity, slow wave activity and sleep homeostasis. Environmental stimuli control Bdnf expression through epigenetic mechanisms, but there are no data on epigenetic regulation of Bdnf by sleep or sleep deprivation. Here we investigated whether 5-methylcytosine (5mC) DNA modification at Bdnf promoters p1, p4 and p9 influences Bdnf1, Bdnf4 and Bdnf9a expression during the normal inactive phase or after sleep deprivation (SD) (3, 6 and 12 h, end-times being ZT3, ZT6 and ZT12) in rats in two brain areas involved in sleep regulation, the basal forebrain and cortex. We found a daytime variation in cortical Bdnf expression: Bdnf1 expression was highest at ZT6 and Bdnf4 lowest at ZT12. Such variation was not observed in the basal forebrain. Also Bdnf p1 and p9 methylation levels differed only in the cortex, while Bdnf p4 methylation did not vary in either area. Factorial analysis revealed that sleep deprivation significantly induced Bdnf1 and Bdnf4 with the similar pattern for Bdnf9a in both basal forebrain and cortex; 12 h of sleep deprivation decreased 5mC levels at the cortical Bdnf p4 and p9. Regression analysis between the 5mC promoter levels and the corresponding Bdnf transcript expression revealed significant negative correlations for the basal forebrain Bdnf1 and cortical Bdnf9a transcripts in only non-deprived rats, while these correlations were lost after sleep deprivation. Our results suggest that Bdnf transcription during the light phase of undisturbed sleep-wake cycle but not after SD is regulated at least partially by brain site-specific DNA methylation. © 2014 European Sleep Research Society.

  1. Cyclic alternating pattern and interictal epileptiform discharges during morning sleep after sleep deprivation in temporal lobe epilepsy.

    PubMed

    Giorgi, Filippo Sean; Maestri, Michelangelo; Guida, Melania; Carnicelli, Luca; Caciagli, Lorenzo; Ferri, Raffaele; Bonuccelli, Ubaldo; Bonanni, Enrica

    2017-08-01

    Sleep deprivation (SD) increases the occurrence of interictal epileptiform discharges (IED) compared to basal EEG in temporal lobe epilepsy (TLE). In adults, EEG after SD is usually performed in the morning after SD. We aimed to evaluate whether morning sleep after SD bears additional IED-inducing effects compared with nocturnal physiological sleep, and whether changes in sleep stability (described by the cyclic alternating pattern-CAP) play a significant role. Adult patients with TLE underwent in-lab night polysomnography (n-PSG) and, within 7days from n-PSG, they underwent also a morning EEG after night SD (SD-EEG). We included only TLE patients in which both recordings showed IED. SD-EEG consisted of waking up patients at 2:00 AM and performing video EEG at 8:00 AM. For both recordings, we obtained the following markers for the first sleep cycle: IED/h (Spike Index, SI), sleep macrostructure, microstructure (NREM CAP rate; A1, A2 and A3 Indices), and SI association with CAP variables. The macrostructure of the first sleep cycle was similar in n-PSG and morning SD-EEG, whereas CAP rate and SI were significantly higher in SD-EEG. SI increase was selectively associated with CAP phases. SD increases the instability of morning recovery sleep compared with n-PSG, and particularly enhances CAP A1 phases, which are associated with the majority of IED. Thus, higher instability of morning recovery sleep may account at least in part for the increased IED yield in SD-EEG in TLE patients. Copyright © 2017 Elsevier Inc. All rights reserved.

  2. Association of Sleep Deprivation With Reduction in Insulin Sensitivity as Assessed by the Hyperglycemic Clamp Technique in Adolescents.

    PubMed

    De Bernardi Rodrigues, Ana Maria; da Silva, Cleliani de Cassia; Vasques, Ana Carolina Junqueira; Camilo, Daniella Fernandes; Barreiro, Francieli; Cassani, Roberta Soares Lara; Zambon, Mariana Porto; Antonio, Maria Ângela Reis de Góes Monteiro; Geloneze, Bruno

    2016-05-01

    The association between short sleep duration and decreased insulin sensitivity in adolescents has been described. However, to our knowledge, no studies have investigated this association measuring insulin sensitivity by the hyperglycemic clamp technique. To compare the distributions of parameters of insulin resistance in adolescents with sleep deprivation vs adequate sleep, and to investigate the association between sleep deprivation and insulin sensitivity. Cross-sectional multicenter study using data from the Brazilian Metabolic Syndrome Study conducted from June 29, 2011, to December 3, 2014, at an obesity outpatient clinic at the University of Campinas and public schools, with a convenience sample of 615 adolescents aged 10 to 19.9 years with a body mass index (BMI; calculated as weight in kilograms divided by height in meters squared) for age and sex at the fifth percentile or higher. A subsample of 81 adolescents underwent the hyperglycemic clamp technique. The self-reported sleep duration was used to classify the population into 2 groups: adolescents with sleep deprivation (<8 hours/night) and adolescents with adequate sleep (≥8 hours/night). Insulin sensitivity was assessed using the hyperglycemic clamp technique. Among the 615 adolescents (56.3% female; median age, 15.9 years [interquartile range, 12.9-17.8 years]) included in the sample, the mean (SD) sleep duration was 7.9 (1.7) hours/night. The adolescents with sleep deprivation (n = 257) compared with those with adequate sleep (n = 358) had a higher median (interquartile range) age (17.0 [15.4-18.3] vs 14.1 [11.8-16.9] years), BMI (25.0 [21.2-29.3] vs 23.1 [19.5-27.6]), waist circumference (83.0 [73.5-95.4] vs 79.0 [68.5-91.0] cm), sagittal abdominal diameter (17.9 [15.8-20.8] vs 17.0 [15.0-19.8] cm), neck circumference (35.2 [33.0-38.0] vs 33.0 [30.0-35.5] cm), uric acid level (4.9 [4.0-5.8] vs 4.5 [3.7-5.5] mg/dL), and white blood cell count (7000 [5900-8200] vs 6600 [5600-7800] cells

  3. Sleep deprivation elevates expectation of gains and attenuates response to losses following risky decisions.

    PubMed

    Venkatraman, Vinod; Chuah, Y M Lisa; Huettel, Scott A; Chee, Michael W L

    2007-05-01

    Using a gambling task, we investigated how 24 hours of sleep deprivation modulates the neural response to the making of risky decisions with potentially loss-bearing outcomes. Two experiments involving sleep-deprived subjects were performed. In the first, neural responses to decision making and reward outcome were evaluated. A second control experiment evaluated responses to reward outcome only. Healthy right-handed adults participated in these experiments (26 [mean age 21.3 years] in Experiment 1 and 13 [mean age 21.7 years] in Experiment 2.) Following sleep deprivation, choices involving higher relative risk elicited greater activation in the right nucleus accumbens, signifying an elevated expectation of the higher reward once the riskier choice was made. Concurrently, activation for losses in the insular and orbitofrontal cortices was reduced, denoting a diminished response to losses. This latter finding of reduced insular activation to losses was also true when volunteers were merely shown the results of the computer's decision, that is, without having to make their own choice. These results suggest that sleep deprivation poses a dual threat to competent decision making by modulating activation in nucleus accumbens and insula, brain regions associated with risky decision making and emotional processing.

  4. Sleep deprivation accelerates delay-related loss of visual short-term memories without affecting precision.

    PubMed

    Wee, Natalie; Asplund, Christopher L; Chee, Michael W L

    2013-06-01

    Visual short-term memory (VSTM) is an important measure of information processing capacity and supports many higher-order cognitive processes. We examined how sleep deprivation (SD) and maintenance duration interact to influence the number and precision of items in VSTM using an experimental design that limits the contribution of lapses at encoding. For each trial, participants attempted to maintain the location and color of three stimuli over a delay. After a retention interval of either 1 or 10 seconds, participants reported the color of the item at the cued location by selecting it on a color wheel. The probability of reporting the probed item, the precision of report, and the probability of reporting a nonprobed item were determined using a mixture-modeling analysis. Participants were studied twice in counterbalanced order, once after a night of normal sleep and once following a night of sleep deprivation. Sleep laboratory. Nineteen healthy college age volunteers (seven females) with regular sleep patterns. Approximately 24 hours of total SD. SD selectively reduced the number of integrated representations that can be retrieved after a delay, while leaving the precision of object information in the stored representations intact. Delay interacted with SD to lower the rate of successful recall. Visual short-term memory is compromised during sleep deprivation, an effect compounded by delay. However, when memories are retrieved, they tend to be intact.

  5. Quantitative Proteomics of Sleep-Deprived Mouse Brains Reveals Global Changes in Mitochondrial Proteins

    PubMed Central

    Li, Tie-Mei; Zhang, Ju-en; Lin, Rui; Chen, She; Luo, Minmin; Dong, Meng-Qiu

    2016-01-01

    Sleep is a ubiquitous, tightly regulated, and evolutionarily conserved behavior observed in almost all animals. Prolonged sleep deprivation can be fatal, indicating that sleep is a physiological necessity. However, little is known about its core function. To gain insight into this mystery, we used advanced quantitative proteomics technology to survey the global changes in brain protein abundance. Aiming to gain a comprehensive profile, our proteomics workflow included filter-aided sample preparation (FASP), which increased the coverage of membrane proteins; tandem mass tag (TMT) labeling, for relative quantitation; and high resolution, high mass accuracy, high throughput mass spectrometry (MS). In total, we obtained the relative abundance ratios of 9888 proteins encoded by 6070 genes. Interestingly, we observed significant enrichment for mitochondrial proteins among the differentially expressed proteins. This finding suggests that sleep deprivation strongly affects signaling pathways that govern either energy metabolism or responses to mitochondrial stress. Additionally, the differentially-expressed proteins are enriched in pathways implicated in age-dependent neurodegenerative diseases, including Parkinson’s, Huntington’s, and Alzheimer’s, hinting at possible connections between sleep loss, mitochondrial stress, and neurodegeneration. PMID:27684481

  6. The effects of early and late night partial sleep deprivation on automatic and selective attention: An ERP study.

    PubMed

    Zerouali, Younes; Jemel, Boutheina; Godbout, Roger

    2010-01-13

    The link between decrease in levels of attention and total sleep deprivation is well known but the respective contributions of slow wave sleep (SWS) and rapid eye movement sleep (REM) is still largely unknown. The aim of this study was to characterize the effects of sleep deprivation during the SWS phase (i.e., early night sleep) and the REM phase (i.e., late night sleep) on tasks that tap automatic and selective attention; these two forms of attention were indexed respectively by "mismatch negativity" (MMN) and "negative difference" (Nd) event-related potential (ERP) difference waves. Ten young adult participants were subjected to a three-night sleep protocol. They were each received one night of full sleep (F), one night of sleep deprivation during the first half of the night (H1), and one night of sleep deprivation during the second half of the night (H2). MMN and Nd were recorded the following morning of each night during two auditory oddball tasks that tapped automatic and selective attention. The effect of sleep deprivation condition was assessed using ERP amplitude measures and standardized low-resolution electromagnetic tomography method (sLORETA). ERP results revealed significant MMN amplitude reduction over frontal and temporal recording areas following the H2 night compared to F and H1, indicating reductions in levels of automatic attention. In addition, Nd amplitude over the parietal recording area was significantly increased following the H2 night compared to F and H1. sLORETA findings show significant changes from F to H2 night in frontal cortex activity, decreasing during the automatic attention task but increasing during the selective attention task. No significant change in brain activity is observed after H1 night. The restoration of attention processes is mainly achieved during REM sleep, which confirms results from previous studies in rat models. The anterior cortex seems to be more sensitive to sleep loss, while the parietal cortex acts as a

  7. Deterioration of the useful visual field with age and sleep deprivation: insight from signal detection theory.

    PubMed

    Rogé, Joceline; Gabaude, Catherine

    2009-08-01

    The goal of this study was to establish whether the deterioration of the useful visual field due to sleep deprivation and age in a screen monitoring activity could be explained by a decrease in perceptual sensitivity and/or a modification of the participant's decision criterion (two indices derived from signal detection theory). In the first experiment, a comparison of three age groups (young, middle-aged, elderly) showed that perceptual sensitivity decreased with age and that the decision criterion became more conservative. In the second experiment, measurement of the useful visual field was carried out on participants who had been deprived of sleep the previous night or had a complete night of sleep. Perceptual sensitivity significantly decreased with sleep debt, and sleep deprivation provoked an increase in the participants' decision criterion. Moreover, the comparison of two age groups (young, middle-aged) indicated that sensitivity decreased with age. The value of using these two indices to explain the deterioration of useful visual field is discussed.

  8. Aging induced endoplasmic reticulum stress alters sleep and sleep homeostasis.

    PubMed

    Brown, Marishka K; Chan, May T; Zimmerman, John E; Pack, Allan I; Jackson, Nicholas E; Naidoo, Nirinjini

    2014-06-01

    Alterations in the quality, quantity, and architecture of baseline and recovery sleep have been shown to occur during aging. Sleep deprivation induces endoplasmic reticular (ER) stress and upregulates a protective signaling pathway termed the unfolded protein response. The effectiveness of the adaptive unfolded protein response is diminished by age. Previously, we showed that endogenous chaperone levels altered recovery sleep in Drosophila melanogaster. We now report that acute administration of the chemical chaperone sodium 4-phenylbutyrate (PBA) reduces ER stress and ameliorates age-associated sleep changes in Drosophila. PBA consolidates both baseline and recovery sleep in aging flies. The behavioral modifications of PBA are linked to its suppression of ER stress. PBA decreased splicing of X-box binding protein 1 and upregulation of phosphorylated elongation initiation factor 2 α, in flies that were subjected to sleep deprivation. We also demonstrate that directly activating ER stress in young flies fragments baseline sleep and alters recovery sleep. Alleviating prolonged or sustained ER stress during aging contributes to sleep consolidation and improves recovery sleep or sleep debt discharge. Copyright © 2014 Elsevier Inc. All rights reserved.

  9. Effects of exercise on depressive behavior and striatal levels of norepinephrine, serotonin and their metabolites in sleep-deprived mice.

    PubMed

    Daniele, Thiago Medeiros da Costa; de Bruin, Pedro Felipe Carvalhedo; Rios, Emiliano Ricardo Vasconcelos; de Bruin, Veralice Meireles Sales

    2017-08-14

    Exercise is a promising adjunctive therapy for depressive behavior, sleep/wake abnormalities, cognition and motor dysfunction. Conversely, sleep deprivation impairs mood, cognition and functional performance. The objective of this study is to evaluate the effects of exercise on anxiety and depressive behavior and striatal levels of norepinephrine (NE), serotonin and its metabolites in mice submitted to 6h of total sleep deprivation (6h-TSD) and 72h of Rapid Eye Movement (REM) sleep deprivation (72h-REMSD). Experimental groups were: (1) mice submitted to 6h-TSD by gentle handling; (2) mice submitted to 72h-REMSD by the flower pot method; (3) exercise (treadmill for 8 weeks); (4) exercise followed by 6h-TSD; (5) exercise followed by 72h-REMSD; (6) control (home cage). Behavioral tests included the Elevated Plus Maze and tail-suspension. NE, serotonin and its metabolites were determined in the striatum using high-performance liquid chromatography (HPLC). Sleep deprivation increased depressive behavior (time of immobilization in the tail-suspension test) and previous exercise hindered it. Sleep deprivation increased striatal NE and previous exercise reduced it. Exercise only was associated with higher levels of serotonin. Furthermore, exercise reduced serotonin turnover associated with sleep deprivation. In brief, previous exercise prevented depressive behavior and reduced striatal high NE levels and serotonin turnover. The present findings confirm the effects of exercise on behavior and neurochemical alterations associated with sleep deprivation. These findings provide new avenues for understanding the mechanisms of exercise. Copyright © 2017 Elsevier B.V. All rights reserved.

  10. Sleep and Nutritional Deprivation and Performance of House Officers.

    ERIC Educational Resources Information Center

    Hawkins, Michael R.; And Others

    1985-01-01

    A study to compare cognitive functioning in acutely and chronically sleep-deprived house officers is described. A multivariate analysis of variance revealed significant deficits in primary mental tasks involving basic rote memory, language, and numeric skills. (Author/MLW)

  11. Dual conception of risk in the Iowa Gambling Task: effects of sleep deprivation and test-retest gap.

    PubMed

    Singh, Varsha

    2013-01-01

    Risk in the Iowa Gambling Task (IGT) is often understood in terms of intertemporal choices, i.e., preference for immediate outcomes in favor of delayed outcomes is considered risky decision making. According to behavioral economics, healthy decision makers are expected to refrain from choosing the short-sighted immediate gain because, over time (10 trials of the IGT), the immediate gains result in a long term loss (net loss). Instead decision makers are expected to maximize their gains by choosing options that, over time (10 trials), result in delayed or long term gains (net gain). However, task choices are sometimes made on the basis of the frequency of reward and punishment such that frequent rewards/infrequent punishments are favored over infrequent rewards/frequent punishments. The presence of these two attributes (intertemporality and frequency of reward) in IGT decision making may correspond to the emotion-cognition dichotomy and reflect a dual conception of risk. Decision making on the basis of the two attributes was tested under two conditions: delay in retest and sleep deprivation. An interaction between sleep deprivation and time delay was expected to attenuate the difference between the two attributes. Participants were 40 male university students. Analysis of the effects of IGT attribute type (intertemporal vs. frequency of reinforcement), sleep deprivation (sleep deprivation vs. no sleep deprivation), and test-retest gap (short vs. long delay) showed a significant within-subjects effect of IGT attribute type thus confirming the difference between the two attributes. Sleep deprivation had no effect on the attributes, but test-retest gap and the three-way interaction between attribute type, test-retest gap, and sleep deprivation were significantly different. Post-hoc tests revealed that sleep deprivation and short test-retest gap attenuated the difference between the two attributes. Furthermore, the results showed an expected trend of increase in

  12. Investigating the effect of acute sleep deprivation on hypothalamic-pituitary-adrenal-axis response to a psychosocial stressor.

    PubMed

    Vargas, Ivan; Lopez-Duran, Nestor

    2017-05-01

    The hypothalamic-pituitary-adrenal (HPA) axis has been previously identified as one potential mechanism that may explain the link between sleep deprivation and negative health outcomes. However, few studies have examined the direct association between sleep deprivation and HPA-axis functioning, particularly in the context of stress. Therefore, the aim of the current study was to investigate the relationship between acute sleep deprivation and HPA-axis reactivity to a psychosocial stressor. Participants included 40 healthy, young adults between the ages of 18-29. The current protocol included spending two nights in the laboratory. After an adaptation night (night 1), participants were randomized into either a sleep deprivation condition (29 consecutive hours awake) or a control condition (night 2). Following the second night, all participants completed the Trier Social Stress Test (TSST). Salivary cortisol was collected before, during, and after the TSST. Results indicated that there were significant group differences in cortisol stress reactivity. Specifically, compared to participants in the control condition, participants in the sleep deprivation condition had greater baseline (i.e., pre-stress) cortisol, yet a blunted cortisol response to the TSST. Taken together, a combination of elevated baseline cortisol (and its subsequent effect on HPA-axis regulatory processes) and a relative 'ceiling' on the amount of cortisol a laboratory stressor can produce may explain why participants in the sleep deprivation condition demonstrated blunted cortisol responses. Copyright © 2017 Elsevier Ltd. All rights reserved.

  13. Skill execution and sleep deprivation: effects of acute caffeine or creatine supplementation - a randomized placebo-controlled trial

    PubMed Central

    2011-01-01

    Background We investigated the effects of sleep deprivation with or without acute supplementation of caffeine or creatine on the execution of a repeated rugby passing skill. Method Ten elite rugby players completed 10 trials on a simple rugby passing skill test (20 repeats per trial), following a period of familiarisation. The players had between 7-9 h sleep on 5 of these trials and between 3-5 h sleep (deprivation) on the other 5. At a time of 1.5 h before each trial, they undertook administration of either: placebo tablets, 50 or 100 mg/kg creatine, 1 or 5 mg/kg caffeine. Saliva was collected before each trial and assayed for salivary free cortisol and testosterone. Results Sleep deprivation with placebo application resulted in a significant fall in skill performance accuracy on both the dominant and non-dominant passing sides (p < 0.001). No fall in skill performance was seen with caffeine doses of 1 or 5 mg/kg, and the two doses were not significantly different in effect. Similarly, no deficit was seen with creatine administration at 50 or 100 mg/kg and the performance effects were not significantly different. Salivary testosterone was not affected by sleep deprivation, but trended higher with the 100 mg/kg creatine dose, compared to the placebo treatment (p = 0.067). Salivary cortisol was elevated (p = 0.001) with the 5 mg/kg dose of caffeine (vs. placebo). Conclusion Acute sleep deprivation affects performance of a simple repeat skill in elite athletes and this was ameliorated by a single dose of either caffeine or creatine. Acute creatine use may help to alleviate decrements in skill performance in situations of sleep deprivation, such as transmeridian travel, and caffeine at low doses appears as efficacious as higher doses, at alleviating sleep deprivation deficits in athletes with a history of low caffeine use. Both options are without the side effects of higher dose caffeine use. PMID:21324203

  14. Skill execution and sleep deprivation: effects of acute caffeine or creatine supplementation - a randomized placebo-controlled trial.

    PubMed

    Cook, Christian J; Crewther, Blair T; Kilduff, Liam P; Drawer, Scott; Gaviglio, Chris M

    2011-02-16

    We investigated the effects of sleep deprivation with or without acute supplementation of caffeine or creatine on the execution of a repeated rugby passing skill. Ten elite rugby players completed 10 trials on a simple rugby passing skill test (20 repeats per trial), following a period of familiarisation. The players had between 7-9 h sleep on 5 of these trials and between 3-5 h sleep (deprivation) on the other 5. At a time of 1.5 h before each trial, they undertook administration of either: placebo tablets, 50 or 100 mg/kg creatine, 1 or 5 mg/kg caffeine. Saliva was collected before each trial and assayed for salivary free cortisol and testosterone. Sleep deprivation with placebo application resulted in a significant fall in skill performance accuracy on both the dominant and non-dominant passing sides (p < 0.001). No fall in skill performance was seen with caffeine doses of 1 or 5 mg/kg, and the two doses were not significantly different in effect. Similarly, no deficit was seen with creatine administration at 50 or 100 mg/kg and the performance effects were not significantly different. Salivary testosterone was not affected by sleep deprivation, but trended higher with the 100 mg/kg creatine dose, compared to the placebo treatment (p = 0.067). Salivary cortisol was elevated (p = 0.001) with the 5 mg/kg dose of caffeine (vs. placebo). Acute sleep deprivation affects performance of a simple repeat skill in elite athletes and this was ameliorated by a single dose of either caffeine or creatine. Acute creatine use may help to alleviate decrements in skill performance in situations of sleep deprivation, such as transmeridian travel, and caffeine at low doses appears as efficacious as higher doses, at alleviating sleep deprivation deficits in athletes with a history of low caffeine use. Both options are without the side effects of higher dose caffeine use.

  15. Possible involvement of GABAergic mechanism in protective effect of melatonin against sleep deprivation-induced behaviour modification and oxidative damage in mice.

    PubMed

    Kumar, Anil; Singh, Anant

    2009-08-01

    Sleep is an important physiological process responsible for the maintenance of physical, mental and emotional health of a living being. Sleep deprivation is considered risky for several pathological diseases such as anxiety and motor and cognitive dysfunctions. Sleep deprivation has recently been reported to cause oxidative damage. This study has been designed to explore the possible involvement of the GABAergic mechanism in protective effects of melatonin against 72-h sleep deprivation-induced behaviour modification and oxidative damage in mice. Mice were sleep-deprived for a period of 72 h using the grid over water suspended method. Animals were divided into groups of 6-8 animals each. Melatonin (5 and 10 mg/kg), flumazenil (0.5 mg/kg), picrotoxin (0.5 mg/kg) and muscimol (0.05 mg/kg) were administered for 5 days starting 2 days before 72-h sleep deprivation. Various behavioural tests (plus maze, zero maze, mirror chamber, actophotometer) and body weight assessment followed by oxidative stress parameters (malondialdehyde level, glutathione, catalase, nitrite and protein) were carried out. The 72-h sleep deprivation caused significant anxiety-like behaviour, weight loss, impaired locomotor activity and oxidative damage as compared with naïve (without sleep deprivation). Treatment with melatonin (5 mg/kg and 10 mg/kg, ip) significantly improved locomotor activity, weight loss and antianxiety effect as compared with control (sleep-deprived). Biochemically, melatonin treatment significantly restored reduced glutathione, catalase activity, attenuated lipid peroxidation and nitrite level as compared with control animals (72-h sleep-deprived). Flumazenil (0.5 mg/kg) and picrotoxin (0.5 mg/kg) pretreatments with a lower dose of melatonin (5 mg/kg) significantly antagonized the protective effect of melatonin. However, muscimol (0.05 mg/kg) pretreatment with melatonin (5 mg/kg, ip) potentiated the protective effect of melatonin which was significant as compared with their

  16. Adenosine, caffeine, and performance: from cognitive neuroscience of sleep to sleep pharmacogenetics.

    PubMed

    Urry, Emily; Landolt, Hans-Peter

    2015-01-01

    An intricate interplay between circadian and sleep-wake homeostatic processes regulate cognitive performance on specific tasks, and individual differences in circadian preference and sleep pressure may contribute to individual differences in distinct neurocognitive functions. Attentional performance appears to be particularly sensitive to time of day modulations and the effects of sleep deprivation. Consistent with the notion that the neuromodulator, adenosine , plays an important role in regulating sleep pressure, pharmacologic and genetic data in animals and humans demonstrate that differences in adenosinergic tone affect sleepiness, arousal and vigilant attention in rested and sleep-deprived states. Caffeine--the most often consumed stimulant in the world--blocks adenosine receptors and normally attenuates the consequences of sleep deprivation on arousal, vigilance, and attention. Nevertheless, caffeine cannot substitute for sleep, and is virtually ineffective in mitigating the impact of severe sleep loss on higher-order cognitive functions. Thus, the available evidence suggests that adenosinergic mechanisms, in particular adenosine A2A receptor-mediated signal transduction, contribute to waking-induced impairments of attentional processes, whereas additional mechanisms must be involved in higher-order cognitive consequences of sleep deprivation. Future investigations should further clarify the exact types of cognitive processes affected by inappropriate sleep. This research will aid in the quest to better understand the role of different brain systems (e.g., adenosine and adenosine receptors) in regulating sleep, and sleep-related subjective state, and cognitive processes. Furthermore, it will provide more detail on the underlying mechanisms of the detrimental effects of extended wakefulness, as well as lead to the development of effective, evidence-based countermeasures against the health consequences of circadian misalignment and chronic sleep restriction.

  17. Hippocampal CA1 Transcriptional Profile of Sleep Deprivation: Relation to Aging and Stress

    PubMed Central

    Porter, Nada M.; Bohannon, Julia H.; Curran-Rauhut, Meredith; Buechel, Heather M.; Dowling, Amy L. S.; Brewer, Lawrence D.; Popovic, Jelena; Thibault, Veronique; Kraner, Susan D.; Chen, Kuey Chu; Blalock, Eric M.

    2012-01-01

    Background Many aging changes seem similar to those elicited by sleep-deprivation and psychosocial stress. Further, sleep architecture changes with age suggest an age-related loss of sleep. Here, we hypothesized that sleep deprivation in young subjects would elicit both stress and aging-like transcriptional responses. Methodology/Principal Findings F344 rats were divided into control and sleep deprivation groups. Body weight, adrenal weight, corticosterone level and hippocampal CA1 transcriptional profiles were measured. A second group of animals was exposed to novel environment stress (NES), and their hippocampal transcriptional profiles measured. A third cohort exposed to control or SD was used to validate transcriptional results with Western blots. Microarray results were statistically contrasted with prior transcriptional studies. Microarray results pointed to sleep pressure signaling and macromolecular synthesis disruptions in the hippocampal CA1 region. Animals exposed to NES recapitulated nearly one third of the SD transcriptional profile. However, the SD -aging relationship was more complex. Compared to aging, SD profiles influenced a significant subset of genes. mRNA associated with neurogenesis and energy pathways showed agreement between aging and SD, while immune, glial, and macromolecular synthesis pathways showed SD profiles that opposed those seen in aging. Conclusions/Significance We conclude that although NES and SD exert similar transcriptional changes, selective presynaptic release machinery and Homer1 expression changes are seen in SD. Among other changes, the marked decrease in Homer1 expression with age may represent an important divergence between young and aged brain response to SD. Based on this, it seems reasonable to conclude that therapeutic strategies designed to promote sleep in young subjects may have off-target effects in the aged. Finally, this work identifies presynaptic vesicular release and intercellular adhesion molecular

  18. Sleep deprivation in resident physicians, work hour limitations, and related outcomes: a systematic review of the literature.

    PubMed

    Mansukhani, Meghna P; Kolla, Bhanu Prakash; Surani, Salim; Varon, Joseph; Ramar, Kannan

    2012-07-01

    Extended work hours, interrupted sleep, and shift work are integral parts of medical training among all specialties. The need for 24-hour patient care coverage and economic factors have resulted in prolonged work hours for resident physicians. This has traditionally been thought to enhance medical educational experience. These long and erratic work hours lead to acute and chronic sleep deprivation and poor sleep quality, resulting in numerous adverse consequences. Impairments may occur in several domains, including attention, cognition, motor skills, and mood. Resident performance, professionalism, safety, and well-being are affected by sleep deprivation, causing potentially adverse implications for patient care. Studies have shown adverse health consequences, motor vehicle accidents, increased alcohol and medication use, and serious medical errors to occur in association with both sleep deprivation and shift work. Resident work hour limitations have been mandated by the Accreditation Council for Graduate Medical Education in response to patient safety concerns. Studies evaluating the impact of these regulations on resident physicians have generated conflicting reports on patient outcomes, demonstrating only a modest increase in sleep duration for resident physicians, along with negative perceptions regarding their education. This literature review summarizes research on the effects of sleep deprivation and shift work, and examines current literature on the impact of recent work hour limitations on resident physicians and patient-related outcomes.

  19. Acute Effects of 24-h Sleep Deprivation on Salivary Cortisol and Testosterone Concentrations and Testosterone to Cortisol Ratio Following Supplementation with Caffeine or Placebo

    PubMed Central

    DONALD, CIARAN MC; MOORE, JOSS; MCINTYRE, ALAN; CARMODY, KEVIN; DONNE, BERNARD

    2017-01-01

    Caffeine has become a popular ergogenic aid amongst athletes and usage to improve athletic performance has been well documented. The effect of caffeine on anabolic and catabolic hormones in a sleep-deprived s tate has had little investigation to date. The purpose of the current study was to investigate the potential of caffeine to offset the effects, if any, of short-term sleep deprivation and exercise on an athlete’s testosterone and cortisol concentrations via salivary technique. Eleven competitive male athletes volunteered to be part of this prospective double-blinded study. Three test days were scheduled for each athlete; one non-sleep deprived, one sleep-deprived with caffeine supplementation (6 mg.kg−1) and one sleep-deprived with placebo ingestion. Sleep deprivation was defined as 24-h without sleep. Each test day was composed of 2 aerobic components: a modified Hoff test and a Yo-Yo test. Testosterone and cortisol concentrations were measured via salivary analysis at 4 different time-points; T1 to T4, representing baseline, and pre- and post-aerobic components, respectively. Overall no significant differences were detected comparing the different sleep states for testosterone or cortisol concentrations. A trend existed whereby the sleep-deprived with caffeine ingestion state mirrored the non-sleep deprived state for cortisol concentration. Therefore, caffeine supplementation may have potential benefits for athletes during short-term aerobic exercise when sleep-deprived. An increase in mean testosterone concentration post-aerobic exercise was only observed in the sleep-deprived with caffeine ingestion state. PMID:28479951

  20. Sleep deprivation attenuates endotoxin-induced cytokine gene expression independent of day length and circulating cortisol in male Siberian hamsters (Phodopus sungorus).

    PubMed

    Ashley, Noah T; Walton, James C; Haim, Achikam; Zhang, Ning; Prince, Laura A; Fruchey, Allison M; Lieberman, Rebecca A; Weil, Zachary M; Magalang, Ulysses J; Nelson, Randy J

    2013-07-15

    Sleep is restorative, whereas reduced sleep leads to negative health outcomes, such as increased susceptibility to disease. Sleep deprivation tends to attenuate inflammatory responses triggered by infection or exposure to endotoxin, such as bacterial lipopolysaccharide (LPS). Previous studies have demonstrated that Siberian hamsters (Phodopus sungorus), photoperiodic rodents, attenuate LPS-induced fever, sickness behavior and upstream pro-inflammatory gene expression when adapted to short day lengths. Here, we tested whether manipulation of photoperiod alters the suppressive effects of sleep deprivation upon cytokine gene expression after LPS challenge. Male Siberian hamsters were adapted to long (16 h:8 h light:dark) or short (8 h:16 h light:dark) photoperiods for >10 weeks, and were deprived of sleep for 24 h using the multiple platform method or remained in their home cage. Hamsters received an intraperitoneal injection of LPS or saline (control) 18 h after starting the protocol, and were killed 6 h later. LPS increased liver and hypothalamic interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF) gene expression compared with vehicle. Among LPS-challenged hamsters, sleep deprivation reduced IL-1 mRNA levels in liver and hypothalamus, but not TNF. IL-1 attenuation was independent of circulating baseline cortisol, which did not increase after sleep deprivation. Conversely, photoperiod altered baseline cortisol, but not pro-inflammatory gene expression in sleep-deprived hamsters. These results suggest that neither photoperiod nor glucocorticoids influence the suppressive effect of sleep deprivation upon LPS-induced inflammation.

  1. What are the effects of sleep deprivation and fatigue in surgical practice?

    PubMed

    Sugden, Colin; Athanasiou, Thanos; Darzi, Ara

    2012-01-01

    Sleep deprivation and fatigue have long been linked with accidents in high-risk industries and serious errors in the medical profession, but their effects on surgical performance are less well understood. This article outlines the important functions that human sleep serves and describes the neurobehavioral effects of wakefulness extension and mental fatigue that are relevant to surgical performance, including attentional failure, risk taking, and decision-making bias. Methods used to explore the effects of sleep deprivation and fatigue on surgical performance, from laboratory studies to outcomes data, are discussed; the findings are summarized; and important deficiencies in the literature are highlighted. Future strategies to mitigate performance decline, such as novel assessment tools and countermeasures with proven efficacy, are presented, and their deployment is discussed in the context of key ethical principles. Copyright © 2012 Elsevier Inc. All rights reserved.

  2. The Neuroprotective Aspects of Sleep.

    PubMed

    Eugene, Andy R; Masiak, Jolanta

    2015-03-01

    Sleep is an important component of human life, yet many people do not understand the relationship between the brain and the process of sleeping. Sleep has been proven to improve memory recall, regulate metabolism, and reduce mental fatigue. A minimum of 7 hours of daily sleep seems to be necessary for proper cognitive and behavioral function. The emotional and mental handicaps associated with chronic sleep loss as well as the highly hazardous situations which can be contributed to the lack of sleep is a serious concern that people need to be aware of. When one sleeps, the brain reorganizes and recharges itself, and removes toxic waste byproducts which have accumulated throughout the day. This evidence demonstrates that sleeping can clear the brain and help maintain its normal functioning. Multiple studies have been done to determine the effects of total sleep deprivation; more recently some have been conducted to show the effects of sleep restriction, which is a much more common occurrence, have the same effects as total sleep deprivation. Each phase of the sleep cycle restores and rejuvenates the brain for optimal function. When sleep is deprived, the active process of the glymphatic system does not have time to perform that function, so toxins can build up, and the effects will become apparent in cognitive abilities, behavior, and judgment. As a background for this paper we have reviewed literature and research of sleep phases, effects of sleep deprivation, and the glymphatic system of the brain and its restorative effect during the sleep cycle.

  3. The Neuroprotective Aspects of Sleep

    PubMed Central

    Eugene, Andy R.; Masiak, Jolanta

    2015-01-01

    Sleep is an important component of human life, yet many people do not understand the relationship between the brain and the process of sleeping. Sleep has been proven to improve memory recall, regulate metabolism, and reduce mental fatigue. A minimum of 7 hours of daily sleep seems to be necessary for proper cognitive and behavioral function. The emotional and mental handicaps associated with chronic sleep loss as well as the highly hazardous situations which can be contributed to the lack of sleep is a serious concern that people need to be aware of. When one sleeps, the brain reorganizes and recharges itself, and removes toxic waste byproducts which have accumulated throughout the day. This evidence demonstrates that sleeping can clear the brain and help maintain its normal functioning. Multiple studies have been done to determine the effects of total sleep deprivation; more recently some have been conducted to show the effects of sleep restriction, which is a much more common occurrence, have the same effects as total sleep deprivation. Each phase of the sleep cycle restores and rejuvenates the brain for optimal function. When sleep is deprived, the active process of the glymphatic system does not have time to perform that function, so toxins can build up, and the effects will become apparent in cognitive abilities, behavior, and judgment. As a background for this paper we have reviewed literature and research of sleep phases, effects of sleep deprivation, and the glymphatic system of the brain and its restorative effect during the sleep cycle. PMID:26594659

  4. Effects of Sleep Deprivation on the Cognitive Performance of Nurses Working in Shift.

    PubMed

    Kaliyaperumal, Deepalakshmi; Elango, Yaal; Alagesan, Murali; Santhanakrishanan, Iswarya

    2017-08-01

    Sleep deprivation and altered circadian rhythm affects the cognitive performance of an individual. Quality of sleep is compromised in those who are frequently involved in extended working hours and shift work which is found to be more common among nurses. Cognitive impairment leads to fatigability, decline in attention and efficiency in their workplace which puts their health and patients' health at risk. To find out the prevalence of sleep deprivation and its impact on cognition among shift working nurses. Sleep deprivation among 97 female and three male healthy nurses of age 20-50 years was assessed by Epworth sleepiness scale (ESS). Cognition was assessed by Montreal Cognitive Assessment (MoCA) questionnaire. Mobile applications were used to test their vigilance, reaction time, photographic memory and numerical cognition. The above said parameters were assessed during end of day shift and 3-4 days after start of night shift. Poor sleep quality was observed among 69% of shift working nurses according to ESS scores. The cognitive performance was analysed using Wilcoxon signed rank test. The MoCA score was found to be lesser among 66% of nurses during night (25.72) than day (26.81). During the night, 32% made more mathematical errors. It was also found that, 71%, 83% and 68% of the nurses scored lesser during night in the Stroop's colour test, vigilance test and memory tests respectively. Thus, impairment in cognitive performance was statistically significant (p<0.001) among shift working nurses. Cognitive performance was found to be impaired among shift working nurses, due to poor sleep quality and decreased alertness during wake state. Thus, shift work poses significant cognitive risks in work performance of nurses.

  5. Effect of bright light on EEG activities and subjective sleepiness to mental task during nocturnal sleep deprivation.

    PubMed

    Yokoi, Mari; Aoki, Ken; Shimomura, Yoshihiro; Iwanaga, Koichi; Katsuura, Tetsuo; Shiomura, Yoshihiro

    2003-11-01

    The purpose of this study was to investigate the effect of the exposure to bright light on EEG activity and subjective sleepiness at rest and at the mental task during nocturnal sleep deprivation. Eight male subjects lay awake in semi-supine in a reclining seat from 21:00 to 04:30 under the bright (BL; >2500 lux) or the dim (DL; <150 lux) light conditions. During the sleep deprivation, the mental task (Stroop color-word conflict test: CWT) was performed each 15 min in one hour. EEG, subjective sleepiness, rectal and mean skin temperatures and urinary melatonin concentrations were measured. The subjective sleepiness increased with time of sleep deprivation during both rest and CWT under the DL condition. The exposure to bright light delayed for 2 hours the increase in subjective sleepiness at rest and suppressed the increase in that during CWT. The bright light exposure also delayed the increase in the theta and alpha wave activities in EEG at rest. In contrast, the effect of the bright light exposure on the theta and alpha wave activities disappeared by CWT. Additionally, under the BL condition, the entire theta activity during CWT throughout nocturnal sleep deprivation increased significantly from that in a rest condition. Our results suggest that the exposure to bright light throughout nocturnal sleep deprivation influences the subjective sleepiness during the mental task and the EEG activity, as well as the subjective sleepiness at rest. However, the effect of the bright light exposure on the EEG activity at the mental task diminishes throughout nocturnal sleep deprivation.

  6. Moderate sleep deprivation produces impairments in cognitive and motor performance equivalent to legally prescribed levels of alcohol intoxication

    PubMed Central

    Williamson, A; Feyer, A.

    2000-01-01

    OBJECTIVES—To compare the relative effects on performance of sleep deprivation and alcohol.
METHODS—Performance effects were studied in the same subjects over a period of 28 hours of sleep deprivation and after measured doses of alcohol up to about 0.1% blood alcohol concentration (BAC). There were 39 subjects, 30 employees from the transport industry and nine from the army.
RESULTS—After 17-19 hours without sleep, corresponding to 2230 and 0100, performance on some tests was equivalent or worse than that at a BAC of 0.05%. Response speeds were up to 50% slower for some tests and accuracy measures were significantly poorer than at this level of alcohol. After longer periods without sleep, performance reached levels equivalent to the maximum alcohol dose given to subjects (BAC of 0.1%).
CONCLUSIONS—These findings reinforce the evidence that the fatigue of sleep deprivation is an important factor likely to compromise performance of speed and accuracy of the kind needed for safety on the road and in other industrial settings.


Keywords: sleep deprivation; performance; alcohol PMID:10984335

  7. Sleep deprivation, low self-control, and delinquency: a test of the strength model of self-control.

    PubMed

    Meldrum, Ryan C; Barnes, J C; Hay, Carter

    2015-02-01

    Recent work provides evidence that sleep deprivation is positively related to delinquency. In this study, we draw on Baumeister and colleagues' strength model of self-control to propose an explanation for this association. Specifically, we argue that low self-control is the construct that bridges the relationship between sleep deprivation and delinquency. To test the proposed model, we examine survey data drawn from a longitudinal multi-city cohort study of adolescents who were followed from birth through age 15 (N = 825; 50% female; 82% non-Hispanic white, 59% two-parent nuclear family). The results from regression models using latent factors indicate: sleep deprivation is positively related to low self-control; low self-control is positively related to delinquency; and the relationship between sleep deprivation and delinquency is indirect and operates through low self-control. Impressively, these relationships emerged when accounting for potential background sources of spuriousness, including neighborhood context, depressive symptoms, parenting practices, unstructured socializing with peers, and prior delinquency. Implications and directions for future research are discussed.

  8. Partial sleep deprivation activates the DNA damage response (DDR) and the senescence-associated secretory phenotype (SASP) in aged adult humans.

    PubMed

    Carroll, Judith E; Cole, Steven W; Seeman, Teresa E; Breen, Elizabeth C; Witarama, Tuff; Arevalo, Jesusa M G; Ma, Jeffrey; Irwin, Michael R

    2016-01-01

    Age-related disease risk has been linked to short sleep duration and sleep disturbances; however, the specific molecular pathways linking sleep loss with diseases of aging are poorly defined. Key cellular events seen with aging, which are thought to contribute to disease, may be particularly sensitive to sleep loss. We tested whether one night of partial sleep deprivation (PSD) would increase leukocyte gene expression indicative of DNA damage responses (DDR), the senescence-associated secretory phenotype (SASP), and senescence indicator p16(INK4a) in older adult humans, who are at increased risk for cellular senescence. Community-dwelling older adults aged 61-86years (n=29; 48% male) underwent an experimental partial sleep deprivation (PSD) protocol over 4 nights, including adaptation, an uninterrupted night of sleep, partial sleep deprivation (sleep restricted 3-7AM), and a subsequent full night of sleep. Blood samples were obtained each morning to assess peripheral blood mononuclear cell (PBMC) gene expression using Illumina HT-12 arrays. Analyses of microarray results revealed that SASP (p<.05) and DDR (p=.08) gene expression were elevated from baseline to PSD nights. Gene expression changes were also observed from baseline to PSD in NFKB2, NBS1 and CHK2 (all p's<.05). The senescence marker p16(INK4a) (CDKN2A) was increased 1day after PSD compared to baseline (p<.01), however confirmatory RT-PCR did not replicate this finding. One night of partial sleep deprivation activates PBMC gene expression patterns consistent with biological aging in this older adult sample. PSD enhanced the SASP and increased the accumulation of damage that initiates cell cycle arrest and promotes cellular senescence. These findings causally link sleep deprivation to the molecular processes associated with biological aging. Copyright © 2015 Elsevier Inc. All rights reserved.

  9. Role of Sleep Deprivation in Fear Conditioning and Extinction: Implications for Treatment of PTSD

    DTIC Science & Technology

    2015-12-01

    and distressing symptoms of PTSD are insomnia and nightmares. The resultant sleep deprivation may actually serve to perpetuate the disorder by...Posttraumatic Stress Disorder (PTSD). Such models have shown fear conditioning disrupts subsequent Rapid Eye Movement Sleep (REM). Here, we provide a

  10. Role of REM Sleep, Melanin Concentrating Hormone and Orexin/Hypocretin Systems in the Sleep Deprivation Pre-Ischemia

    PubMed Central

    Pace, Marta; Adamantidis, Antoine; Facchin, Laura; Bassetti, Claudio

    2017-01-01

    Study Objectives Sleep reduction after stroke is linked to poor recovery in patients. Conversely, a neuroprotective effect is observed in animals subjected to acute sleep deprivation (SD) before ischemia. This neuroprotection is associated with an increase of the sleep, melanin concentrating hormone (MCH) and orexin/hypocretin (OX) systems. This study aims to 1) assess the relationship between sleep and recovery; 2) test the association between MCH and OX systems with the pathological mechanisms of stroke. Methods Sprague-Dawley rats were assigned to four experimental groups: (i) SD_IS: SD performed before ischemia; (ii) IS: ischemia; (iii) SD_Sham: SD performed before sham surgery; (iv) Sham: sham surgery. EEG and EMG were recorded. The time-course of the MCH and OX gene expression was measured at 4, 12, 24 hours and 3, 4, 7 days following ischemic surgery by qRT-PCR. Results A reduction of infarct volume was observed in the SD_IS group, which correlated with an increase of REM sleep observed during the acute phase of stroke. Conversely, the IS group showed a reduction of REM sleep. Furthermore, ischemia induces an increase of MCH and OX systems during the acute phase of stroke, although, both systems were still increased for a long period of time only in the SD_IS group. Conclusions Our data indicates that REM sleep may be involved in the neuroprotective effect of SD pre-ischemia, and that both MCH and OX systems were increased during the acute phase of stroke. Future studies should assess the role of REM sleep as a prognostic marker, and test MCH and OXA agonists as new treatment options in the acute phase of stroke. PMID:28061506

  11. Frontal Underactivation During Working Memory Processing in Adults With Acute Partial Sleep Deprivation: A Near-Infrared Spectroscopy Study.

    PubMed

    Yeung, Michael K; Lee, Tsz L; Cheung, Winnie K; Chan, Agnes S

    2018-01-01

    Individuals with partial sleep deprivation may have working memory (WM) impairment, but the underlying neural mechanism of this phenomenon is relatively unknown. The present study examined neural processing during WM performance in individuals with and without partial sleep deprivation using near-infrared spectroscopy (NIRS). Forty college students (10 males) were equally split into Sufficient Sleep (SS) and Insufficient Sleep (IS) groups based on self-reports of previous night's sleep duration. Participants in the SS group obtained the recommended amounts of sleep according to various sleep organizations (i.e., >7.0 h), whereas those in the IS group obtained amounts of sleep no greater than the lower limit of the recommendation (i.e., ≤7.0 h). All participants underwent an n -back paradigm with a WM load (i.e., 3-back) and a control condition (i.e., 0-back) while their prefrontal hemodynamics were recorded by NIRS. The IS and SS groups performed the tasks comparably well. However, unlike the SS group, which exhibited bilateral frontal activation indicated by increased oxyhemoglobin concentration and decreased deoxyhemoglobin concentration during WM processing (i.e., 3-back > 0-back), the IS group did not exhibit such activation. In addition, levels of WM-related frontal activation, especially those on the left side, correlated with sleep duration the night before, even when habitual sleep duration was controlled for. The findings suggest the presence of frontal lobe dysfunction in the absence of evident WM difficulties in individuals with acute partial sleep deprivation. They also highlight the importance of a good night's sleep to brain health.

  12. Gray Matter-Specific Changes in Brain Bioenergetics after Acute Sleep Deprivation: A 31P Magnetic Resonance Spectroscopy Study at 4 Tesla

    PubMed Central

    Plante, David T.; Trksak, George H.; Jensen, J. Eric; Penetar, David M.; Ravichandran, Caitlin; Riedner, Brady A.; Tartarini, Wendy L.; Dorsey, Cynthia M.; Renshaw, Perry F.; Lukas, Scott E.; Harper, David G.

    2014-01-01

    Study Objectives: A principal function of sleep may be restoration of brain energy metabolism caused by the energetic demands of wakefulness. Because energetic demands in the brain are greater in gray than white matter, this study used linear mixed-effects models to examine tissue-type specific changes in high-energy phosphates derived using 31P magnetic resonance spectroscopy (MRS) after sleep deprivation and recovery sleep. Design: Experimental laboratory study. Setting: Outpatient neuroimaging center at a private psychiatric hospital. Participants: A total of 32 MRS scans performed in eight healthy individuals (mean age 35 y; range 23-51 y). Interventions: Phosphocreatine (PCr) and β-nucleoside triphosphate (NTP) were measured using 31P MRS three dimensional-chemical shift imaging at high field (4 Tesla) after a baseline night of sleep, acute sleep deprivation, and 2 nights of recovery sleep. Novel linear mixed-effects models were constructed using spectral and tissue segmentation data to examine changes in bioenergetics in gray and white matter. Measurements and Results: PCr increased in gray matter after 2 nights of recovery sleep relative to sleep deprivation with no significant changes in white matter. Exploratory analyses also demonstrated that increases in PCr were associated with increases in electroencephalographic slow wave activity during recovery sleep. No significant changes in β-NTP were observed. Conclusions: These results demonstrate that sleep deprivation and subsequent recovery-induced changes in high-energy phosphates primarily occur in gray matter, and increases in phosphocreatine after recovery sleep may be related to sleep homeostasis. Citation: Plante DT, Trksak GH, Jensen JE, Penetar DM, Ravichandran C, Riedner BA, Tartarini WL, Dorsey CM, Renshaw PF, Lukas SE, Harper DG. Gray matter-specific changes in brain bioenergetics after acute sleep deprivation: a 31P magnetic resonance spectroscopy study at 4 Tesla. SLEEP 2014

  13. Oxidative stress, cancer, and sleep deprivation: is there a logical link in this association?

    PubMed

    Noguti, Juliana; Andersen, Monica Levy; Cirelli, Chiara; Ribeiro, Daniel Araki

    2013-09-01

    Sleep disorders are associated with various human pathologies and interfere with biological processes essential for health and quality of life. On the other hand, cancer is one of the most common diseases worldwide with an average of 1,500 deaths per day in the USA. Is there a factor common to both sleep disorders and cancer that serves to link these conditions? It is a normal process for cellular metabolism to produce reactive oxidant series (ROS). However, when the production of ROS overcomes the antioxidant capacity of the cell to eliminate these products, the resulting state is called oxidative stress. Oxidative DNA damage may participate in ROS-induced carcinogenesis. Moreover, ROS are also produced in the sleep deprivation process. The aim of this article is to review pathways and mechanisms that may point to oxidative stress as a link between sleep deprivation and cancer.

  14. Sleep in Othello

    PubMed Central

    Dimsdale, Joel E.

    2009-01-01

    Some of our best descriptions of sleep disorders come from literature. While Shakespeare is well known for his references to insomnia and sleep walking, his works also demonstrate a keen awareness of many other sleep disorders. This paper examines sleep themes in Shakespeare's play Othello. The play indicates Shakespeare's astute eye for sleep deprivation, sexual parasomnias, and effects of stress and drugs on sleep. Citation: Dimsdale JE. Sleep in Othello. J Clin Sleep Med 2009;5(3):280-281. PMID:19960651

  15. Sleep: A Health Imperative

    PubMed Central

    Luyster, Faith S.; Strollo, Patrick J.; Zee, Phyllis C.; Walsh, James K.

    2012-01-01

    Chronic sleep deficiency, defined as a state of inadequate or mistimed sleep, is a growing and underappreciated determinant of health status. Sleep deprivation contributes to a number of molecular, immune, and neural changes that play a role in disease development, independent of primary sleep disorders. These changes in biological processes in response to chronic sleep deficiency may serve as etiological factors for the development and exacerbation of cardiovascular and metabolic diseases and, ultimately, a shortened lifespan. Sleep deprivation also results in significant impairments in cognitive and motor performance which increase the risk of motor vehicle crashes and work-related injuries and fatal accidents. The American Academy of Sleep Medicine and the Sleep Research Society have developed this statement to communicate to national health stakeholders the current knowledge which ties sufficient sleep and circadian alignment in adults to health. Citation: Luyster FS; Strollo PJ; Zee PC; Walsh JK. Sleep: a health imperative. SLEEP 2012;35(6):727-734. PMID:22654183

  16. Validation of sleep-2-Peak: A smartphone application that can detect fatigue-related changes in reaction times during sleep deprivation.

    PubMed

    Brunet, Jean-François; Dagenais, Dominique; Therrien, Marc; Gartenberg, Daniel; Forest, Geneviève

    2017-08-01

    Despite its high sensitivity and validity in the context of sleep loss, the Psychomotor Vigilance Test (PVT) could be improved. The aim of the present study was to validate a new smartphone PVT-type application called sleep-2-Peak (s2P) by determining its ability to assess fatigue-related changes in alertness in a context of extended wakefulness. Short 3-min versions of s2P and of the classic PVT were administered at every even hour during a 35-h total sleep deprivation protocol. In addition, subjective measures of sleepiness were collected. The outcomes on these tests were then compared using Pearson product-moment correlations, t tests, and repeated measures within-groups analyses of variance. The results showed that both tests significantly correlated on all outcome variables, that both significantly distinguished between the alert and sleepy states in the same individual, and that both varied similarly through the sleep deprivation protocol as sleep loss accumulated. All outcome variables on both tests also correlated significantly with the subjective measures of sleepiness. These results suggest that a 3-min version of s2P is a valid tool for differentiating alert from sleepy states and is as sensitive as the PVT for tracking fatigue-related changes during extended wakefulness and sleep loss. Unlike the PVT, s2P does not provide feedback to subjects on each trial. We discuss how this feature of s2P raises the possibility that the performance results measured by s2P could be less impacted by motivational confounds, giving this tool added value in particular clinical and/or research settings.

  17. Spatial and reversal learning in the Morris water maze are largely resistant to six hours of REM sleep deprivation following training

    PubMed Central

    Walsh, Christine M.; Booth, Victoria; Poe, Gina R.

    2011-01-01

    This first test of the role of REM (rapid eye movement) sleep in reversal spatial learning is also the first attempt to replicate a much cited pair of papers reporting that REM sleep deprivation impairs the consolidation of initial spatial learning in the Morris water maze. We hypothesized that REM sleep deprivation following training would impair both hippocampus-dependent spatial learning and learning a new target location within a familiar environment: reversal learning. A 6-d protocol was divided into the initial spatial learning phase (3.5 d) immediately followed by the reversal phase (2.5 d). During the 6 h following four or 12 training trials/day of initial or reversal learning phases, REM sleep was eliminated and non-REM sleep left intact using the multiple inverted flowerpot method. Contrary to our hypotheses, REM sleep deprivation during four or 12 trials/day of initial spatial or reversal learning did not affect training performance. However, some probe trial measures indicated REM sleep-deprivation–associated impairment in initial spatial learning with four trials/day and enhancement of subsequent reversal learning. In naive animals, REM sleep deprivation during normal initial spatial learning was followed by a lack of preference for the subsequent reversal platform location during the probe. Our findings contradict reports that REM sleep is essential for spatial learning in the Morris water maze and newly reveal that short periods of REM sleep deprivation do not impair concurrent reversal learning. Effects on subsequent reversal learning are consistent with the idea that REM sleep serves the consolidation of incompletely learned items. PMID:21677190

  18. Socializing by Day May Affect Performance by Night: Vulnerability to Sleep Deprivation is Differentially Mediated by Social Exposure in Extraverts vs Introverts

    PubMed Central

    Rupp, Tracy L.; Killgore, William D.S.; Balkin, Thomas J.

    2010-01-01

    Study Objectives: To examine the effects of socially enriched versus socially impoverished environments on performance and alertness decline during sleep deprivation in extraverts versus introverts. Design: Participants (n = 29 men, n = 19 women) were assigned to socially enriched (n = 24; 13 introverts, 11 extraverts) or socially impoverished (n = 24; 12 introverts, 12 extraverts) conditions (activities matched) for 12 hours (1000–2200) on Day 1 followed by 22 hours of sleep deprivation (2200-2000; 36 h awake total), monitored by actigraphy. The median split of volunteers' Eysenck Extraversion scores was used for extravert/introvert categorization. The Psychomotor Vigilance Task (PVT), modified Maintenance of Wakefulness Test (MWT), and Stanford Sleepiness Scale (SSS) were administered every 2 hours throughout. PVT speed, transformed lapses, modified MWT sleep-onset latency, and SSS were analyzed using mixed-model analyses of variance, with covariates of age and total actigraphic activity during enrichment or impoverishment. Setting: Residential sleep/performance testing facility. Participants: Forty-eight healthy adults (aged 18–39). Interventions: Twelve hours of socially enriched or isolated environments in extraverts and introverts prior to sleep deprivation. Results Social experience interacted with personality type to affect alertness and vigilance. Social enrichment, as compared with social impoverishment, was associated with more PVT lapses at 04:00 overall. Similarly, following social enrichment, PVT speed was significantly slower among extraverts than among introverts during sleep deprivation, but no personality-group differences emerged following social impoverishment. MWT sleep latency and SSS subjective sleepiness did not show significant personality or social-condition effects during sleep deprivation. Conclusions: The effect of social exposure on vulnerability or resiliency to sleep deprivation was modulated by introversion and extraversion

  19. The role of omega-3 on modulation of cognitive deficiency induced by REM sleep deprivation in rats.

    PubMed

    Nasehi, Mohammad; Nezhad, Seyed Moslem Mousavi; Khakpai, Fatemeh; Zarrindast, Mohammad-Reza

    2018-06-02

    Prolonged sleep deprivation causes cognitive deficits. In rats, for instance, sleep deprivation weakens spatial learning and long-term potentiation (LTP). We examined the effects of omega-3 on cognitive deficiency induced by REM sleep deprivation (RSD). For this purpose, we used a fear conditioning paradigm, forced swim test (FST) apparatus, and hot plate test. Intravenously omega-3 injection was performed during 3 consecutive days. Rats trained in the fear conditioning apparatus after 24 hours. During conditioning, animals were received foot shocks, either alone or paired with a sound. Sleep deprivation paradigm was carried out in which REM sleep was completely prevented and non-REM sleep was intensely declined for 24 hours. Then, context-dependent retention, anxiety behaviors, and hot plate tests were done. Auditory-dependent retention, anxiety behaviors, and FST were carried out 24 hours later. 24 hours of RSD impaired cognitive function, however intravenously administration of omega-3 improved (0.25, 0.5 and 1 mg/kg) context- or auditory-dependent memory, induced anxiolytic (1 mg/kg), antidepressant (1.25 mg/kg), and anti-nociceptive (0.25 mg/kg) effects. The results revealed that RSD interferes with the neural systems underlying cognitive functions and supports the involvement of omega-3 in the modulation of cognitive functions. Copyright © 2018. Published by Elsevier B.V.

  20. Sleep deprivation alters choice strategy without altering uncertainty or loss aversion preferences

    PubMed Central

    Mullette-Gillman, O'Dhaniel A.; Kurnianingsih, Yoanna A.; Liu, Jean C. J.

    2015-01-01

    Sleep deprivation alters decision making; however, it is unclear what specific cognitive processes are modified to drive altered choices. In this manuscript, we examined how one night of total sleep deprivation (TSD) alters economic decision making. We specifically examined changes in uncertainty preferences dissociably from changes in the strategy with which participants engage with presented choice information. With high test-retest reliability, we show that TSD does not alter uncertainty preferences or loss aversion. Rather, TSD alters the information the participants rely upon to make their choices. Utilizing a choice strategy metric which contrasts the influence of maximizing and satisficing information on choice behavior, we find that TSD alters the relative reliance on maximizing information and satisficing information, in the gains domain. This alteration is the result of participants both decreasing their reliance on cognitively-complex maximizing information and a concomitant increase in the use of readily-available satisficing information. TSD did not result in a decrease in overall information use in either domain. These results show that sleep deprivation alters decision making by altering the informational strategies that participants employ, without altering their preferences. PMID:26500479

  1. Creatine supplementation reduces sleep need and homeostatic sleep pressure in rats.

    PubMed

    Dworak, Markus; Kim, Tae; Mccarley, Robert W; Basheer, Radhika

    2017-06-01

    Sleep has been postulated to promote brain energy restoration. It is as yet unknown if increasing the energy availability within the brain reduces sleep need. The guanidine amino acid creatine (Cr) is a well-known energy booster in cellular energy homeostasis. Oral Cr-monohydrate supplementation (CS) increases exercise performance and has been shown to have substantial effects on cognitive performance, neuroprotection and circadian rhythms. The effect of CS on cellular high-energy molecules and sleep-wake behaviour is unclear. Here, we examined the sleep-wake behaviour and brain energy metabolism before and after 4-week-long oral administration of CS in the rat. CS decreased total sleep time and non-rapid eye movement (NREM) sleep significantly during the light (inactive) but not during the dark (active) period. NREM sleep and NREM delta activity were decreased significantly in CS rats after 6 h of sleep deprivation. Biochemical analysis of brain energy metabolites showed a tendency to increase in phosphocreatine after CS, while cellular adenosine triphosphate (ATP) level decreased. Microdialysis analysis showed that the sleep deprivation-induced increase in extracellular adenosine was attenuated after CS. These results suggest that CS reduces sleep need and homeostatic sleep pressure in rats, thereby indicating its potential in the treatment of sleep-related disorders. © 2017 European Sleep Research Society.

  2. TNFα G308A polymorphism is associated with resilience to sleep deprivation-induced psychomotor vigilance performance impairment in healthy young adults.

    PubMed

    Satterfield, Brieann C; Wisor, Jonathan P; Field, Stephanie A; Schmidt, Michelle A; Van Dongen, Hans P A

    2015-07-01

    Cytokines such as TNFα play an integral role in sleep/wake regulation and have recently been hypothesized to be involved in cognitive impairment due to sleep deprivation. We examined the effect of a guanine to adenine substitution at position 308 in the TNFα gene (TNFα G308A) on psychomotor vigilance performance impairment during total sleep deprivation. A total of 88 healthy women and men (ages 22-40) participated in one of five laboratory total sleep deprivation experiments. Performance on a psychomotor vigilance test (PVT) was measured every 2-3h. The TNFα 308A allele, which is less common than the 308G allele, was associated with greater resilience to psychomotor vigilance performance impairment during total sleep deprivation (regardless of time of day), and also provided a small performance benefit at baseline. The effect of genotype on resilience persisted when controlling for between-subjects differences in age, gender, race/ethnicity, and baseline sleep duration. The TNFα G308A polymorphism predicted less than 10% of the overall between-subjects variance in performance impairment during sleep deprivation. Nonetheless, the differential effect of the polymorphism at the peak of performance impairment was more than 50% of median performance impairment at that time, which is sizeable compared to the effects of other genotypes reported in the literature. Our findings provided evidence for a role of TNFα in the effects of sleep deprivation on psychomotor vigilance performance. Furthermore, the TNFα G308A polymorphism may have predictive potential in a biomarker panel for the assessment of resilience to psychomotor vigilance performance impairment due to sleep deprivation. Copyright © 2014 Elsevier Inc. All rights reserved.

  3. In Vivo Imaging of the Central and Peripheral Effects of Sleep Deprivation and Suprachiasmatic Nuclei Lesion on PERIOD-2 Protein in Mice

    PubMed Central

    Curie, Thomas; Maret, Stephanie; Emmenegger, Yann; Franken, Paul

    2015-01-01

    Study Objectives: That sleep deprivation increases the brain expression of various clock genes has been well documented. Based on these and other findings we hypothesized that clock genes not only underlie circadian rhythm generation but are also implicated in sleep homeostasis. However, long time lags have been reported between the changes in the clock gene messenger RNA levels and their encoded proteins. It is therefore crucial to establish whether also protein levels increase within the time frame known to activate a homeostatic sleep response. We report on the central and peripheral effects of sleep deprivation on PERIOD-2 (PER2) protein both in intact and suprachiasmatic nuclei-lesioned mice. Design: In vivo and in situ PER2 imaging during baseline, sleep deprivation, and recovery. Settings: Mouse sleep-recording facility. Participants: Per2::Luciferase knock-in mice. Interventions: N/A. Measurements and Results: Six-hour sleep deprivation increased PER2 not only in the brain but also in liver and kidney. Remarkably, the effects in the liver outlasted those observed in the brain. Within the brain the increase in PER2 concerned the cerebral cortex mainly, while leaving suprachiasmatic nuclei (SCN) levels unaffected. Against expectation, sleep deprivation did not increase PER2 in the brain of arrhythmic SCN-lesioned mice because of higher PER2 levels in baseline. In contrast, liver PER2 levels did increase in these mice similar to the sham and partially lesioned controls. Conclusions: Our results stress the importance of considering both sleep-wake dependent and circadian processes when quantifying clock-gene levels. Because sleep deprivation alters PERIOD-2 in the brain as well as in the periphery, it is tempting to speculate that clock genes constitute a common pathway mediating the shared and well-known adverse effects of both chronic sleep loss and disrupted circadian rhythmicity on metabolic health. Citation: Curie T, Maret S, Emmenegger Y, Franken P. In

  4. Sustained Partial Sleep Deprivation: Effects on Immune Modulation and Growth Factors

    NASA Technical Reports Server (NTRS)

    Mullington, Janet M.

    1999-01-01

    The vulnerability to medical emergencies is greatest in space where there are real limits to the availability or effectiveness of ground based assistance. Moreover, astronaut safety and health maintenance will be of increasing importance as we venture out into space for extended periods of time. It is therefore critical to understand the mechanisms of the regulatory physiology of homeostatic systems (sleep, circadian, neuroendocrine, fluid and nutritional balance) and the key roles played in adaptation. This synergy project has combined aims of the "Human Performance Factors, Sleep and Chronobiology Team"; the "Immunology, Infection and Hematology Team"; and the "Muscle Alterations and Atrophy Team", to broadly address the effects of long term sleep reduction, as is frequently encountered in space exploration, on neuroendocrine, neuroimmune and circulating growth factors. Astronaut sleep is frequently curtailed to averages of between 4- 6.5 hours per night. There is evidence that this amount of sleep is inadequate for maintaining optimal daytime functioning. However, there is a lack of information concerning the effects of chronic sleep restriction, or reduction, on regulatory physiology in general, and there have been no controlled studies of the cumulative effects of chronic sleep reduction on neuroendocrine and neuroimmune parameters. This synergy project represents a pilot study designed to characterize the effects of chronic partial sleep deprivation (PSD) on neuroendocrine, neuroimmune and growth factors. This project draws its subjects from two (of 18) conditions of the larger NSBRI project, "Countermeasures to Neurobehavioral Deficits from Cumulative Partial Sleep Deprivation During Space Flight", one of the projects on the "Human Performance Factors, Sleep and Chronobiology Team ". For the purposes of this study, to investigate the effects of chronic sleep loss on neuroendocrine and neuroimmune function, we have focused on the two extreme sleep conditions

  5. Effects of Sleep Deprivation on Color-Word, Emotional, and Specific Stroop Interference and on Self-Reported Anxiety

    ERIC Educational Resources Information Center

    Sagaspe, Patricia; Sanchez-Ortuno, Montserrat; Charles, Andre; Taillard, Jacques; Valtat, Cedric; Bioulac, Bernard; Philip, Pierre

    2006-01-01

    The aim of this study was principally to assess the impact of sleep deprivation on interference performance in short Stroop tasks (Color-Word, Emotional, and Specific) and on subjective anxiety. Subjective sleepiness and performance on a psychomotor sustained attention task were also investigated to validate our protocol of sleep deprivation.…

  6. Socializing by Day May Affect Performance by Night: Vulnerability to Sleep Deprivation is Differentially Mediated by Social Exposure in Extraverts vs Introverts.

    PubMed

    Rupp, Tracy L; Killgore, William D S; Balkin, Thomas J

    2010-11-01

    to examine the effects of socially enriched versus socially impoverished environments on performance and alertness decline during sleep deprivation in extraverts versus introverts. participants (n = 29 men, n = 19 women) were assigned to socially enriched (n = 24; 13 introverts, 11 extraverts) or socially impoverished (n = 24; 12 introverts, 12 extraverts) conditions (activities matched) for 12 hours (1000-2200) on Day 1 followed by 22 hours of sleep deprivation (2200-2000; 36 h awake total), monitored by actigraphy. The median split of volunteers' Eysenck Extraversion scores was used for extravert/introvert categorization. The Psychomotor Vigilance Task (PVT), modified Maintenance of Wakefulness Test (MWT), and Stanford Sleepiness Scale (SSS) were administered every 2 hours throughout. PVT speed, transformed lapses, modified MWT sleep-onset latency, and SSS were analyzed using mixed-model analyses of variance, with covariates of age and total actigraphic activity during enrichment or impoverishment. residential sleep/performance testing facility. forty-eight healthy adults (aged 18-39). Twelve hours of socially enriched or isolated environments in extraverts and introverts prior to sleep deprivation. Social experience interacted with personality type to affect alertness and vigilance. Social enrichment, as compared with social impoverishment, was associated with more PVT lapses at 04:00 overall. Similarly, following social enrichment, PVT speed was significantly slower among extraverts than among introverts during sleep deprivation, but no personality-group differences emerged following social impoverishment. MWT sleep latency and SSS subjective sleepiness did not show significant personality or social-condition effects during sleep deprivation. the effect of social exposure on vulnerability or resiliency to sleep deprivation was modulated by introversion and extraversion. Extraverts exposed to social environments were more vulnerable to subsequent sleep

  7. Large-Scale Brain Network Coupling Predicts Total Sleep Deprivation Effects on Cognitive Capacity

    PubMed Central

    Wang, Lubin; Zhai, Tianye; Zou, Feng; Ye, Enmao; Jin, Xiao; Li, Wuju; Qi, Jianlin; Yang, Zheng

    2015-01-01

    Interactions between large-scale brain networks have received most attention in the study of cognitive dysfunction of human brain. In this paper, we aimed to test the hypothesis that the coupling strength of large-scale brain networks will reflect the pressure for sleep and will predict cognitive performance, referred to as sleep pressure index (SPI). Fourteen healthy subjects underwent this within-subject functional magnetic resonance imaging (fMRI) study during rested wakefulness (RW) and after 36 h of total sleep deprivation (TSD). Self-reported scores of sleepiness were higher for TSD than for RW. A subsequent working memory (WM) task showed that WM performance was lower after 36 h of TSD. Moreover, SPI was developed based on the coupling strength of salience network (SN) and default mode network (DMN). Significant increase of SPI was observed after 36 h of TSD, suggesting stronger pressure for sleep. In addition, SPI was significantly correlated with both the visual analogue scale score of sleepiness and the WM performance. These results showed that alterations in SN-DMN coupling might be critical in cognitive alterations that underlie the lapse after TSD. Further studies may validate the SPI as a potential clinical biomarker to assess the impact of sleep deprivation. PMID:26218521

  8. Chronic escitalopram treatment attenuated the accelerated rapid eye movement sleep transitions after selective rapid eye movement sleep deprivation: a model-based analysis using Markov chains.

    PubMed

    Kostyalik, Diána; Vas, Szilvia; Kátai, Zita; Kitka, Tamás; Gyertyán, István; Bagdy, Gyorgy; Tóthfalusi, László

    2014-11-19

    Shortened rapid eye movement (REM) sleep latency and increased REM sleep amount are presumed biological markers of depression. These sleep alterations are also observable in several animal models of depression as well as during the rebound sleep after selective REM sleep deprivation (RD). Furthermore, REM sleep fragmentation is typically associated with stress procedures and anxiety. The selective serotonin reuptake inhibitor (SSRI) antidepressants reduce REM sleep time and increase REM latency after acute dosing in normal condition and even during REM rebound following RD. However, their therapeutic outcome evolves only after weeks of treatment, and the effects of chronic treatment in REM-deprived animals have not been studied yet. Chronic escitalopram- (10 mg/kg/day, osmotic minipump for 24 days) or vehicle-treated rats were subjected to a 3-day-long RD on day 21 using the flower pot procedure or kept in home cage. On day 24, fronto-parietal electroencephalogram, electromyogram and motility were recorded in the first 2 h of the passive phase. The observed sleep patterns were characterized applying standard sleep metrics, by modelling the transitions between sleep phases using Markov chains and by spectral analysis. Based on Markov chain analysis, chronic escitalopram treatment attenuated the REM sleep fragmentation [accelerated transition rates between REM and non-REM (NREM) stages, decreased REM sleep residence time between two transitions] during the rebound sleep. Additionally, the antidepressant avoided the frequent awakenings during the first 30 min of recovery period. The spectral analysis showed that the SSRI prevented the RD-caused elevation in theta (5-9 Hz) power during slow-wave sleep. Conversely, based on the aggregate sleep metrics, escitalopram had only moderate effects and it did not significantly attenuate the REM rebound after RD. In conclusion, chronic SSRI treatment is capable of reducing several effects on sleep which might be the consequence

  9. Homeostatic response to sleep/rest deprivation by constant water flow in larval zebrafish in both dark and light conditions.

    PubMed

    Aho, Vilma; Vainikka, Maija; Puttonen, Henri A J; Ikonen, Heidi M K; Salminen, Tiia; Panula, Pertti; Porkka-Heiskanen, Tarja; Wigren, Henna-Kaisa

    2017-06-01

    Sleep-or sleep-like states-have been reported in adult and larval zebrafish using behavioural criteria. These reversible quiescent periods, displaying circadian rhythmicity, have been used in pharmacological, genetic and neuroanatomical studies of sleep-wake regulation. However, one of the important criteria for sleep, namely sleep homeostasis, has not been demonstrated unequivocally. To study rest homeostasis in zebrafish larvae, we rest-deprived 1-week-old larvae with a novel, ecologically relevant method: flow of water. Stereotyped startle responses to sensory stimuli were recorded after the rest deprivation to study arousal threshold using a high-speed camera, providing an appropriate time resolution to detect species-specific behavioural responses occurring in a millisecond time-scale. Rest-deprived larvae exhibited fewer startle responses than control larvae during the remaining dark phase and the beginning of the light phase, which can be interpreted as a sign of rest homeostasis-often used as equivalent of sleep homeostasis. To address sleep homeostasis further, we probed the adenosinergic system, which in mammals regulates sleep homeostasis. The adenosine A1 receptor agonist, cyclohexyladenosine, administered during the light period, decreased startle responses and increased immobility bouts, while the adenosine antagonist, caffeine, administered during the dark period, decreased immobility bouts. These results suggest that the regulation of sleep homeostasis in zebrafish larvae consists of the same elements as that of other species. © 2017 European Sleep Research Society.

  10. In Vivo Imaging of the Central and Peripheral Effects of Sleep Deprivation and Suprachiasmatic Nuclei Lesion on PERIOD-2 Protein in Mice.

    PubMed

    Curie, Thomas; Maret, Stephanie; Emmenegger, Yann; Franken, Paul

    2015-09-01

    That sleep deprivation increases the brain expression of various clock genes has been well documented. Based on these and other findings we hypothesized that clock genes not only underlie circadian rhythm generation but are also implicated in sleep homeostasis. However, long time lags have been reported between the changes in the clock gene messenger RNA levels and their encoded proteins. It is therefore crucial to establish whether also protein levels increase within the time frame known to activate a homeostatic sleep response. We report on the central and peripheral effects of sleep deprivation on PERIOD-2 (PER2) protein both in intact and suprachiasmatic nuclei-lesioned mice. In vivo and in situ PER2 imaging during baseline, sleep deprivation, and recovery. Mouse sleep-recording facility. Per2::Luciferase knock-in mice. N/A. Six-hour sleep deprivation increased PER2 not only in the brain but also in liver and kidney. Remarkably, the effects in the liver outlasted those observed in the brain. Within the brain the increase in PER2 concerned the cerebral cortex mainly, while leaving suprachiasmatic nuclei (SCN) levels unaffected. Against expectation, sleep deprivation did not increase PER2 in the brain of arrhythmic SCN-lesioned mice because of higher PER2 levels in baseline. In contrast, liver PER2 levels did increase in these mice similar to the sham and partially lesioned controls. Our results stress the importance of considering both sleep-wake dependent and circadian processes when quantifying clock-gene levels. Because sleep deprivation alters PERIOD-2 in the brain as well as in the periphery, it is tempting to speculate that clock genes constitute a common pathway mediating the shared and well-known adverse effects of both chronic sleep loss and disrupted circadian rhythmicity on metabolic health. © 2015 Associated Professional Sleep Societies, LLC.

  11. Enhanced emotional reactivity after selective REM sleep deprivation in humans: an fMRI study

    PubMed Central

    Rosales-Lagarde, Alejandra; Armony, Jorge L.; del Río-Portilla, Yolanda; Trejo-Martínez, David; Conde, Ruben; Corsi-Cabrera, Maria

    2012-01-01

    Converging evidence from animal and human studies suggest that rapid eye movement (REM) sleep modulates emotional processing. The aim of the present study was to explore the effects of selective REM sleep deprivation (REM-D) on emotional responses to threatening visual stimuli and their brain correlates using functional magnetic resonance imaging (fMRI). Twenty healthy subjects were randomly assigned to two groups: selective REM-D, by awakening them at each REM sleep onset, or non-rapid eye movement sleep interruptions (NREM-I) as control for potential non-specific effects of awakenings and lack of sleep. In a within-subject design, a visual emotional reactivity task was performed in the scanner before and 24 h after sleep manipulation. Behaviorally, emotional reactivity was enhanced relative to baseline (BL) in the REM deprived group only. In terms of fMRI signal, there was, as expected, an overall decrease in activity in the NREM-I group when subjects performed the task the second time, particularly in regions involved in emotional processing, such as occipital and temporal areas, as well as in the ventrolateral prefrontal cortex, involved in top-down emotion regulation. In contrast, activity in these areas remained the same level or even increased in the REM-D group, compared to their BL level. Taken together, these results suggest that lack of REM sleep in humans is associated with enhanced emotional reactivity, both at behavioral and neural levels, and thus highlight the specific role of REM sleep in regulating the neural substrates for emotional responsiveness. PMID:22719723

  12. Functional brain imaging of a complex navigation task following one night of total sleep deprivation

    NASA Technical Reports Server (NTRS)

    Strangman, Gary; Thompson, John H.; Strauss, Monica M.; Marshburn, Thomas H.; Sutton, Jeffrey P.

    2006-01-01

    Study Objectives: To assess the cerebral effects associated with sleep deprivation in a simulation of a complex, real-world, high-risk task. Design and Interventions: A two-week, repeated measures, cross-over experimental protocol, with counterbalanced orders of normal sleep (NS) and total sleep deprivation (TSD). Setting: Each subject underwent functional magnetic resonance imaging (fMRI) while performing a dual-joystick, 3D sensorimotor navigation task (simulated orbital docking). Scanning was performed twice per subject, once following a night of normal sleep (NS), and once following a single night of total sleep deprivation (TSD). Five runs (eight 24s docking trials each) were performed during each scanning session. Participants: Six healthy, young, right-handed volunteers (2 women; mean age 20) participated. Measurements and Results: Behavioral performance on multiple measures was comparable in the two sleep conditions. Neuroimaging results within sleep conditions revealed similar locations of peak activity for NS and TSD, including left sensorimotor cortex, left precuneus (BA 7), and right visual areas (BA 18/19). However, cerebral activation following TSD was substantially larger and exhibited higher amplitude modulations from baseline. When directly comparing NS and TSD, most regions exhibited TSD>NS activity, including multiple prefrontal cortical areas (BA 8/9,44/45,47), lateral parieto-occipital areas (BA 19/39, 40), superior temporal cortex (BA 22), and bilateral thalamus and amygdala. Only left parietal cortex (BA 7) demonstrated NS>TSD activity. Conclusions: The large network of cerebral differences between the two conditions, even with comparable behavioral performance, suggests the possibility of detecting TSD-induced stress via functional brain imaging techniques on complex tasks before stress-induced failures.

  13. The effects of slow-wave sleep (SWS) deprivation and time of night on behavioral performance upon awakening.

    PubMed

    Ferrara, M; De Gennaro, L; Bertini, M

    The aim of the present study is to evaluate the effects of selective SWS deprivation on the motor and sensory motor performance impairment immediately after awakening from nocturnal sleep at different times of the night. Ten normal males slept for 6 consecutive nights in the laboratory: one adaptation, two baseline, two selective SWS deprivation, and one recovery night. During the last 4 nights performance was assessed four times: (a) before sleep, as a baseline measure; (b) within 30 s from the first nighttime awakening, after 2 h of sleep; (c) within 30 s from the second nighttime awakening, after 5 h of sleep; (d) within 30 s from the final morning awakening. After each awakening, following a 3-min cognitive test, a simple Auditory Reaction Time task (ART, about 5 min) and a Finger Tapping Task (FTT, 3 min) were administered. Median of Reaction Times (RT) and of Intertapping Intervals (ITI), 10% fastest RT, 10% slowest RT, and number of misses were considered as dependent variables. The selective SWS deprivation was very effective: SWS percentage during both the deprivation nights was close to zero. This strong manipulation of SWS amount interacted with time-of-night factors in influencing sleep inertia. The SWS deprivation procedure caused a worsening of behavioral performance during the deprivation nights. as well as upon the final awakening of the recovery night. Behavioral performance slowing upon awakening is accounted for by: (1) a general decrement in overall response speed (median of RT); (2) an "optimum response shift", i.e., a decrease in speed of the fastest responses; (3) an increase of lapsing, with more marked response delays resulting in a further decrease in response speed in the "lapse domain". Finally, our results do not support the existence of a circadian rhythm of sleep inertia linked to body temperature rhythm.

  14. Sleep in elite athletes and nutritional interventions to enhance sleep.

    PubMed

    Halson, Shona L

    2014-05-01

    Sleep has numerous important physiological and cognitive functions that may be particularly important to elite athletes. Recent evidence, as well as anecdotal information, suggests that athletes may experience a reduced quality and/or quantity of sleep. Sleep deprivation can have significant effects on athletic performance, especially submaximal, prolonged exercise. Compromised sleep may also influence learning, memory, cognition, pain perception, immunity and inflammation. Furthermore, changes in glucose metabolism and neuroendocrine function as a result of chronic, partial sleep deprivation may result in alterations in carbohydrate metabolism, appetite, food intake and protein synthesis. These factors can ultimately have a negative influence on an athlete's nutritional, metabolic and endocrine status and hence potentially reduce athletic performance. Research has identified a number of neurotransmitters associated with the sleep-wake cycle. These include serotonin, gamma-aminobutyric acid, orexin, melanin-concentrating hormone, cholinergic, galanin, noradrenaline, and histamine. Therefore, nutritional interventions that may act on these neurotransmitters in the brain may also influence sleep. Carbohydrate, tryptophan, valerian, melatonin and other nutritional interventions have been investigated as possible sleep inducers and represent promising potential interventions. In this review, the factors influencing sleep quality and quantity in athletic populations are examined and the potential impact of nutritional interventions is considered. While there is some research investigating the effects of nutritional interventions on sleep, future research may highlight the importance of nutritional and dietary interventions to enhance sleep.

  15. Effect of sleep deprivation after a night shift duty on simulated crisis management by residents in anaesthesia. A randomised crossover study.

    PubMed

    Arzalier-Daret, Ségolène; Buléon, Clément; Bocca, Marie-Laure; Denise, Pierre; Gérard, Jean-Louis; Hanouz, Jean-Luc

    2018-04-01

    Sleep deprivation has been associated with an increased incidence of medical errors and can jeopardise patients' safety during medical crisis management. The aim of the study was to assess the effect of sleep deprivation on the management of simulated anaesthesia crisis by residents in anaesthesiology. A randomised, comparative, monocentric crossover study involving 48 residents in anaesthesia was performed on a high fidelity patient simulator. Each resident was evaluated in a sleep-deprived state (deprived group, after a night shift duty) and control state (control group, after a night of sleep). Performance was assessed through points obtained during crisis scenario 1 (oesophageal intubation followed by anaphylactic shock) and scenario 2 (anaesthesia-related bronchospasm followed by ventricular tachycardia). Sleep periods were recorded by actigraphy. Two independent observers assessed the performances. The primary endpoint of the study was the score obtained for each scenario. Resident's crisis management performance is associated with sleep deprivation (scenario 1: control=39 [33-42] points vs. deprived=26 [19-40] points, P=0.02; scenario 2: control=21 [17-24] vs. deprived=14 [12-19], P=0.01). The main errors observed were: error in drug administration and dose, delay in identification of hypotension, and missing communication with the surgical team about situation. The present study showed that sleep deprivation is associated with impairment of performance to manage crisis situations by residents in anaesthesia. Copyright © 2017 Société française d’anesthésie et de réanimation (Sfar). Published by Elsevier Masson SAS. All rights reserved.

  16. The effects of age, sleep deprivation, and altitude on complex performance.

    DOT National Transportation Integrated Search

    1985-05-01

    Little research has been concerned with the combined effects on performance of age, sleep deprivation, and altitude. This study examined their potential interaction with laboratory tasks measuring aviation-related psychological functions. : Healthy m...

  17. The trait of Introversion-Extraversion predicts vulnerability to sleep deprivation.

    PubMed

    Killgore, William D S; Richards, Jessica M; Killgore, Desiree B; Kamimori, Gary H; Balkin, Thomas J

    2007-12-01

    According to Eysenck's theory of Introversion-Extroversion (I-E), introverts demonstrate higher levels of basal activity within the reticular-thalamic-cortical loop, yielding higher tonic cortical arousal than Extraverts, who are described conversely as chronically under-aroused and easily bored. We hypothesized that higher scores on the trait of Extraversion would be associated with greater declines in psychomotor vigilance performance during prolonged wakefulness. We evaluated the relationship between I-E and overnight psychomotor vigilance performance during 77 h of continuous sleep deprivation in a sample of 23 healthy adult military personnel (19 men; four women), ranging in age from 20 to 35 years. At baseline, volunteers completed the Revised NEO Personality Inventory (NEO PI-R) and completed psychomotor vigilance testing at approximately 10-min intervals from 00:15 to 08:50 hours over three nights of continuous sleep deprivation. In addition, 12 participants received four repeated administrations of caffeine (200 mg) every 2 h each night. Analysis of covariance and stepwise multiple regression analyses showed that, above and beyond the effects of caffeine, higher Extraversion was significantly related to more extensive declines in speed of responding and more frequent attentional lapses, but only for the first overnight testing session. Sub-factors of Extraversion, including Gregariousness and higher Activity level were most predictive of these changes following sleep loss. These findings are consistent with Eysenck's cortico-reticular activation theory of I-E and suggest that individual differences in the trait of Extraversion confer some vulnerability/resistance to the adverse effects of sleep loss on attention and vigilance.

  18. Role of Sleep Deprivation in Fear Conditioning and Extinction: Implications for Treatment of PTSD

    DTIC Science & Technology

    2015-10-01

    distressing symptoms of PTSD are insomnia and nightmares. The resultant sleep deprivation may actually serve to perpetuate the disorder by interfering with...response  Treating sleep =  response to PTSD treatment 19 +Acknowledgments  DoD grant DM102425  VA San Diego Center of Excellence in Stress and Mental

  19. The effect of sleep deprivation on vocal expression of emotion in adolescents and adults.

    PubMed

    McGlinchey, Eleanor L; Talbot, Lisa S; Chang, Keng-Hao; Kaplan, Katherine A; Dahl, Ronald E; Harvey, Allison G

    2011-09-01

    Investigate the impact of sleep deprivation on vocal expression of emotion. Within-group repeated measures analysis involving sleep deprivation and rested conditions. Experimental laboratory setting. Fifty-five healthy participants (24 females), including 38 adolescents aged 11-15 y and 17 adults aged 30-60 y. A multimethod approach was used to examine vocal expression of emotion in interviews conducted at 22:30 and 06:30. On that night, participants slept a maximum of 2 h. Interviews were analyzed for vocal expression of emotion via computerized text analysis, human rater judgments, and computerized acoustic properties. Computerized text analysis and human rater judgments indicated decreases in positive emotion in all participants at 06:30 relative to 22:30, and adolescents displayed a significantly greater decrease in positive emotion via computerized text analysis relative to adults. Increases in negative emotion were observed among all participants using human rater judgments. Results for the computerized acoustic properties indicated decreases in pitch, bark energy (intensity) in certain high frequency bands, and vocal sharpness (reduction in high frequency bands > 1000 Hz). These findings support the importance of sleep for healthy emotional functioning in adults, and further suggest that adolescents are differentially vulnerable to the emotional consequences of sleep deprivation.

  20. Sleep and memory. I: The influence of different sleep stages on memory.

    PubMed

    Rotenberg, V S

    1992-01-01

    A new approach to the sleep stages role in memory is discussed in the context of the two opposite patterns of behavior-search activity and renunciation of search. Search activity is activity designed to change the situation (or the subjects attitudes to it) in the absence of a definite forecast of the results of such activity, but with the constant consideration of these results at all stages of activity. Search activity increases general adaptability and body resistance while renunciation of search decreases adaptability and requires REM sleep for its compensation. Unprepared learning, which is often accompanied by failures on the first steps of learning, is suggested to produce renunciation of search, which decreases learning ability, suppress retention, and increase REM sleep requirement. A prolonged REM sleep deprivation before training causes learned helplessness and disturbs the learning process, while short REM sleep deprivation cause the "rebound" of the compensatory search activity that interferes with passive avoidance. REM sleep deprivation performed after a training session can increase distress caused by a training procedure, with the subsequent negative outcome on retention.

  1. Voluntary exercise impact on cognitive impairments in sleep-deprived intact female rats.

    PubMed

    Rajizadeh, Mohammad Amin; Esmaeilpour, Khadijeh; Masoumi-Ardakani, Yaser; Bejeshk, Mohammad Abbas; Shabani, Mohammad; Nakhaee, Nouzar; Ranjbar, Mohammad Pour; Borzadaran, Fatemeh Mohtashami; Sheibani, Vahid

    2018-05-01

    Sleep loss is a common problem in modern societies affecting different aspects of individuals' lives. Many studies have reported that sleep deprivation (SD) leads to impairments in various types of learning and memory. Physical exercise has been suggested to attenuate the cognitive impairments induced by sleep deprivation in male rats. Our previous studies have shown that forced exercise by treadmill improved learning and memory impairments following SD. The aim of the current study was to investigate the effects of voluntary exercise by running wheel on cognitive, motor and anxiety-like behavior functions of female rats following 72 h SD. Intact female rats were used in the present study. The multiple platform method was applied for the induction of 72 h SD. The exercise protocol was 4 weeks of running wheel and the cognitive function was evaluated using Morris water maze (MWM), passive avoidance and novel object recognition tests. Open field test and measurement of plasma corticosterone level were performed for evaluation of anxiety-like behaviors. Motor balance evaluation was surveyed by rotarod test. In this study, remarkable learning and long-term memory impairments were observed in sleep deprived rats in comparison to the other groups. Running wheel exercise ameliorated the SD-induced learning and memory impairments. Voluntary and mandatory locomotion and balance situation were not statistically significant among the different groups. Our study confirmed the negative effects of SD on cognitive function and approved protective effects of voluntary exercise on these negative effects. Copyright © 2018 Elsevier Inc. All rights reserved.

  2. Flavanol-rich chocolate acutely improves arterial function and working memory performance counteracting the effects of sleep deprivation in healthy individuals.

    PubMed

    Grassi, Davide; Socci, Valentina; Tempesta, Daniela; Ferri, Claudio; De Gennaro, Luigi; Desideri, Giovambattista; Ferrara, Michele

    2016-07-01

    Sleep deprivation is a risk factor for cardiovascular disease. Cocoa flavonoids exert cardiovascular benefits and neuroprotection. Whether chocolate consumption may mitigate detrimental effects of sleep loss on cognitive performance and cardiovascular parameters has never been studied. We investigated the effects of flavanol-rich chocolate consumption on cognitive skills and cardiovascular parameters after sleep deprivation. Thirty-two healthy participants underwent two baseline sessions after one night of undisturbed sleep and two experimental sessions after one night of total sleep deprivation. Two hours before each testing session, participants were randomly assigned to consume high or poor flavanol chocolate bars. During the tests were evaluated, the Psychomotor Vigilance Task and a working memory task, office SBP and DBP, flow-mediated dilation and pulse-wave velocity. Sleep deprivation increased SBP/DBP. SBP/DBP and pulse pressure were lower after flavanol-rich treatment respect to flavanol-poor treatment (SBP: 116.9 ± 1.6 vs. 120.8 ± 1.9 mmHg, respectively, P = 0.00005; DBP: 70.5 ± 1.2 vs. 72.3 ± 1.2 mmHg, respectively, P = 0.01; pulse pressure: 46.4 ± 1.3 vs. 48.4 ± 1.5 mmHg, P = 0.004). Sleep deprivation impaired flow-mediated dilation (5.5 ± 0.5 vs. 6.5 ± 0.6%, P = 0.02), flavanol-rich, but not flavanol-poor chocolate counteracted this alteration (flavanol-rich/flavanol-poor chocolate: 7.0 ± 0.6 vs. 5.0 ± 0.4%, P = 0.000001). Flavanol-rich chocolate mitigated the pulse-wave velocity increase (P = 0.001). Flavanol-rich chocolate preserved working memory accuracy in women after sleep deprivation. Flow-mediated dilation correlated with working memory performance accuracy in the sleep condition (P = 0.04). Flavanol-rich chocolate counteracted vascular impairment after sleep deprivation and restored working memory performance. Improvement in cognitive performance could be because

  3. Sleep deprivation alters functioning within the neural network underlying the covert orienting of attention.

    PubMed

    Mander, Bryce A; Reid, Kathryn J; Davuluri, Vijay K; Small, Dana M; Parrish, Todd B; Mesulam, M-Marsel; Zee, Phyllis C; Gitelman, Darren R

    2008-06-27

    One function of spatial attention is to enable goal-directed interactions with the environment through the allocation of neural resources to motivationally relevant parts of space. Studies have shown that responses are enhanced when spatial attention is predictively biased towards locations where significant events are expected to occur. Previous studies suggest that the ability to bias attention predictively is related to posterior cingulate cortex (PCC) activation [Small, D.M., et al., 2003. The posterior cingulate and medial prefrontal cortex mediate the anticipatory allocation of spatial attention. Neuroimage 18, 633-41]. Sleep deprivation (SD) impairs selective attention and reduces PCC activity [Thomas, M., et al., 2000. Neural basis of alertness and cognitive performance impairments during sleepiness. I. Effects of 24 h of sleep deprivation on waking human regional brain activity. J. Sleep Res. 9, 335-352]. Based on these findings, we hypothesized that SD would affect PCC function and alter the ability to predictively allocate spatial attention. Seven healthy, young adults underwent functional magnetic resonance imaging (fMRI) following normal rest and 34-36 h of SD while performing a task in which attention was shifted in response to peripheral targets preceded by spatially informative (valid), misleading (invalid), or uninformative (neutral) cues. When rested, but not when sleep-deprived, subjects responded more quickly to targets that followed valid cues than those after neutral or invalid cues. Brain activity during validly cued trials with a reaction time benefit was compared to activity in trials with no benefit. PCC activation was greater during trials with a reaction time benefit following normal rest. In contrast, following SD, reaction time benefits were associated with activation in the left intraparietal sulcus, a region associated with receptivity to stimuli at unexpected locations. These changes may render sleep-deprived individuals less able

  4. Sleep deprivation: a mind-body approach.

    PubMed

    Aguirre, Claudia C

    2016-11-01

    The purpose of this review is to summarize recent advances in our understanding of the impact sleep disturbances have on our health, with particular focus on the brain. The present review considers the influence of sleep disturbance on the neurovascular unit; the role of sleep disturbance in neurodegenerative diseases; and relevant strategies of neuro-immuno-endocrine interactions that likely contribute to the restorative power of sleep. Given the latest discoveries about the brain's waste clearance system and its relationship to neurodegenerative diseases like Alzheimer's disease, this review gives a brief overview on the molecular mechanisms behind sleep loss-related impairments. Recent evidence indicates that sleep plays a vital role in neuro-immuno-endocrine homeostasis. Sleep loss has been linked to elevated risks for cognitive and mood disorders, underscored by impaired synaptic transmission. The glymphatic system has been shown to be modulated by sleep and implicated in neurodegenerative disorders. Interactions between sleep quality, the immune system, and neurodegenerative disease are complex and a challenge to distil. These interactions are frequently bidirectional, because of sleep's characterization as an early symptom and as a potential factor contributing to the development and progression of mood and cognitive disorders. VIDEO ABSTRACT.

  5. Building a self-regulatory model of sleep deprivation and deception: the role of caffeine and social influence.

    PubMed

    Welsh, David T; Ellis, Aleksander P J; Christian, Michael S; Mai, Ke Michael

    2014-11-01

    Employees are getting less sleep, which has been shown to deplete self-regulatory resources and increase unethical behavior (Barnes, Schaubroeck, Huth, & Ghumman, 2011; Christian & Ellis, 2011). In this study, we extend the original mediated model by examining the role of 2 moderators in the relationship between sleep deprivation, depletion, and deceptive behavior. First, we derive psychological arguments from the psychopharmacology literature to hypothesize that caffeine moderates the relationship between sleep deprivation and depletion by replenishing self-regulatory resources. Second, we draw from recent research in social psychology to hypothesize that social influence moderates the relationship between depletion and deceptive behavior, such that depleted individuals are less able to resist the negative influence of others. Results of a laboratory study provide support for our expanded model combining mediation and moderation, adding to our understanding of the role of sleep deprivation in the incidence of workplace deception. (PsycINFO Database Record (c) 2014 APA, all rights reserved).

  6. EphA4 is Involved in Sleep Regulation but Not in the Electrophysiological Response to Sleep Deprivation.

    PubMed

    Freyburger, Marlène; Pierre, Audrey; Paquette, Gabrielle; Bélanger-Nelson, Erika; Bedont, Joseph; Gaudreault, Pierre-Olivier; Drolet, Guy; Laforest, Sylvie; Blackshaw, Seth; Cermakian, Nicolas; Doucet, Guy; Mongrain, Valérie

    2016-03-01

    Optimal sleep is ensured by the interaction of circadian and homeostatic processes. Although synaptic plasticity seems to contribute to both processes, the specific players involved are not well understood. The EphA4 tyrosine kinase receptor is a cell adhesion protein regulating synaptic plasticity. We investigated the role of EphA4 in sleep regulation using electrocorticography in mice lacking EphA4 and gene expression measurements. EphA4 knockout (KO) mice, Clock(Δ19/Δ19) mutant mice and littermates, C57BL/6J and CD-1 mice, and Sprague-Dawley rats were studied under a 12 h light: 12 h dark cycle, under undisturbed conditions or 6 h sleep deprivation (SLD), and submitted to a 48 h electrophysiological recording and/or brain sampling at different time of day. EphA4 KO mice showed less rapid eye movement sleep (REMS), enhanced duration of individual bouts of wakefulness and nonrapid eye movement sleep (NREMS) during the light period, and a blunted daily rhythm of NREMS sigma activity. The NREMS delta activity response to SLD was unchanged in EphA4 KO mice. However, SLD increased EphA4 expression in the thalamic/hypothalamic region in C57BL/6J mice. We further show the presence of E-boxes in the promoter region of EphA4, a lower expression of EphA4 in Clock mutant mice, a rhythmic expression of EphA4 ligands in several brain areas, expression of EphA4 in the suprachiasmatic nuclei of the hypothalamus (SCN), and finally an unchanged number of cells expressing Vip, Grp and Avp in the SCN of EphA4 KO mice. Our results suggest that EphA4 is involved in circadian sleep regulation. © 2016 Associated Professional Sleep Societies, LLC.

  7. Socially Isolated Mice Exhibit a Blunted Homeostatic Sleep Response to Acute Sleep Deprivation Compared to Socially Paired Mice

    PubMed Central

    Kaushal, Navita; Nair, Deepti; Gozal, David; Ramesh, Vijay

    2012-01-01

    Sleep is an important physiological process underlying maintenance of physical, mental and emotional health. Consequently, sleep deprivation (SD) is associated with adverse consequences and increases the risk for anxiety, immune, and cognitive disorders. SD is characterized by increased energy expenditure responses and sleep rebound upon recovery that are regulated by homeostatic processes, which in turn are influenced by stress. Since all previous studies on SD were conducted in a setting of social isolation, the impact of the social contextual setting is unknown. Therefore, we used a relatively stress-free SD paradigm in mice to assess the impact of social isolation on sleep, wakefulness and delta electroencephalogram (EEG) power during non-rapid eye movement (NREM) sleep. Paired or isolated C57BL/6J adult chronically-implanted male mice were exposed to SD for 6 hours and telemetric polygraphic recordings were conducted, including 18 hours recovery. Recovery from SD in the paired group showed a significant decrease in wake and significant increase in NREM sleep and rapid eye movement (REM), and a similar, albeit less robust response occurred in the isolated mice. Delta power during NREM sleep was increased in both groups immediately following SD, but paired mice exhibited significantly higher delta power throughout the dark period. The increase in body temperature and gross motor activity observed during the SD procedure was decreased during the dark period. In both open field and elevated plus maze tests, socially isolated mice showed significantly higher anxiety than paired mice. The homeostatic processes altered by SD are differentially affected in paired and isolated mice, suggesting that the social context of isolation stress may adversely affect the quantity and quality of sleep in mice. PMID:22498175

  8. Leukocytosis and natural killer cell function parallel neurobehavioral fatigue induced by 64 hours of sleep deprivation.

    PubMed

    Dinges, D F; Douglas, S D; Zaugg, L; Campbell, D E; McMann, J M; Whitehouse, W G; Orne, E C; Kapoor, S C; Icaza, E; Orne, M T

    1994-05-01

    The hypothesis that sleep deprivation depresses immune function was tested in 20 adults, selected on the basis of their normal blood chemistry, monitored in a laboratory for 7 d, and kept awake for 64 h. At 2200 h each day measurements were taken of total leukocytes (WBC), monocytes, granulocytes, lymphocytes, eosinophils, erythrocytes (RBC), B and T lymphocyte subsets, activated T cells, and natural killer (NK) subpopulations (CD56/CD8 dual-positive cells, CD16-positive cells, CD57-positive cells). Functional tests included NK cytotoxicity, lymphocyte stimulation with mitogens, and DNA analysis of cell cycle. Sleep loss was associated with leukocytosis and increased NK cell activity. At the maximum sleep deprivation, increases were observed in counts of WBC, granulocytes, monocytes, NK activity, and the proportion of lymphocytes in the S phase of the cell cycle. Changes in monocyte counts correlated with changes in other immune parameters. Counts of CD4, CD16, CD56, and CD57 lymphocytes declined after one night without sleep, whereas CD56 and CD57 counts increased after two nights. No changes were observed in other lymphocyte counts, in proliferative responses to mitogens, or in plasma levels of cortisol or adrenocorticotropin hormone. The physiologic leukocytosis and NK activity increases during deprivation were eliminated by recovery sleep in a manner parallel to neurobehavioral function, suggesting that the immune alterations may be associated with biological pressure for sleep.

  9. Leukocytosis and natural killer cell function parallel neurobehavioral fatigue induced by 64 hours of sleep deprivation.

    PubMed Central

    Dinges, D F; Douglas, S D; Zaugg, L; Campbell, D E; McMann, J M; Whitehouse, W G; Orne, E C; Kapoor, S C; Icaza, E; Orne, M T

    1994-01-01

    The hypothesis that sleep deprivation depresses immune function was tested in 20 adults, selected on the basis of their normal blood chemistry, monitored in a laboratory for 7 d, and kept awake for 64 h. At 2200 h each day measurements were taken of total leukocytes (WBC), monocytes, granulocytes, lymphocytes, eosinophils, erythrocytes (RBC), B and T lymphocyte subsets, activated T cells, and natural killer (NK) subpopulations (CD56/CD8 dual-positive cells, CD16-positive cells, CD57-positive cells). Functional tests included NK cytotoxicity, lymphocyte stimulation with mitogens, and DNA analysis of cell cycle. Sleep loss was associated with leukocytosis and increased NK cell activity. At the maximum sleep deprivation, increases were observed in counts of WBC, granulocytes, monocytes, NK activity, and the proportion of lymphocytes in the S phase of the cell cycle. Changes in monocyte counts correlated with changes in other immune parameters. Counts of CD4, CD16, CD56, and CD57 lymphocytes declined after one night without sleep, whereas CD56 and CD57 counts increased after two nights. No changes were observed in other lymphocyte counts, in proliferative responses to mitogens, or in plasma levels of cortisol or adrenocorticotropin hormone. The physiologic leukocytosis and NK activity increases during deprivation were eliminated by recovery sleep in a manner parallel to neurobehavioral function, suggesting that the immune alterations may be associated with biological pressure for sleep. PMID:7910171

  10. [Hygiene in Sleep: Problems of Sleeping Habits in Shift Workers].

    PubMed

    Takada, Masumi

    2018-01-01

    Since World War II, Japan has achieved remarkable economic development and has become an advanced country. Particularly in the industrial field, a production system has been developed to reduce the loss of machining time by adopting a shiftwork in factories operating 24 hours a day, which contributes to the improvement of productivity. Nowadays, this shiftwork practice has spread from the industrial field to other businesses such as 24-hour entertainment facilities and convenience stores, which lead to sleep deprivation in Japanese society. Even at home, certain conditions adversely affect sleeping habits. We are concerned about the risks of physical and mental health, impairments posed by the use of tablets, PCs, smartphones, and other devices so popular in today's Japan, as they delay sleep. It is urgent to improve poor sleeping habits because their outcomes such as sleep disorders and deprivation may also lead to traffic and industrial accidents.

  11. Sleep is not just for the brain: transcriptional responses to sleep in peripheral tissues

    PubMed Central

    2013-01-01

    Background Many have assumed that the primary function of sleep is for the brain. We evaluated the molecular consequences of sleep and sleep deprivation outside the brain, in heart and lung. Using microarrays we compared gene expression in tissue from sleeping and sleep deprived mice euthanized at the same diurnal times. Results In each tissue, nearly two thousand genes demonstrated statistically significant differential expression as a function of sleep/wake behavioral state. To mitigate the influence of an artificial deprivation protocol, we identified a subset of these transcripts as specifically sleep-enhanced or sleep-repressed by requiring that their expression also change over the course of unperturbed sleep. 3% and 6% of the assayed transcripts showed “sleep specific” changes in the lung and heart respectively. Sleep specific transcripts in these tissues demonstrated highly significant overlap and shared temporal dynamics. Markers of cellular stress and the unfolded protein response were reduced during sleep in both tissues. These results mirror previous findings in brain. Sleep-enhanced pathways reflected the unique metabolic functions of each tissue. Transcripts related to carbohydrate and sulfur metabolic processes were enhanced by sleep in the lung, and collectively favor buffering from oxidative stress. DNA repair and protein metabolism annotations were significantly enriched among the sleep-enhanced transcripts in the heart. Our results also suggest that sleep may provide a Zeitgeber, or synchronizing cue, in the lung as a large cluster of transcripts demonstrated systematic changes in inter-animal variability as a function of both sleep duration and circadian time. Conclusion Our data support the notion that the molecular consequences of sleep/wake behavioral state extend beyond the brain to include peripheral tissues. Sleep state induces a highly overlapping response in both heart and lung. We conclude that sleep enhances organ specific

  12. Sleep is not just for the brain: transcriptional responses to sleep in peripheral tissues.

    PubMed

    Anafi, Ron C; Pellegrino, Renata; Shockley, Keith R; Romer, Micah; Tufik, Sergio; Pack, Allan I

    2013-05-30

    Many have assumed that the primary function of sleep is for the brain. We evaluated the molecular consequences of sleep and sleep deprivation outside the brain, in heart and lung. Using microarrays we compared gene expression in tissue from sleeping and sleep deprived mice euthanized at the same diurnal times. In each tissue, nearly two thousand genes demonstrated statistically significant differential expression as a function of sleep/wake behavioral state. To mitigate the influence of an artificial deprivation protocol, we identified a subset of these transcripts as specifically sleep-enhanced or sleep-repressed by requiring that their expression also change over the course of unperturbed sleep. 3% and 6% of the assayed transcripts showed "sleep specific" changes in the lung and heart respectively. Sleep specific transcripts in these tissues demonstrated highly significant overlap and shared temporal dynamics. Markers of cellular stress and the unfolded protein response were reduced during sleep in both tissues. These results mirror previous findings in brain. Sleep-enhanced pathways reflected the unique metabolic functions of each tissue. Transcripts related to carbohydrate and sulfur metabolic processes were enhanced by sleep in the lung, and collectively favor buffering from oxidative stress. DNA repair and protein metabolism annotations were significantly enriched among the sleep-enhanced transcripts in the heart. Our results also suggest that sleep may provide a Zeitgeber, or synchronizing cue, in the lung as a large cluster of transcripts demonstrated systematic changes in inter-animal variability as a function of both sleep duration and circadian time. Our data support the notion that the molecular consequences of sleep/wake behavioral state extend beyond the brain to include peripheral tissues. Sleep state induces a highly overlapping response in both heart and lung. We conclude that sleep enhances organ specific molecular functions and that it has a

  13. Spatial and Reversal Learning in the Morris Water Maze Are Largely Resistant to Six Hours of REM Sleep Deprivation Following Training

    ERIC Educational Resources Information Center

    Walsh, Christine M.; Booth, Victoria; Poe, Gina R.

    2011-01-01

    This first test of the role of REM (rapid eye movement) sleep in reversal spatial learning is also the first attempt to replicate a much cited pair of papers reporting that REM sleep deprivation impairs the consolidation of initial spatial learning in the Morris water maze. We hypothesized that REM sleep deprivation following training would impair…

  14. Heightened sexual interest and sleep disturbance

    NASA Technical Reports Server (NTRS)

    Zarcone, V.; De La Pena, A.; Dement, W. C.

    1974-01-01

    The study demonstrates a behavioral effect of selective sleep disturbance in normal human subjects. Ten male subjects were selectively REM-deprived for two nights by awakening them at the onset of REM sleep. In addition, there were baseline and non-REM awakening conditions. Heightened sexual interest was defined by the number of film frames (using a Mackworth camera) in which subjects fixated on parts of the female figure in photographs. The largest mean difference in sexual interest was found between baseline and REM-deprivation. Both the non-REM awakenings and REM-sleep deprivation enhanced sexual interest. The failure to demonstrate a significant difference between REM-deprivation and non-REM awakenings may be due to the fact that subjects were REM-sleep-deprived in both conditions. It is suggested that REM-sleep loss may lead to increased selective attention and preoccupation with any cues which are usually interesting.

  15. Quantitative EEG Monitoring of Vigilance: Effects of Sleep Deprivation, Circadian Phase and Sympathetic Activation

    NASA Technical Reports Server (NTRS)

    Dijk, Derk-Jan

    1999-01-01

    Shuttle astronauts typically sleep only 6 to 6.5 hours per day while in orbit. This sleep loss is related to recurrent sleep cycle shifting--due to mission-dependent orbital mechanics and mission duration requirements-- and associated circadian displacement of sleep, the operational demands of space flight, noise and space motion sickness. Such sleep schedules are known to produce poor subjective sleep quality, daytime sleepiness, reduced attention, negative mood, slower reaction times, and impaired daytime alertness. Countermeasures to allow crew members to obtain an adequate amount of sleep and maintain adequate levels of neurobehavioral performance are being developed and investigated. However, it is necessary to develop methods that allow effective and attainable in-flight monitoring of vigilance to evaluate the effectiveness of these countermeasures and to detect and predict online critical decrements in alertness/performance. There is growing evidence to indicate that sleep loss and associated decrements in neurobehavioral function are reflected in the spectral composition of the electroencephalogram (EEG) during wakefulness as well as in the incidence of slow eye movements recorded by the electro-oculogram (EOG). Further-more, our preliminary data indicated that these changes in the EEG during wakefulness are more pronounced when subjects are in a supine posture, which mimics some of the physiologic effects of microgravity. Therefore, we evaluate the following hypotheses: (1) that during a 40-hour period of wakefulness (i.e., one night of total sleep deprivation) neurobehavioral function deteriorates, the incidence of slow eye-movements and EEG power density in the theta frequencies increases especially in frontal areas of the brain; (2) that the sleep deprivation induced deterioration of neurobehavioral function and changes in the incidence of slow eye movements and the spectral composition of the EEG are more pronounced when subjects are in a supine

  16. Increased interhemispheric resting-state functional connectivity after sleep deprivation: a resting-state fMRI study.

    PubMed

    Zhu, Yuanqiang; Feng, Zhiyan; Xu, Junling; Fu, Chang; Sun, Jinbo; Yang, Xuejuan; Shi, Dapeng; Qin, Wei

    2016-09-01

    Several functional imaging studies have investigated the regional effects of sleep deprivation (SD) on impaired brain function; however, potential changes in the functional interactions between the cerebral hemispheres after SD are not well understood. In this study, we used a recently validated approach, voxel-mirrored homotopic connectivity (VMHC), to directly examine the changes in interhemispheric homotopic resting-state functional connectivity (RSFC) after SD. Resting-state functional MRI (fMRI) was performed in 28 participants both after rest wakefulness (RW) and a total night of SD. An interhemispheric RSFC map was obtained by calculating the Pearson correlation (Fisher Z transformed) between each pair of homotopic voxel time series for each subject in each condition. The between-condition differences in interhemispheric RSFC were then examined at global and voxelwise levels separately. Significantly increased global VMHC was found after sleep deprivation; specifically, a significant increase in VMHC was found in specific brain regions, including the thalamus, paracentral lobule, supplementary motor area, postcentral gyrus and lingual gyrus. No regions showed significantly reduced VMHC after sleep deprivation. Further analysis indicates that these findings did not depend on the various sizes of smoothing kernels that were adopted in the preprocessing steps and that the differences in these regions were still significant with or without global signal regression. Our data suggest that the increased VMHC might reflect the compensatory involvement of bilateral brain areas, especially the bilateral thalamus, to prevent cognitive performance deterioration when sleep pressure is elevated after sleep deprivation. Our findings provide preliminary evidence of interhemispheric correlation changes after SD and contribute to a better understanding of the neural mechanisms of SD.

  17. Sleep Deprivation in Humans, Immunodepression and Glutamine Supplementation

    DTIC Science & Technology

    2005-04-15

    and lymphocytes, cell types which are known to be affected by sleep deprivation, changed in terms of intracellular cytokine production ? (2) What is...ability and enhanced cytokine production . Bassitt et al. attributed these findings to the maintenance of p[Gln] via BCAA precursors. Bacarau et...took BCAA for four weeks prior to a race (Hiscock et al., 2001). Leptin The ob gene product leptin is released from adipose tissue. Although

  18. Sleep and Cognition

    PubMed Central

    Deak, Maryann C.; Stickgold, Robert

    2018-01-01

    Sleep is a complex physiologic state, the importance of which has long been recognized. Lack of sleep is detrimental to humans and animals. Over the past decade, an important link between sleep and cognitive processing has been established. Sleep plays an important role in consolidation of different types of memory and contributes to insightful, inferential thinking. While the mechanism by which memories are processed in sleep remains unknown, several experimental models have been proposed. This article explores the link between sleep and cognition by reviewing (1) the effects of sleep deprivation on cognition, (2) the influence of sleep on consolidation of declarative and non-declarative memory, and 3) some proposed models of how sleep facilitates memory consolidation in sleep. PMID:26271496

  19. Impact of sleep deprivation on anaesthesia residents' non-technical skills: a pilot simulation-based prospective randomized trial.

    PubMed

    Neuschwander, A; Job, A; Younes, A; Mignon, A; Delgoulet, C; Cabon, P; Mantz, J; Tesniere, A

    2017-07-01

    Sleep deprivation is common in anaesthesia residents, but its impact on performance remains uncertain. Non-technical skills (team working, situation awareness, decision making, and task management) are key components of quality of care in anaesthesia, particularly in crisis situations occurring in the operating room. The impact of sleep deprivation on non-technical skills is unknown. We tested the hypothesis that in anaesthesia residents sleep deprivation is associated with impaired non-technical skills. Twenty anaesthesia residents were randomly allocated to undergo a simulation session after a night shift [sleep-deprived (SLD) group, n =10] or after a night of rest [rested (R) group, n =10] from January to March 2015. The simulated scenario was a situation of crisis management in the operating room. The primary end point was a composite score of anaesthetists' non-technical skills (ANTS) assessed by two blinded evaluators. Non-technical skills were significantly impaired in the SLD group [ANTS score 12.2 (interquartile range 10.5-13)] compared with the R group [14.5 (14-15), P <0.02]. This difference was mainly accounted for by a difference in the team working item. On the day of simulation, the SLD group showed increased sleepiness and decreased confidence in anaesthesia skills. In this randomized pilot trial, sleep deprivation was associated with impaired non-technical skills of anaesthesia residents in a simulated anaesthesia intraoperative crisis scenario. NCT02622217. © The Author 2017. Published by Oxford University Press on behalf of the British Journal of Anaesthesia. All rights reserved. For Permissions, please email: journals.permissions@oup.com

  20. Sleep deprivation reduces perceived emotional intelligence and constructive thinking skills.

    PubMed

    Killgore, William D S; Kahn-Greene, Ellen T; Lipizzi, Erica L; Newman, Rachel A; Kamimori, Gary H; Balkin, Thomas J

    2008-07-01

    Insufficient sleep can adversely affect a variety of cognitive abilities, ranging from simple alertness to higher-order executive functions. Although the effects of sleep loss on mood and cognition are well documented, there have been no controlled studies examining its effects on perceived emotional intelligence (EQ) and constructive thinking, abilities that require the integration of affect and cognition and are central to adaptive functioning. Twenty-six healthy volunteers completed the Bar-On Emotional Quotient Inventory (EQi) and the Constructive Thinking Inventory (CTI) at rested baseline and again after 55.5 and 58 h of continuous wakefulness, respectively. Relative to baseline, sleep deprivation was associated with lower scores on Total EQ (decreased global emotional intelligence), Intrapersonal functioning (reduced self-regard, assertiveness, sense of independence, and self-actualization), Interpersonal functioning (reduced empathy toward others and quality of interpersonal relationships), Stress Management skills (reduced impulse control and difficulty with delay of gratification), and Behavioral Coping (reduced positive thinking and action orientation). Esoteric Thinking (greater reliance on formal superstitions and magical thinking processes) was increased. These findings are consistent with the neurobehavioral model suggesting that sleep loss produces temporary changes in cerebral metabolism, cognition, emotion, and behavior consistent with mild prefrontal lobe dysfunction.

  1. Sleep Health: Reciprocal Regulation of Sleep and Innate Immunity

    PubMed Central

    Irwin, Michael R; Opp, Mark R

    2017-01-01

    Sleep disturbances including insomnia independently contribute to risk of inflammatory disorders and major depressive disorder. This review and overview provides an integrated understanding of the reciprocal relationships between sleep and the innate immune system and considers the role of sleep in the nocturnal regulation of the inflammatory biology dynamics; the impact of insomnia complaints, extremes of sleep duration, and experimental sleep deprivation on genomic, cellular, and systemic markers of inflammation; and the influence of sleep complaints and insomnia on inflammaging and molecular processes of cellular aging. Clinical implications of this research include discussion of the contribution of sleep disturbance to depression and especially inflammation-related depressive symptoms. Reciprocal action of inflammatory mediators on the homeostatic regulation of sleep continuity and sleep macrostructure, and the potential of interventions that target insomnia to reverse inflammation, are also reviewed. Together, interactions between sleep and inflammatory biology mechanisms underscore the implications of sleep disturbance for inflammatory disease risk, and provide a map to guide the development of treatments that modulate inflammation, improve sleep, and promote sleep health. PMID:27510422

  2. Cognitive consequences of sleep deprivation, shiftwork, and heat exposure for underground miners.

    PubMed

    Legault, Glenn; Clement, Alexandra; Kenny, Glen P; Hardcastle, Stephen; Keller, Nancy

    2017-01-01

    Sleep deprivation, abnormal sleep patterns arising from working rotating shifts, and exposure to high ambient temperatures contribute to physical and cognitive dysfunction. We examined the effects of these on 19 (41.5 ± 5.1 years) male underground miners. Data were collected for 28 to 30 consecutive days such that the participants experienced their full rotating shift schedule, including days off. Objective measures of sleep quality (actigraphy), attentional capacity (psychomotor vigilance task), core body temperature (visceral pill), executive function (BRIEF-A) and subjective measures of fatigue (Karolinska and Epworth Sleepiness scales) were obtained over the 28-30 day period. Non-parametric analyses (χ(2), Wilcoxen Signed ranks) were used to determine differences between shift types and days off. Z-tests were used to compare sample data to population norms. These revealed that the participants experienced poor quality of sleep relative to age-matched norms irrespective of the shift being worked or if the participant was on a scheduled day off [30-39 year olds: z = -14.62, p < 0.001; 40-49 year olds: z = -4.44, p < 0.001]. Participants when working day shift experienced less sleep prior to beginning work compared to their days off or night shift; however, no differences in total sleep time between when participants worked day or night shifts were observed [χ(2) (2, n = 18) = 13.44, p < 0.01]. When measured subjectively, the only time participants reported excessive sleepiness was after a night shift. Objective measures of attentional capacity showed best performance at the beginning of night shifts in contrast to any other time that the task was completed; however, performance degraded dramatically over the course of the night shift [χ(2) (2, n = 12) = 6.50, p < 0.05]. We show that underground miners reported for work sleep deprived. The cognitive consequences of this poor sleep were most pronounced during night shift when their

  3. Gray matter-specific changes in brain bioenergetics after acute sleep deprivation: a 31P magnetic resonance spectroscopy study at 4 Tesla.

    PubMed

    Plante, David T; Trksak, George H; Jensen, J Eric; Penetar, David M; Ravichandran, Caitlin; Riedner, Brady A; Tartarini, Wendy L; Dorsey, Cynthia M; Renshaw, Perry F; Lukas, Scott E; Harper, David G

    2014-12-01

    A principal function of sleep may be restoration of brain energy metabolism caused by the energetic demands of wakefulness. Because energetic demands in the brain are greater in gray than white matter, this study used linear mixed-effects models to examine tissue-type specific changes in high-energy phosphates derived using 31P magnetic resonance spectroscopy (MRS) after sleep deprivation and recovery sleep. Experimental laboratory study. Outpatient neuroimaging center at a private psychiatric hospital. A total of 32 MRS scans performed in eight healthy individuals (mean age 35 y; range 23-51 y). Phosphocreatine (PCr) and β-nucleoside triphosphate (NTP) were measured using 31P MRS three dimensional-chemical shift imaging at high field (4 Tesla) after a baseline night of sleep, acute sleep deprivation (SD), and 2 nights of recovery sleep. Novel linear mixed-effects models were constructed using spectral and tissue segmentation data to examine changes in bioenergetics in gray and white matter. PCr increased in gray matter after 2 nights of recovery sleep relative to SD with no significant changes in white matter. Exploratory analyses also demonstrated that increases in PCr were associated with increases in electroencephalographic slow wave activity during recovery sleep. No significant changes in β-NTP were observed. These results demonstrate that sleep deprivation and subsequent recovery-induced changes in high-energy phosphates primarily occur in gray matter, and increases in PCr after recovery sleep may be related to sleep homeostasis. © 2014 Associated Professional Sleep Societies, LLC.

  4. The impact of sleep loss on hippocampal function

    PubMed Central

    Prince, Toni-Moi; Abel, Ted

    2013-01-01

    Hippocampal cellular and molecular processes critical for memory consolidation are affected by the amount and quality of sleep attained. Questions remain with regard to how sleep enhances memory, what parameters of sleep after learning are optimal for memory consolidation, and what underlying hippocampal molecular players are targeted by sleep deprivation to impair memory consolidation and plasticity. In this review, we address these topics with a focus on the detrimental effects of post-learning sleep deprivation on memory consolidation. Obtaining adequate sleep is challenging in a society that values “work around the clock.” Therefore, the development of interventions to combat the negative cognitive effects of sleep deprivation is key. However, there are a limited number of therapeutics that are able to enhance cognition in the face of insufficient sleep. The identification of molecular pathways implicated in the deleterious effects of sleep deprivation on memory could potentially yield new targets for the development of more effective drugs. PMID:24045505

  5. The perilipin homologue, lipid storage droplet 2, regulates sleep homeostasis and prevents learning impairments following sleep loss.

    PubMed

    Thimgan, Matthew S; Suzuki, Yasuko; Seugnet, Laurent; Gottschalk, Laura; Shaw, Paul J

    2010-08-31

    Extended periods of waking result in physiological impairments in humans, rats, and flies. Sleep homeostasis, the increase in sleep observed following sleep loss, is believed to counter the negative effects of prolonged waking by restoring vital biological processes that are degraded during sleep deprivation. Sleep homeostasis, as with other behaviors, is influenced by both genes and environment. We report here that during periods of starvation, flies remain spontaneously awake but, in contrast to sleep deprivation, do not accrue any of the negative consequences of prolonged waking. Specifically, the homeostatic response and learning impairments that are a characteristic of sleep loss are not observed following prolonged waking induced by starvation. Recently, two genes, brummer (bmm) and Lipid storage droplet 2 (Lsd2), have been shown to modulate the response to starvation. bmm mutants have excess fat and are resistant to starvation, whereas Lsd2 mutants are lean and sensitive to starvation. Thus, we hypothesized that bmm and Lsd2 may play a role in sleep regulation. Indeed, bmm mutant flies display a large homeostatic response following sleep deprivation. In contrast, Lsd2 mutant flies, which phenocopy aspects of starvation as measured by low triglyceride stores, do not exhibit a homeostatic response following sleep loss. Importantly, Lsd2 mutant flies are not learning impaired after sleep deprivation. These results provide the first genetic evidence, to our knowledge, that lipid metabolism plays an important role in regulating the homeostatic response and can protect against neuronal impairments induced by prolonged waking.

  6. Soluble TNF-alpha receptor 1 and IL-6 plasma levels in humans subjected to the sleep deprivation model of spaceflight

    NASA Technical Reports Server (NTRS)

    Shearer, W. T.; Reuben, J. M.; Mullington, J. M.; Price, N. J.; Lee, B. N.; Smith, E. O.; Szuba, M. P.; Van Dongen, H. P.; Dinges, D. F.

    2001-01-01

    BACKGROUND: The extent to which sleep loss may predispose astronauts to a state of altered immunity during extended space travel prompts evaluation with ground-based models. OBJECTIVE: We sought to measure plasma levels of selected cytokines and their receptors, including the putative sleep-regulation proteins soluble TNF-alpha receptor (sTNF-alpha R) I and IL-6, in human subjects undergoing 2 types of sleep deprivation during environmental confinement with performance demands. METHODS: Healthy adult men (n = 42) were randomized to schedules that varied in severity of sleep loss: 4 days (88 hours) of partial sleep deprivation (PSD) involving two 2-hour naps per day or 4 days of total sleep deprivation (TSD). Plasma samples were obtained every 6 hours across 5 days and analyzed by using enzyme-linked immunoassays for sTNF-alpha RI, sTNF-alpha RII, IL-6, soluble IL-2 receptor, IL-10, and TNF-alpha. RESULTS: Interactions between the effects of time and sleep deprivation level were detected for sTNF-alpha RI and IL-6 but not for sTNF-alpha RII, soluble IL-2 receptor, IL-10, and TNF-alpha. Relative to the PSD condition, subjects in the TSD condition had elevated plasma levels of sTNF-alpha RI on day 2 (P =.04), day 3 (P =.01), and across days 2 to 4 of sleep loss (P =.01) and elevated levels of IL-6 on day 4 (P =.04). CONCLUSIONS: Total sleep loss produced significant increases in plasma levels of sTNF-alpha RI and IL-6, messengers that connect the nervous, endocrine, and immune systems. These changes appeared to reflect elevations of the homeostatic drive for sleep because they occurred in TSD but not PSD, suggesting that naps may serve as the basis for a countermeasures approach to prolonged spaceflight.

  7. Functional neuroimaging and behavioral correlates of capacity decline in visual short-term memory after sleep deprivation.

    PubMed

    Chee, Michael W L; Chuah, Y M Lisa

    2007-05-29

    Sleep deprivation (SD) impairs short-term memory, but it is unclear whether this is because of reduced storage capacity or processes contributing to appropriate information encoding. We evaluated 30 individuals twice, once after a night of normal sleep and again after 24 h of SD. In each session, we evaluated visual memory capacity by presenting arrays of one to eight colored squares. Additionally, we measured cortical responses to varying visual array sizes without engaging memory. The magnitude of intraparietal sulcus activation and memory capacity after normal sleep were highly correlated. SD elicited a pattern of activation in both tasks, indicating that deficits in visual processing and visual attention accompany and could account for loss of short-term memory capacity. Additionally, a comparison between better and poorer performers showed that preservation of precuneus and temporoparietal junction deactivation with increasing memory load corresponds to less performance decline when one is sleep-deprived.

  8. Dose-dependent model of caffeine effects on human vigilance during total sleep deprivation.

    PubMed

    Ramakrishnan, Sridhar; Laxminarayan, Srinivas; Wesensten, Nancy J; Kamimori, Gary H; Balkin, Thomas J; Reifman, Jaques

    2014-10-07

    Caffeine is the most widely consumed stimulant to counter sleep-loss effects. While the pharmacokinetics of caffeine in the body is well-understood, its alertness-restoring effects are still not well characterized. In fact, mathematical models capable of predicting the effects of varying doses of caffeine on objective measures of vigilance are not available. In this paper, we describe a phenomenological model of the dose-dependent effects of caffeine on psychomotor vigilance task (PVT) performance of sleep-deprived subjects. We used the two-process model of sleep regulation to quantify performance during sleep loss in the absence of caffeine and a dose-dependent multiplier factor derived from the Hill equation to model the effects of single and repeated caffeine doses. We developed and validated the model fits and predictions on PVT lapse (number of reaction times exceeding 500 ms) data from two separate laboratory studies. At the population-average level, the model captured the effects of a range of caffeine doses (50-300 mg), yielding up to a 90% improvement over the two-process model. Individual-specific caffeine models, on average, predicted the effects up to 23% better than population-average caffeine models. The proposed model serves as a useful tool for predicting the dose-dependent effects of caffeine on the PVT performance of sleep-deprived subjects and, therefore, can be used for determining caffeine doses that optimize the timing and duration of peak performance. Published by Elsevier Ltd.

  9. Cognitive and hippocampus biochemical changes following sleep deprivation in the adult male rat.

    PubMed

    Nabaee, Ebrahim; Kesmati, Mahnaz; Shahriari, Ali; Khajehpour, Lotfollah; Torabi, Mozhgan

    2018-05-14

    Sleep deprivation (SD) influences physiological processes such as cognitive function. The balance of oxidant and antioxidant markers, neurotrophic factors and magnesium are affected by sleep deprivation but there is no difference between pre and post training sleep deprivation. This study was designed to investigate memory retrieval and biochemical factors such as oxidant and antioxidant enzyme, brain-derived neurotrophic factor (BDNF) and magnesium levels in the hippocampus following pre and post-training sleep deprivation. Male Wistar rats (weighing 200 ± 20 g) in below groups were used: control 1, 24, 48 and 72 h SD before training groups, control2, 24 h SD1 after training (being evaluated 24 h after training) and SD2 24 after training (being evaluated 48 h after training). Memory was evaluated 90 min, 24 h or 48 h after training by step-through passive avoidance apparatus. Multiple platforms method was used to induce SD. Oxidant and antioxidant markers including glutathione (GSH), glutathione reductase (GPx), malonedialdehyde (MDA), Total antioxidant concentration, catalase, superoxide dismutase (SOD), magnesium and BDNF were assessed in the hippocampus or/and brain. 72 h pre-training SD impaired short and long-term memory significantly. There was no significant difference in hippocampus oxidant and antioxidant markers compared to control. Hippocampal BDNF and magnesium did not show any changes in all SD groups. Lack of correlation between memory impairment and levels of BDNF, magnesium and/or oxidant and antioxidant balance in the hippocampus is likely to be related to animal locomotor activity in the multiple platforms method. More research is needed to clarify the role of neurochemical systems. Copyright © 2018 Elsevier Masson SAS. All rights reserved.

  10. Residency training: the King-Devick test and sleep deprivation: study in pre- and post-call neurology residents.

    PubMed

    Davies, Emma C; Henderson, Sam; Balcer, Laura J; Galetta, Steven L

    2012-04-24

    The current study investigates the effect of sleep deprivation on the speed and accuracy of eye movements as measured by the King-Devick (K-D) test, a <1-minute test that involves rapid number naming. In this cohort study, neurology residents and staff from the University of Pennsylvania Health System underwent baseline followed by postcall K-D testing (n = 25); those not taking call (n = 10) also completed baseline and follow-up K-D testing. Differences in the times and errors between baseline and follow-up K-D scores were compared between the 2 groups. Residents taking call had less improvement from baseline K-D times when compared to participants not taking call (p < 0.0001, Wilcoxon rank sum test). For both groups, the change in K-D time from baseline was correlated to amount of sleep obtained (r(s) = -0.50, p = 0.002) and subjective evaluation of level of alertness (r(s) = 0.33, p = 0.05) but had no correlation to time since last caffeine consumption (r(s) = -0.13, p = 0.52). For those residents on their actual call night, the duration of sleep obtained did not correlate with change in K-D scores from baseline (r(s) = 0.13, p = 0.54). The K-D test is sensitive to the effects of sleep deprivation on cognitive functioning, including rapid eye movements, concentration, and language function. As with other measures of sleep deprivation, K-D performance demonstrated significant interindividual variability in vulnerability to sleep deprivation. Severe fatigue appears to reduce the degree of improvement typically observed in K-D testing.

  11. Involvement of the α1-adrenoceptor in sleep-waking and sleep loss-induced anxiety behavior in zebrafish.

    PubMed

    Singh, A; Subhashini, N; Sharma, S; Mallick, B N

    2013-08-15

    Sleep is a universal phenomenon in vertebrates, and its loss affects various behaviors. Independent studies have reported that sleep loss increases anxiety; however, the detailed mechanism is unknown. Because sleep deprivation increases noradrenalin (NA), which modulates many behaviors and induces patho-physiological changes, this study utilized zebrafish as a model to investigate whether sleep loss-induced increased anxiety is modulated by NA. Continuous behavioral quiescence for at least 6s was considered to represent sleep in zebrafish; although some authors termed it as a sleep-like state, in this study we have termed it as sleep. The activity of fish that signified sleep-waking was recorded in light-dark, during continuous dark and light; the latter induced sleep loss in fish. The latency, number of entries, time spent and distance travelled in the light chamber were assessed in a light-dark box test to estimate the anxiety behavior of normal, sleep-deprived and prazosin (PRZ)-treated fish. Zebrafish showed increased waking during light and complete loss of sleep upon continuous exposure to light for 24h. PRZ significantly increased sleep in normal fish. Sleep-deprived fish showed an increased preference for dark (expression of increased anxiety), and this effect was prevented by PRZ, which increased sleep as well. Our findings suggest that sleep loss-induced anxiety-like behavior in zebrafish is likely to be mediated by NA's action on the α1-adrenoceptor. Copyright © 2013 IBRO. Published by Elsevier Ltd. All rights reserved.

  12. Sleeping brain, learning brain. The role of sleep for memory systems.

    PubMed

    Peigneux, P; Laureys, S; Delbeuck, X; Maquet, P

    2001-12-21

    The hypothesis that sleep participates in the consolidation of recent memory traces has been investigated using four main paradigms: (1) effects of post-training sleep deprivation on memory consolidation, (2) effects of learning on post-training sleep, (3) effects of within sleep stimulation on the sleep pattern and on overnight memories, and (4) re-expression of behavior-specific neural patterns during post-training sleep. These studies convincingly support the idea that sleep is deeply involved in memory functions in humans and animals. However, the available data still remain too scarce to confirm or reject unequivocally the recently upheld hypothesis that consolidations of non-declarative and declarative memories are respectively dependent upon REM and NREM sleep processes.

  13. Impairment of male reproductive function after sleep deprivation.

    PubMed

    Alvarenga, Tathiana A; Hirotsu, Camila; Mazaro-Costa, Renata; Tufik, Sergio; Andersen, Monica L

    2015-05-01

    To evaluate the influence of sleep loss on sexual behavior, hormone levels, sperm parameters, and testis-specific gene expression in male rats. Experimental research. Animal laboratory. Male adult Wistar-Hannover rats. Sexually experienced rats were subjected to paradoxic sleep deprivation (PSD) for 96 hours or sleep restriction (SR) for 21 days or kept in their home cage as control (CTRL). Sexual behavior, hormone levels, sperm parameters and expression of stress and nitric oxide-related genes were evaluated. PSD significantly decreased sexual behavior compared with the CTRL group, whereas SR had no effect. The PSD group had significantly lower testosterone levels than the CTRL group. Both PSD and SR groups had lower sperm viabilities than the CTRL group. The decrease in the number of live sperm compared with the CTRL group was larger in the PSD group than in the SR group. Regarding testicular gene expression, both PSD and SR led to an increase of iNOS and hydroxysteroid 11β-dehydrogenase 1 expressions compared with the CTRL group. These changes were more pronounced in the PSD group. A significant increase in endothelial nitric oxide synthase expression was observed in the PSD groups compared with the CTRL group. No changes were observed in dimethylarginine dimethylaminohydrolase 1 and casein kinase 2β-polypeptide expressions. Sleep loss can promote marked changes in the male reproductive system of rats, particularly affecting spermatic function in part by interfering in the testicular nitric oxide pathway. Copyright © 2015 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.

  14. The influence of sleep deprivation and oscillating motion on sleepiness, motion sickness, and cognitive and motor performance.

    PubMed

    Kaplan, Janna; Ventura, Joel; Bakshi, Avijit; Pierobon, Alberto; Lackner, James R; DiZio, Paul

    2017-01-01

    Our goal was to determine how sleep deprivation, nauseogenic motion, and a combination of motion and sleep deprivation affect cognitive vigilance, visual-spatial perception, motor learning and retention, and balance. We exposed four groups of subjects to different combinations of normal 8h sleep or 4h sleep for two nights combined with testing under stationary conditions or during 0.28Hz horizontal linear oscillation. On the two days following controlled sleep, all subjects underwent four test sessions per day that included evaluations of fatigue, motion sickness, vigilance, perceptual discrimination, perceptual learning, motor performance and learning, and balance. Sleep loss and exposure to linear oscillation had additive or multiplicative relationships to sleepiness, motion sickness severity, decreases in vigilance and in perceptual discrimination and learning. Sleep loss also decelerated the rate of adaptation to motion sickness over repeated sessions. Sleep loss degraded the capacity to compensate for novel robotically induced perturbations of reaching movements but did not adversely affect adaptive recovery of accurate reaching. Overall, tasks requiring substantial attention to cognitive and motor demands were degraded more than tasks that were more automatic. Our findings indicate that predicting performance needs to take into account in addition to sleep loss, the attentional demands and novelty of tasks, the motion environment in which individuals will be performing and their prior susceptibility to motion sickness during exposure to provocative motion stimulation. Copyright © 2016 Elsevier B.V. All rights reserved.

  15. Sleep, sport, and the brain.

    PubMed

    Halson, Shona L; Juliff, Laura E

    2017-01-01

    The recognition that sleep is one of the foundations of athlete performance is increasing both in the elite athlete arena as well as applied performance research. Sleep, as identified through sleep deprivation and sleep extension investigations, has a role in performance, illness, injury, metabolism, cognition, memory, learning, and mood. Elite athletes have been identified as having poorer quality and quantity of sleep in comparison to the general population. This is likely the result on training times, competition stress/anxiety, muscle soreness, caffeine use, and travel. Sleep, in particular slow wave sleep, provides a restorative function to the body to recover from prior wakefulness and fatigue by repairing processes and restoring energy. In addition, research in the general population is highlighting the importance of sleep on neurophysiology, cognitive function, and mood which may have implications for elite athlete performance. It is thus increased understanding of both the effects of sleep deprivation and potential mechanisms of influence on performance that may allow scientists and practitioners to positively influence sleep in athletes and ultimately maximize performances. © 2017 Elsevier B.V. All rights reserved.

  16. [Non-linear research of alertness levels under sleep deprivation].

    PubMed

    Xue, Ranting; Zhou, Peng; Gao, Xiang; Dong, Xinming; Wang, Xiaolu; Ming, Dong; Qi, Hongzhi; Wang, Xuemin

    2014-06-01

    We applied Lempel-Ziv complexity (LZC) combined with brain electrical activity mapping (BEAM) to study the change of alertness under sleep deprivation in our research. Ten subjects were involved in 36 hours sleep deprivation (SD), during which spontaneous electroencephalogram (EEG) experiments and auditory evoked EEG experiments-Oddball were recorded once every 6 hours. Spontaneous and evoked EEG data were calculated and BEAMs were structured. Results showed that during the 36 hours of SD, alertness could be divided into three stages, i. e. the first 12 hours as the high stage, the middle 12 hours as the rapid decline stage and the last 12 hours as the low stage. During the period SD, LZC of Spontaneous EEG decreased over the whole brain to some extent, but remained consistent with the subjective scales. By BEAMs of event related potential, LZC on frontal cortex decreased, but kept consistent with the behavioral responses. Therefore, LZC can be effective to reflect the change of brain alertness. At the same time LZC could be used as a practical index to monitor real-time alertness because of its simple computation and fast calculation.

  17. Effects of Time of Day and Sleep Deprivation on Motorcycle-Driving Performance

    PubMed Central

    Bougard, Clément; Espié, Stéphane; Larnaudie, Bruno; Moussay, Sébastien; Davenne, Damien

    2012-01-01

    The aim of this study was to investigate whether motorcycle handling capabilities – measured by means of the efficiency of emergency manoeuvres – were dependent on prior sleep deprivation and time of day. Twelve male participants voluntarily took part in four test sessions, starting at 6 a.m., 10 a.m., 2 p.m., and 6 p.m., following a night either with or without sleep. Each test session comprised temperature and sleepiness measurements, before three different types of motorcycling tests were initiated: (1) stability in straight ahead riding at low speed (in “slow motion” mode and in “brakes and clutch” mode), (2) emergency braking and (3) crash avoidance tasks performed at 20 kph and 40 kph. The results indicate that motorcycle control at low speed depends on time of day, with an improvement in performance throughout the day. Emergency braking performance is affected at both speeds by time of day, with poorer performance (longer total stopping distance, reaction time and braking distance) in the morning, and also by sleep deprivation, from measurements obtained at 40 kph (incorrect initial speed). Except for a tendency observed after the sleepless night to deviate from the initial speed, it seems that crash avoidance capabilities are quite unaffected by the two disturbance factors. Consequently, some motorcycle handling capabilities (stability at low speed and emergency braking) change in the same way as the diurnal fluctuation observed in body temperature and sleepiness, whereas for others (crash avoidance) the participants were able to maintain their initial performance level despite the high levels of sleepiness recorded after a sleepless night. Motorcycle riders have to be aware that their handling capabilities are limited in the early morning and/or after sleep deprivation. Both these situations can increase the risk of falls and of being involved in a road accident. PMID:22761881

  18. Sleep restriction alters the hypothalamic-pituitary-adrenal response to stress

    NASA Technical Reports Server (NTRS)

    Meerlo, P.; Koehl, M.; van der Borght, K.; Turek, F. W.

    2002-01-01

    Chronic sleep restriction is an increasing problem in many countries and may have many, as yet unknown, consequences for health and well being. Studies in both humans and rats suggest that sleep deprivation may activate the hypothalamic-pituitary-adrenal (HPA) axis, one of the main neuroendocrine stress systems. However, few attempts have been made to examine how sleep loss affects the HPA axis response to subsequent stressors. Furthermore, most studies applied short-lasting total sleep deprivation and not restriction of sleep over a longer period of time, as often occurs in human society. Using the rat as our model species, we investigated: (i) the HPA axis activity during and after sleep deprivation and (ii) the effect of sleep loss on the subsequent HPA response to a novel stressor. In one experiment, rats were subjected to 48 h of sleep deprivation by placing them in slowly rotating wheels. Control rats were placed in nonrotating wheels. In a second experiment, rats were subjected to an 8-day sleep restriction protocol allowing 4 h of sleep each day. To test the effects of sleep loss on subsequent stress reactivity, rats were subjected to a 30-min restraint stress. Blood samples were taken at several time points and analysed for adrenocorticotropic hormone (ACTH) and corticosterone. The results show that ACTH and corticosterone concentrations were elevated during sleep deprivation but returned to baseline within 4 h of recovery. After 1 day of sleep restriction, the ACTH and corticosterone response to restraint stress did not differ between control and sleep deprived rats. However, after 48 h of total sleep deprivation and after 8 days of restricted sleep, the ACTH response to restraint was significantly reduced whereas the corticosterone response was unaffected. These results show that sleep loss not only is a mild activator of the HPA axis itself, but also affects the subsequent response to stress. Alterations in HPA axis regulation may gradually appear under

  19. Acute Sleep Deprivation Induces a Local Brain Transfer Information Increase in the Frontal Cortex in a Widespread Decrease Context.

    PubMed

    Alonso, Joan F; Romero, Sergio; Mañanas, Miguel A; Alcalá, Marta; Antonijoan, Rosa M; Giménez, Sandra

    2016-04-14

    Sleep deprivation (SD) has adverse effects on mental and physical health, affecting the cognitive abilities and emotional states. Specifically, cognitive functions and alertness are known to decrease after SD. The aim of this work was to identify the directional information transfer after SD on scalp EEG signals using transfer entropy (TE). Using a robust methodology based on EEG recordings of 18 volunteers deprived from sleep for 36 h, TE and spectral analysis were performed to characterize EEG data acquired every 2 h. Correlation between connectivity measures and subjective somnolence was assessed. In general, TE showed medium- and long-range significant decreases originated at the occipital areas and directed towards different regions, which could be interpreted as the transfer of predictive information from parieto-occipital activity to the rest of the head. Simultaneously, short-range increases were obtained for the frontal areas, following a consistent and robust time course with significant maps after 20 h of sleep deprivation. Changes during sleep deprivation in brain network were measured effectively by TE, which showed increased local connectivity and diminished global integration. TE is an objective measure that could be used as a potential measure of sleep pressure and somnolence with the additional property of directed relationships.

  20. REM sleep deprivation induces endothelial dysfunction and hypertension in middle-aged rats: Roles of the eNOS/NO/cGMP pathway and supplementation with L-arginine.

    PubMed

    Jiang, Jiaye; Gan, Zhongyuan; Li, Yuan; Zhao, Wenqi; Li, Hanqing; Zheng, Jian-Pu; Ke, Yan

    2017-01-01

    Sleep loss can induce or aggravate the development of cardiovascular and cerebrovascular diseases. However, the molecular mechanism underlying this phenomenon is poorly understood. The present study was designed to investigate the effects of REM sleep deprivation on blood pressure in rats and the underlying mechanisms of these effects. After Sprague-Dawley rats were subjected to REM sleep deprivation for 5 days, their blood pressures and endothelial function were measured. In addition, one group of rats was given continuous access to L-arginine supplementation (2% in distilled water) for the 5 days before and the 5 days of REM sleep deprivation to reverse sleep deprivation-induced pathological changes. The results showed that REM sleep deprivation decreased body weight, increased blood pressure, and impaired endothelial function of the aortas in middle-aged rats but not young rats. Moreover, nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) concentrations as well as endothelial NO synthase (eNOS) phosphorylation in the aorta were decreased by REM sleep deprivation. Supplementation with L-arginine could protect against REM sleep deprivation-induced hypertension, endothelial dysfunction, and damage to the eNOS/NO/cGMP signaling pathway. The results of the present study suggested that REM sleep deprivation caused endothelial dysfunction and hypertension in middle-aged rats via the eNOS/NO/cGMP pathway and that these pathological changes could be inhibited via L-arginine supplementation. The present study provides a new strategy to inhibit the signaling pathways involved in insomnia-induced or insomnia-enhanced cardiovascular diseases.

  1. Cognitive Performance Degradation on Sonar Operator and Torpedo Data Control Unit Operator after One Night of Sleep Deprivation

    DTIC Science & Technology

    1985-09-01

    8 II. SLEEP AND SOME CHARACTERISTICS . . . . . o . . 13 A. C"YCLE AND CYCLE EFFECT ... ......... 11 B. SLEEP DEPRIVATION...17 E. NAP: RESTORATIVE POWER AND SIDE EFFECTS OF THE NAP o . . o o o o e o o . o * o e o . 19 III. SLEEP LOSS AND...war periods. The effect of this situ- ation is a requirement for long hours of physically and mentally exhausting work without sleep. The silent war

  2. [Sleep psychiatry].

    PubMed

    Chiba, Shigeru

    2013-01-01

    Sleep disorders are serious issues in modern society. There has been marked scientific interest in sleep for a century, with the discoveries of the electrical activity of the brain (EEG), sleep-wake system, rapid eye movement (REM) sleep, and circadian rhythm system. Additionally, the advent of video-polysomnography in clinical research has revealed some of the consequences of disrupted sleep and sleep deprivation in psychiatric disorders. Decades of clinical research have demonstrated that sleep disorders are intimately tied to not only physical disease (e. g., lifestyle-related disease) but psychiatric illness. According to The International Classification of Sleep Disorders (2005), sleep disorders are classified into 8 major categories: 1) insomnia, 2) sleep-related breathing disorders, 3) hypersomnias of central origin, 4) circadian rhythm sleep disorders, 5) parasomnias, 6) sleep-related movement disorders, 7) isolated symptoms, and 8) other sleep disorders. Several sleep disorders, including obstructive sleep apnea syndrome, restless legs syndrome, periodic limb movement disorder, sleepwalking, REM sleep behavior disorder, and narcolepsy, may be comorbid or possibly mimic numerous psychiatric disorders, and can even occur due to psychiatric pharmacotherapy. Moreover, sleep disorders may exacerbate underlying psychiatric disorders when left untreated. Therefore, psychiatrists should pay attention to the intimate relationship between sleep disorders and psychiatric symptoms. Sleep psychiatry is an academic field focusing on interrelations between sleep medicine and psychiatry. This mini-review summarizes recent findings in sleep psychiatry. Future research on the bidirectional relation between sleep disturbance and psychiatric symptoms will shed light on the pathophysiological view of psychiatric disorders and sleep disorders.

  3. Emotional memory processing is influenced by sleep quality.

    PubMed

    Tempesta, Daniela; De Gennaro, Luigi; Natale, Vincenzo; Ferrara, Michele

    2015-07-01

    The recall of emotional memory is enhanced after sleep and is hindered by sleep deprivation. We used an emotional memory task to assess whether poor sleep quality, as well as sleep deprivation, may influence the accuracy of memory recognition, but also the affective tone associated with the memory. Seventy-five subjects, divided into poor sleeper (PS), good sleeper (GS), and sleep deprivation (SD) groups, completed two recall (R) sessions: R1, 1 h after the encoding phase; and R2, after one night of sleep for PS and GS groups and after one night of sleep deprivation for the SD group. During the encoding phase, the participants rated valence and arousal of 90 pictures. During R1 and R2, the participants first made a yes/no memory judgment of the 45 target pictures intermingled with 30 non-target pictures, then rated valence and arousal of each picture. Recognition accuracy was higher for the PS and GS groups compared to the SD group for all pictures. Emotional valence of the remembered pictures was more negative after sleep deprivation and poor quality sleep, while it was preserved after a good sleep. These results provide the first evidence that poor sleep quality negatively affects emotional valence of memories, within the context of preserved emotional memory consolidation. It is suggested that low sleep quality and lack of sleep may impose a more negative affective tone to memories. The reported effects are not to be ascribed to depressive mood, but to a specific influence of poor sleep quality. Copyright © 2015 Elsevier B.V. All rights reserved.

  4. Sleep deprivation and activation of morning levels of cellular and genomic markers of inflammation.

    PubMed

    Irwin, Michael R; Wang, Minge; Campomayor, Capella O; Collado-Hidalgo, Alicia; Cole, Steve

    2006-09-18

    Inflammation is associated with increased risk of cardiovascular disorders, arthritis, diabetes mellitus, and mortality. The effects of sleep loss on the cellular and genomic mechanisms that contribute to inflammatory cytokine activity are not known. In 30 healthy adults, monocyte intracellular proinflammatory cytokine production was repeatedly assessed during the day across 3 baseline periods and after partial sleep deprivation (awake from 11 pm to 3 am). We analyzed the impact of sleep loss on transcription of proinflammatory cytokine genes and used DNA microarray analyses to characterize candidate transcription-control pathways that might mediate the effects of sleep loss on leukocyte gene expression. In the morning after a night of sleep loss, monocyte production of interleukin 6 and tumor necrosis factor alpha was significantly greater compared with morning levels following uninterrupted sleep. In addition, sleep loss induced a more than 3-fold increase in transcription of interleukin 6 messenger RNA and a 2-fold increase in tumor necrosis factor alpha messenger RNA. Bioinformatics analyses suggested that the inflammatory response was mediated by the nuclear factor kappaB inflammatory signaling system as well as through classic hormone and growth factor response pathways. Sleep loss induces a functional alteration of the monocyte proinflammatory cytokine response. A modest amount of sleep loss also alters molecular processes that drive cellular immune activation and induce inflammatory cytokines; mapping the dynamics of sleep loss on molecular signaling pathways has implications for understanding the role of sleep in altering immune cell physiologic characteristics. Interventions that target sleep might constitute new strategies to constrain inflammation with effects on inflammatory disease risk.

  5. Sleep, circadian rhythms, and psychomotor vigilance.

    PubMed

    Van Dongen, Hans P A; Dinges, David F

    2005-04-01

    Psychomotor vigilance performance is highly relevant to athletic performance. It is influenced by a sleep homeostatic process, which builds up pressure for sleep during wakefulness and dissipates this pressure during sleep, and a circadian rhythm process, which produces a waxing and waning of pressure for wakefulness over a 24 hours of the day. During total sleep deprivation, these two processes cause performance to deteriorate progressively over days, modulated within days by further performance reductions at night and relative improvements during the daytime. As the homeostatic pressure for sleep builds up higher across prolonged wakefulness, the rate of dissipation of that pressure during subsequent sleep is enhanced exponentially, so that even brief periods of sleep provide significant performance recuperation. Nevertheless, sleep restriction practiced on a chronic basis induces cumulative performance deficits of the same order of magnitude as observed during total sleep deprivation. There are also considerable individual differences in the degree of vulnerability to performance impairment from sleep loss, and these differences represent a trait.

  6. Sleep and cognition.

    PubMed

    Deak, Maryann C; Stickgold, Robert

    2010-07-01

    Sleep is a complex physiologic state, the importance of which has long been recognized. Lack of sleep is detrimental to humans and animals. Over the past decade, an important link between sleep and cognitive processing has been established. Sleep plays an important role in consolidation of different types of memory and contributes to insightful, inferential thinking. While the mechanism by which memories are processed in sleep remains unknown, several experimental models have been proposed. This article explores the link between sleep and cognition by reviewing (1) the effects of sleep deprivation on cognition, (2) the influence of sleep on consolidation of declarative and non-declarative memory, and (3) some proposed models of how sleep facilitates memory consolidation in sleep. Copyright © 2010 John Wiley & Sons, Ltd. For further resources related to this article, please visit the WIREs website. Copyright © 2010 John Wiley & Sons, Ltd.

  7. Sleep deprivation impairs object-selective attention: a view from the ventral visual cortex.

    PubMed

    Lim, Julian; Tan, Jiat Chow; Parimal, Sarayu; Dinges, David F; Chee, Michael W L

    2010-02-05

    Most prior studies on selective attention in the setting of total sleep deprivation (SD) have focused on behavior or activation within fronto-parietal cognitive control areas. Here, we evaluated the effects of SD on the top-down biasing of activation of ventral visual cortex and on functional connectivity between cognitive control and other brain regions. Twenty-three healthy young adult volunteers underwent fMRI after a normal night of sleep (RW) and after sleep deprivation in a counterbalanced manner while performing a selective attention task. During this task, pictures of houses or faces were randomly interleaved among scrambled images. Across different blocks, volunteers responded to house but not face pictures, face but not house pictures, or passively viewed pictures without responding. The appearance of task-relevant pictures was unpredictable in this paradigm. SD resulted in less accurate detection of target pictures without affecting the mean false alarm rate or response time. In addition to a reduction of fronto-parietal activation, attending to houses strongly modulated parahippocampal place area (PPA) activation during RW, but this attention-driven biasing of PPA activation was abolished following SD. Additionally, SD resulted in a significant decrement in functional connectivity between the PPA and two cognitive control areas, the left intraparietal sulcus and the left inferior frontal lobe. SD impairs selective attention as evidenced by reduced selectivity in PPA activation. Further, reduction in fronto-parietal and ventral visual task-related activation suggests that it also affects sustained attention. Reductions in functional connectivity may be an important additional imaging parameter to consider in characterizing the effects of sleep deprivation on cognition.

  8. Fragmentation of Rapid Eye Movement and Nonrapid Eye Movement Sleep without Total Sleep Loss Impairs Hippocampus-Dependent Fear Memory Consolidation.

    PubMed

    Lee, Michael L; Katsuyama, Ângela M; Duge, Leanne S; Sriram, Chaitra; Krushelnytskyy, Mykhaylo; Kim, Jeansok J; de la Iglesia, Horacio O

    2016-11-01

    Sleep is important for consolidation of hippocampus-dependent memories. It is hypothesized that the temporal sequence of nonrapid eye movement (NREM) sleep and rapid eye movement (REM) sleep is critical for the weakening of nonadaptive memories and the subsequent transfer of memories temporarily stored in the hippocampus to more permanent memories in the neocortex. A great body of evidence supporting this hypothesis relies on behavioral, pharmacological, neural, and/or genetic manipulations that induce sleep deprivation or stage-specific sleep deprivation. We exploit an experimental model of circadian desynchrony in which intact animals are not deprived of any sleep stage but show fragmentation of REM and NREM sleep within nonfragmented sleep bouts. We test the hypothesis that the shortening of NREM and REM sleep durations post-training will impair memory consolidation irrespective of total sleep duration. When circadian-desynchronized animals are trained in a hippocampus-dependent contextual fear-conditioning task they show normal short-term memory but impaired long-term memory consolidation. This impairment in memory consolidation is positively associated with the post-training fragmentation of REM and NREM sleep but is not significantly associated with the fragmentation of total sleep or the total amount of delta activity. We also show that the sleep stage fragmentation resulting from circadian desynchrony has no effect on hippocampus-dependent spatial memory and no effect on hippocampus-independent cued fear-conditioning memory. Our findings in an intact animal model, in which sleep deprivation is not a confounding factor, support the hypothesis that the stereotypic sequence and duration of sleep stages play a specific role in long-term hippocampus-dependent fear memory consolidation. © 2016 Associated Professional Sleep Societies, LLC.

  9. Genes Involved in the Astrocyte-Neuron Lactate Shuttle (ANLS) Are Specifically Regulated in Cortical Astrocytes Following Sleep Deprivation in Mice

    PubMed Central

    Petit, Jean-Marie; Gyger, Joël; Burlet-Godinot, Sophie; Fiumelli, Hubert; Martin, Jean-Luc; Magistretti, Pierre J.

    2013-01-01

    Study Objectives: There is growing evidence indicating that in order to meet the neuronal energy demands, astrocytes provide lactate as an energy substrate for neurons through a mechanism called “astrocyte-neuron lactate shuttle” (ANLS). Since neuronal activity changes dramatically during vigilance states, we hypothesized that the ANLS may be regulated during the sleep-wake cycle. To test this hypothesis we investigated the expression of genes associated with the ANLS specifically in astrocytes following sleep deprivation. Astrocytes were purified by fluorescence-activated cell sorting from transgenic mice expressing the green fluorescent protein (GFP) under the control of the human astrocytic GFAP-promoter. Design: 6-hour instrumental sleep deprivation (TSD). Setting: Animal sleep research laboratory. Participants: Young (P23-P27) FVB/N-Tg (GFAP-GFP) 14Mes/J (Tg) mice of both sexes and 7-8 week male Tg and FVB/Nj mice. Interventions: Basal sleep recordings and sleep deprivation achieved using a modified cage where animals were gently forced to move. Measurements and Results: Since Tg and FVB/Nj mice displayed a similar sleep-wake pattern, we performed a TSD in young Tg mice. Total RNA was extracted from the GFP-positive and GFP-negative cells sorted from cerebral cortex. Quantitative RT-PCR analysis showed that levels of Glut1, α-2-Na/K pump, Glt1, and Ldha mRNAs were significantly increased following TSD in GFP-positive cells. In GFP-negative cells, a tendency to increase, although not significant, was observed for Ldha, Mct2, and α-3-Na/K pump mRNAs. Conclusions: This study shows that TSD induces the expression of genes associated with ANLS specifically in astrocytes, underlying the important role of astrocytes in the maintenance of the neuro-metabolic coupling across the sleep-wake cycle. Citation: Petit JM; Gyger J; Burlet-Godinot S; Fiumelli H; Martin JL; Magistretti PJ. Genes involved in the astrocyte-neuron lactate shuttle (ANLS) are specifically

  10. Sleep At Camp: A Survey.

    ERIC Educational Resources Information Center

    Pravda, Myra

    1997-01-01

    Among 40 camp directors surveyed, the majority believed that campers get enough sleep, but that staff members and directors do not get enough sleep. Addresses how sleep deprivation can affect job performance and offers strategies for helping staff understand the importance of sleep to keep them alert and functioning in their job. Includes…

  11. The cognitive cost of sleep lost

    PubMed Central

    McCoy, John G.; Strecker, Robert E.

    2013-01-01

    A substantial body of literature supports the intuitive notion that a good night’s sleep can facilitate human cognitive performance the next day. Deficits in attention, learning & memory, emotional reactivity, and higher-order cognitive processes, such as executive function and decision making, have all been documented following sleep disruption in humans. Thus, whilst numerous clinical and experimental studies link human sleep disturbance to cognitive deficits, attempts to develop valid and reliable rodent models of these phenomena are fewer, and relatively more recent. This review focuses primarily on the cognitive impairments produced by sleep disruption in rodent models of several human patterns of sleep loss/sleep disturbance. Though not an exclusive list, this review will focus on four specific types of sleep disturbance: total sleep deprivation, experimental sleep fragmentation, selective REM sleep deprivation, and chronic sleep restriction. The use of rodent models can provide greater opportunities to understand the neurobiological changes underlying sleep loss induced cognitive impairments. Thus, this review concludes with a description of recent neurobiological findings concerning the neuroplastic changes and putative brain mechanisms that may underlie the cognitive deficits produced by sleep disturbances. PMID:21875679

  12. Dopamine agonist suppression of rapid-eye-movement sleep is secondary to sleep suppression mediated via limbic structures

    DOE Office of Scientific and Technical Information (OSTI.GOV)

    Miletich, R.S.

    The effects of pergolide, a direct dopamine receptor agonist, on sleep and wakefulness, motor behavior and /sup 3/H-spiperone specific binding in limbic structures and striatum in rats was studied. The results show that pergolide induced a biphasic dose effect, with high doses increasing wakefulness and suppressing sleep while low dose decreased wakefulness, but increased sleep. It was shown that pergolide-induced sleep suppression was blocked by ..cap alpha..-glupenthixol and pimozide, two dopamine receptor antagonists. It was further shown that pergolide merely delayed the rebound resulting from rapid-eye-movement (REM) sleep deprivation, that dopamine receptors stimulation had no direct effect on the period,more » phase or amplitude of the circadian rhythm of REM sleep propensity and that there was no alteration in the coupling of REM sleep episodes with S/sub 2/ episodes. Rapid-eye-movement sleep deprivation resulted in increased sensitivity to the pergolide-induced wakefulness stimulation and sleep suppression and pergolide-induced motor behaviors of locomotion and head bobbing. /sup 3/H-spiperone specific binding to dopamine receptors was shown to be altered by REM sleep deprivation in the subcortical limbic structures. It is concluded that the REM sleep suppressing action of dopamine receptor stimulation is secondary to sleep suppression per se and not secondary to a unique effect on the REM sleep. Further, it is suggested that the wakefulness stimulating action of dopamine receptor agonists is mediated by activation of the dopamine receptors in the terminal areas of the mesolimbocortical dopamine projection system.« less

  13. Impact of sleep deprivation and obstructive sleep apnea syndrome on daytime vigilance and driving performance: a laboratory perspective.

    PubMed

    Pizza, F; Contardi, S; Mondini, S; Cirignotta, F

    2012-01-01

    To study the impact of sleepiness, a well-established cause of car accidents, on driving ability, we designed a 30-min monotonous simulated driving task. Our simulated driving task encompasses both primary vehicle control (standard deviation of lane position, crash occurrence) and secondary tasks (type and reaction times to divided attention tasks). Driving simulator data were correlated to subjective (state/trait) and objective (MSLT/MWT) sleepiness measures in healthy subjects undergoing sleep deprivation (SD) and in obstructive sleep apnea (OSAS) patients. SD induced severe sleepiness during nighttime, when state sleepiness increased while primary vehicle control ability worsened. After SD, driving ability decreased and was inversely correlated to subjective and objective sleepiness at MSLT. OSAS patients driving ability was well correlated to objective sleepiness, with inverse correlation to sleep propensity at the MSLT and even more strict relation with the ability to maintain wakefulness at the MWT. Sleepiness worsens driving ability in healthy subjects after SD and in OSAS patients. Driving ability correlates with subjective and objective sleepiness measures, in particular to the ability to maintain wakefulness.

  14. The Effects of Sleep Continuity Disruption on Positive Mood and Sleep Architecture in Healthy Adults.

    PubMed

    Finan, Patrick H; Quartana, Phillip J; Smith, Michael T

    2015-11-01

    The purpose of this study was to test an experimental model of the effects of sleep continuity disturbance on sleep architecture and positive mood in order to better understand the mechanisms linking insomnia and depression. Participants were randomized to receive 3 consecutive nights of sleep continuity disruption via forced nocturnal awakenings (FA, n = 21), or one of two control conditions: restricted sleep opportunity (RSO, n = 17) or uninterrupted sleep (US, n = 24). The study was set in an inpatient clinical research suite. Healthy, good-sleeping men and women were included. Polysomnography was used to measure sleep architecture, and mood was assessed via self-report each day. Compared to restricted sleep opportunity controls, forced awakenings subjects had significantly less slow wave sleep (P < 0.05) after the first night of sleep deprivation, and significantly lower positive mood (P < 0.05) after the second night of sleep deprivation. The differential change in slow wave sleep statistically mediated the observed group differences in positive mood (P = 0.002). To our knowledge, this is the first human experimental study to demonstrate that, despite comparable reductions in total sleep time, partial sleep loss from sleep continuity disruption is more detrimental to positive mood than partial sleep loss from delaying bedtime, even when controlling for concomitant increases in negative mood. With these findings, we provide temporal evidence in support of a putative biologic mechanism (slow wave sleep deficit) that could help explain the strong comorbidity between insomnia and depression. © 2015 Associated Professional Sleep Societies, LLC.

  15. Sleep deprivation affects fear memory consolidation: bi-stable amygdala connectivity with insula and ventromedial prefrontal cortex.

    PubMed

    Feng, Pan; Becker, Benjamin; Zheng, Yong; Feng, Tingyong

    2018-02-01

    Sleep plays an important role for successful fear memory consolidation. Growing evidence suggests that sleep disturbances might contribute to the development and the maintenance of posttraumatic stress disorder (PTSD), a disorders characterized by dysregulations in fear learning mechanisms, as well as exaggerated arousal and salience processing. Against this background, the present study examined the effects of sleep deprivation (SD) on the acquisition of fear and the subsequent neural consolidation. To this end, the present study assessed fear acquisition and associated changes in fMRI-based amygdala-functional connectivity following 24 h of SD. Relative to non-sleep deprived controls, SD subjects demonstrated increased fear ratings and skin conductance responses (SCR) during fear acquisition. During fear consolidation SD inhibited increased amygdala-ventromendial prefrontal cortex (vmPFC) connectivity and concomitantly increased changes in amygdala-insula connectivity. Importantly, whereas in controls fear indices during acquisition were negatively associated with amygdala-vmPFC connectivity during consolidation, fear indices were positively associated with amygdala-insula coupling following SD. Together the findings suggest that SD may interfere with vmPFC control of the amygdala and increase bottom-up arousal signaling in the amygdala-insula pathway during fear consolidation, which might mediate the negative impact of sleep disturbances on PSTD symptomatology.

  16. Acute Total and Chronic Partial Sleep Deprivation: Effects on Neurobehavioral Functions, Waking EEG and Renin-Angiotensin System

    NASA Technical Reports Server (NTRS)

    Dijk, Derk-Jan

    1999-01-01

    Total sleep deprivation leads to decrements in neurobehavioral performance and changes in electroencephalographic (EEG) oscillations as well as the incidence of slow eye movements ad detected in the electro-oculogram (EOG) during wakefulness. Although total sleep deprivation is a powerful tool to investigate the association of EEG/EOG and neurobehavioral decrements, sleep loss during space flight is usual only partial. Furthermore exposure to the microgravity environment leads to changes in sodium and volume homeostasis and associated renal and cardio-endocrine responses. Some of these changes can be induced in head down tilt bedrest studies. We integrate research tools and research projects to enhance the fidelity of the simulated conditions of space flight which are characterized by complexity and mutual interactions. The effectiveness of countermeasures and physiologic mechanisms underlying neurobehavioral changes and renal-cardio endocrine changes are investigated in Project 3 of the Human Performance Team and Project 3 of the Cardiovascular Alterations Team respectively. Although the. specific aims of these two projects are very different, they employ very similar research protocols. Thus, both projects investigate the effects of posture/bedrest and sleep deprivation (total or partial) on outcome measures relevant to their specific aims. The main aim of this enhancement grant is to exploit the similarities in research protocols by including the assessment of outcome variables relevant to the Renal-Cardio project in the research protocol of Project 3 of the Human Performance Team and by including the assessment of outcome variables relevant to the Quantitative EEG and Sleep Deprivation Project in the research protocols of Project 3 of the Cardiovascular Alterations team. In particular we will assess Neurobehavioral Function and Waking EEG in the research protocols of the renal-cardio endocrine project and renin-angiotensin and cardiac function in the research

  17. The inappropriate occurrence of rapid eye movement sleep in narcolepsy is not due to a defect in homeostatic regulation of rapid eye movement sleep.

    PubMed

    Roman, Alexis; Meftah, Soraya; Arthaud, Sébastien; Luppi, Pierre-Hervé; Peyron, Christelle

    2018-06-01

    Narcolepsy type 1 is a disabling disorder with four primary symptoms: excessive-daytime-sleepiness, cataplexy, hypnagogic hallucinations, and sleep paralysis. The later three symptoms together with a short rapid eye movement (REM) sleep latency have suggested impairment in REM sleep homeostatic regulation with an enhanced propensity for (i.e. tendency to enter) REM sleep. To test this hypothesis, we challenged REM sleep homeostatic regulation in a recognized model of narcolepsy, the orexin knock-out (Orex-KO) mice and their wild-type (WT) littermates. We first performed 48 hr of REM sleep deprivation using the classic small-platforms-over-water method. We found that narcoleptic mice are similarly REM sleep deprived to WT mice. Although they had shorter sleep latency, Orex-KO mice recovered similarly to WT during the following 10 hr of recovery. Interestingly, Orex-KO mice also had cataplexy episodes immediately after REM sleep deprivation, anticipating REM sleep rebound, at a time of day when cataplexy does not occur in baseline condition. We then evaluated REM sleep propensity using our new automated method of deprivation that performs a specific and efficient REM sleep deprivation. We showed that REM sleep propensity is similar during light phase in Orex-KO and WT mice. However, during the dark phase, REM sleep propensity was not suppressed in Orex-KO mice when hypocretin/orexin neuropeptides are normally released. Altogether our data suggest that in addition to the well-known wake-promoting role of hypocretin/orexin, these neuropeptides would also suppress REM sleep. Therefore, hypocretin/orexin deficiency would facilitate the occurrence of REM sleep at any time of day in an opportunistic manner as seen in human narcolepsy.

  18. Fragmentation of Rapid Eye Movement and Nonrapid Eye Movement Sleep without Total Sleep Loss Impairs Hippocampus-Dependent Fear Memory Consolidation

    PubMed Central

    Lee, Michael L.; Katsuyama, Ângela M.; Duge, Leanne S.; Sriram, Chaitra; Krushelnytskyy, Mykhaylo; Kim, Jeansok J.; de la Iglesia, Horacio O.

    2016-01-01

    Study Objectives: Sleep is important for consolidation of hippocampus-dependent memories. It is hypothesized that the temporal sequence of nonrapid eye movement (NREM) sleep and rapid eye movement (REM) sleep is critical for the weakening of nonadaptive memories and the subsequent transfer of memories temporarily stored in the hippocampus to more permanent memories in the neocortex. A great body of evidence supporting this hypothesis relies on behavioral, pharmacological, neural, and/or genetic manipulations that induce sleep deprivation or stage-specific sleep deprivation. Methods: We exploit an experimental model of circadian desynchrony in which intact animals are not deprived of any sleep stage but show fragmentation of REM and NREM sleep within nonfragmented sleep bouts. We test the hypothesis that the shortening of NREM and REM sleep durations post-training will impair memory consolidation irrespective of total sleep duration. Results: When circadian-desynchronized animals are trained in a hippocampus-dependent contextual fear-conditioning task they show normal short-term memory but impaired long-term memory consolidation. This impairment in memory consolidation is positively associated with the post-training fragmentation of REM and NREM sleep but is not significantly associated with the fragmentation of total sleep or the total amount of delta activity. We also show that the sleep stage fragmentation resulting from circadian desynchrony has no effect on hippocampus-dependent spatial memory and no effect on hippocampus-independent cued fear-conditioning memory. Conclusions: Our findings in an intact animal model, in which sleep deprivation is not a confounding factor, support the hypothesis that the stereotypic sequence and duration of sleep stages play a specific role in long-term hippocampus-dependent fear memory consolidation. Citation: Lee ML, Katsuyama AM, Duge LS, Sriram C, Krushelnytskyy M, Kim JJ, de la Iglesia HO. Fragmentation of rapid eye movement

  19. One night of partial sleep deprivation impairs recovery from a single exercise training session.

    PubMed

    Rae, Dale E; Chin, Tayla; Dikgomo, Kagiso; Hill, Lee; McKune, Andrew J; Kohn, Tertius A; Roden, Laura C

    2017-04-01

    The effects of sleep deprivation on physical performance are well documented, but data on the consequence of sleep deprivation on recovery from exercise are limited. The aim was to compare cyclists' recovery from a single bout of high-intensity interval training (HIIT) after which they were given either a normal night of sleep (CON, 7.56 ± 0.63 h) or half of their usual time in bed (DEP, 3.83 ± 0.33 h). In this randomized cross-over intervention study, 16 trained male cyclists (age 32 ± 7 years), relative peak power output (PPO 4.6 ± 0.7 W kg -1 ) performed a HIIT session at ±18:00 followed by either the CON or DEP sleep condition. Recovery from the HIIT session was assessed the following day by comparing pre-HIIT variables to those measured 12 and 24 h after the session. Following a 2-week washout, cyclists repeated the trial, but under the alternate sleep condition. PPO was reduced more 24 h after the HIIT session in the DEP (ΔPPO -0.22 ± 0.22 W kg -1 ; range -0.75 to 0.1 W kg -1 ) compared to the CON condition (ΔPPO -0.05 ± 0.09 W kg -1 , range -0.19 to 0.17 W kg -1 , p = 0.008, d = -2.16). Cyclists were sleepier (12 h: p = 0.002, d = 1.90; 24 h: p = 0.001, d = 1.41) and felt less motivated to train (12 h, p = 0.012, d = -0.89) during the 24 h recovery phase when the HIIT session was followed by the DEP condition. The exercise-induced 24 h reduction in systolic blood pressure observed in the CON condition was absent in the DEP condition (p = 0.039, d = 0.75). One night of partial sleep deprivation impairs recovery from a single HIIT session in cyclists. Further research is needed to understand the mechanisms behind this observation.

  20. Perceptions of pre-clerkship medical students and academic advisors about sleep deprivation and its relationship to academic performance: a cross-sectional perspective from Saudi Arabia.

    PubMed

    AlFakhri, Lama; Sarraj, Jumana; Kherallah, Shouq; Kuhail, Khulood; Obeidat, Akef; Abu-Zaid, Ahmed

    2015-12-01

    The medical student population is believed to be at an increased risk for sleep deprivation. Little is known about students' perceptions towards sleep deprivation and its relationship to academic performance. The aim of study is to explore the perceptions of medical students and their academic advisors about sleep deprivation and its relationship to academic performance. The study took place at Alfaisal University, College of Medicine, Riyadh, Saudi Arabia. An online, anonymous, cross-sectional, self-rating survey was administered to first-, third-year students and their academic advisors. Two-tailed Mann-Whitney U test was used to compare the mean 5-point Likert scale responses between students according to gender, academic year and cumulative grade point average (cGPA). A total of 259 students and 21 academic advisors participated in the survey (response rates: 70.6 and 84%, respectively). The vast majority of students agreed that sleep deprivation negatively affects academic performance (78.8%) and mood (78.4%). Around 62.2 and 73.7% of students agreed that the demanding medical curriculum and stress of final exams lead to sleep deprivation, respectively. While 36.7% of students voiced the need for incorporation of curricular separate courses about healthy sleep patterns into medical curriculum, a much greater proportion of students (45.9%) expressed interest in extracurricular activities about healthy sleep patterns. Interestingly, only 13.5% of students affirmed that they were counselled about sleep patterns and academic performance by their academic advisors. There were several statistically significant differences of means of students' perceptions according to gender, academic year and cGPA. Despite almost all academic advisors (95.5%) asserted the importance of sleep patterns to academic performance, none (0%) inquired about sleep patterns when counselling students. Nineteen academic advisors (90.5%) recommended incorporation of sleep patterns related

  1. Frontal predominance of a relative increase in sleep delta and theta EEG activity after sleep loss in humans

    NASA Technical Reports Server (NTRS)

    Cajochen, C.; Foy, R.; Dijk, D. J.; Czeisler, C. A. (Principal Investigator)

    1999-01-01

    The effect of sleep deprivation (40 h) on topographic and temporal aspects of electroencephalographic (EEG) activity during sleep was investigated by all night spectral analysis in six young volunteers. The sleep-deprivation-induced increase of EEG power density in the delta and theta frequencies (1-7 Hz) during nonREM sleep, assessed along the antero-posterior axis (midline: Fz, Cz, Pz, Oz), was significantly larger in the more frontal derivations (Fz, Cz) than in the more parietal derivations (Pz, Oz). This frequency-specific frontal predominance was already present in the first 30 min of recovery sleep, and dissipated in the course of the 8-h sleep episode. The data demonstrate that the enhancement of slow wave EEG activity during sleep following extended wakefulness is most pronounced in frontal cortical areas.

  2. The Effects of Sleep Continuity Disruption on Positive Mood and Sleep Architecture in Healthy Adults

    PubMed Central

    Finan, Patrick H.; Quartana, Phillip J.; Smith, Michael T.

    2015-01-01

    Objective: The purpose of this study was to test an experimental model of the effects of sleep continuity disturbance on sleep architecture and positive mood in order to better understand the mechanisms linking insomnia and depression. Design: Participants were randomized to receive 3 consecutive nights of sleep continuity disruption via forced nocturnal awakenings (FA, n = 21), or one of two control conditions: restricted sleep opportunity (RSO, n = 17) or uninterrupted sleep (US, n = 24). Setting: The study was set in an inpatient clinical research suite. Participants: Healthy, good-sleeping men and women were included. Measurement and Results: Polysomnography was used to measure sleep architecture, and mood was assessed via self-report each day. Compared to restricted sleep opportunity controls, forced awakenings subjects had significantly less slow wave sleep (P < 0.05) after the first night of sleep deprivation, and significantly lower positive mood (P < 0.05) after the second night of sleep deprivation. The differential change in slow wave sleep statistically mediated the observed group differences in positive mood (P = 0.002). Conclusions: To our knowledge, this is the first human experimental study to demonstrate that, despite comparable reductions in total sleep time, partial sleep loss from sleep continuity disruption is more detrimental to positive mood than partial sleep loss from delaying bedtime, even when controlling for concomitant increases in negative mood. With these findings, we provide temporal evidence in support of a putative biologic mechanism (slow wave sleep deficit) that could help explain the strong comorbidity between insomnia and depression. Citation: Finan PH, Quartana PJ, Smith MT. The effects of sleep continuity disruption on positive mood and sleep architecture in healthy adults. SLEEP 2015;38(11):1735–1742. PMID:26085289

  3. Impact of sleep duration on seizure frequency in adults with epilepsy: a sleep diary study.

    PubMed

    Cobabe, Maurine M; Sessler, Daniel I; Nowacki, Amy S; O'Rourke, Colin; Andrews, Noah; Foldvary-Schaefer, Nancy

    2015-02-01

    Prolonged sleep deprivation activates epileptiform EEG abnormalities and seizures in people with epilepsy. Few studies have addressed the effect of chronic partial sleep deprivation on seizure occurrence in populations with epilepsy. We tested the primary hypothesis that partial sleep deprivation over 24- and 72-hour periods increases seizure occurrence in adults with epilepsy. Forty-four subjects completed a series of self-reported instruments, as well as 1-month sleep and seizure diaries, to characterize their sleep and quality of life. Diaries were used to determine the relationship between seizure occurrence and total sleep time 24 and 72h before seizure occurrence using random effects models and a logistic regression model fit by generalized estimating equations. A total of 237 seizures were recorded during 1295 diary days, representing 5.5±7.0 (mean±SD) seizures per month. Random effects models for 24- and 72-hour total sleep times showed no clinically or statistically significant differences in the total sleep time between preseizure periods and seizure-free periods. The average 24-hour total sleep time during preseizure 24-hour periods was 8min shorter than that during seizure-free periods (p=0.51). The average 72-hour total sleep time during preseizure periods was 20min longer than that during seizure-free periods (p=0.86). The presence of triggers was a significant predictor of seizure occurrence, with stress/anxiety noted most often as a trigger. Mean total sleep time was 9h, and subjects took an average of 12±10 naps per month, having a mean duration of 1.9±1.2h. Daytime sleepiness, fatigue, and insomnia symptoms were commonly reported. Small degrees of sleep loss were not associated with seizure occurrence in our sample of adults with epilepsy. Our results also include valuable observations of the altered sleep times and frequent napping habits of adults with refractory epilepsy and the potential contribution of these habits to quality of life and

  4. Some effects of sleep deprivation on tracking performance in static and dynamic environments.

    DOT National Transportation Integrated Search

    1976-01-01

    The influence of approximately 34 and 55 h of sleep deprivation on performance scores derived from manually tracking the localizer needle on an aircraft instrument was assessed under both static (no motion) and dynamic (whole-body angular acceleratio...

  5. Characterization of Sleep in Aplysia californica

    PubMed Central

    Vorster, Albrecht P.A.; Krishnan, Harini C.; Cirelli, Chiara; Lyons, Lisa C.

    2014-01-01

    Study Objective: To characterize sleep in the marine mollusk, Aplysia californica. Design: Animal behavior and activity were assessed using video recordings to measure activity, resting posture, resting place preference, and behavior after rest deprivation. Latencies for behavioral responses were measured for appetitive and aversive stimuli for animals in the wake and rest states. Setting: Circadian research laboratory for Aplysia. Patients or Participants: A. californica from the Pacific Ocean. Interventions: N/A. Measurements and Results: Aplysia rest almost exclusively during the night in a semi-contracted body position with preferential resting locations in the upper corners of their tank. Resting animals demonstrate longer latencies in head orientation and biting in response to a seaweed stimulus and less frequent escape response steps following an aversive salt stimulus applied to the tail compared to awake animals at the same time point. Aplysia exhibit rebound rest the day following rest deprivation during the night, but not after similar handling stimulation during the day. Conclusions: Resting behavior in Aplysia fulfills all invertebrate characteristics of sleep including: (1) a specific sleep body posture, (2) preferred resting location, (3) reversible behavioral quiescence, (4) elevated arousal thresholds for sensory stimuli during sleep, and (5) compensatory sleep rebound after sleep deprivation. Citation: Vorster AP, Krishnan HC, Cirelli C, Lyons LC. Characterization of sleep in Aplysia californica. SLEEP 2014;37(9):1453-1463. PMID:25142567

  6. Increased Sleep Depth in Developing Neural Networks: New Insights from Sleep Restriction in Children

    PubMed Central

    Kurth, Salome; Dean, Douglas C.; Achermann, Peter; O’Muircheartaigh, Jonathan; Huber, Reto; Deoni, Sean C. L.; LeBourgeois, Monique K.

    2016-01-01

    Brain networks respond to sleep deprivation or restriction with increased sleep depth, which is quantified as slow-wave activity (SWA) in the sleep electroencephalogram (EEG). When adults are sleep deprived, this homeostatic response is most pronounced over prefrontal brain regions. However, it is unknown how children’s developing brain networks respond to acute sleep restriction, and whether this response is linked to myelination, an ongoing process in childhood that is critical for brain development and cortical integration. We implemented a bedtime delay protocol in 5- to 12-year-old children to obtain partial sleep restriction (1-night; 50% of their habitual sleep). High-density sleep EEG was assessed during habitual and restricted sleep and brain myelin content was obtained using mcDESPOT magnetic resonance imaging. The effect of sleep restriction was analyzed using statistical non-parametric mapping with supra-threshold cluster analysis. We observed a localized homeostatic SWA response following sleep restriction in a specific parieto-occipital region. The restricted/habitual SWA ratio was negatively associated with myelin water fraction in the optic radiation, a developing fiber bundle. This relationship occurred bilaterally over parieto-temporal areas and was adjacent to, but did not overlap with the parieto-occipital region showing the most pronounced homeostatic SWA response. These results provide evidence for increased sleep need in posterior neural networks in children. Sleep need in parieto-temporal areas is related to myelin content, yet it remains speculative whether age-related myelin growth drives the fading of the posterior homeostatic SWA response during the transition to adulthood. Whether chronic insufficient sleep in the sensitive period of early life alters the anatomical generators of deep sleep slow-waves is an important unanswered question. PMID:27708567

  7. Effects of Sleep Deprivation on U.S. Navy Watchstander Performance Onboard the Independence Class Littoral Combat Ship (LCS 2)

    DTIC Science & Technology

    2013-09-01

    obtained .........................................................................8 Table 2. NPS theses relating to work schedule, sleep , and/or fatigue ...an analysis of performance issues related to sleep deprivation and fatigue aboard the Independence Class Littoral Combat Ship (LCS 2). The unique...rotation led to “fragmented sleep of generally less than 6 hours in duration.” Efforts to correct the issue of fatigue within the Navy were at a

  8. Two nights of sleep deprivation with or without energy restriction does not impair the thermal response to cold.

    PubMed

    Oliver, Samuel J; Harper Smith, Adam D; Costa, Ricardo J S; Maassen, Norbert; Bilzon, James L J; Walsh, Neil P

    2015-10-01

    In persons completing exhaustive daily exercise, sleep and energy restriction have been highlighted as risk factors for hypothermia in cold environments. The present study therefore sought to determine the effect of sleep deprivation (SDEP), with and without energy restriction, on the thermal response to cold. In a random order, ten recreationally active men (mean ± SD: age 25 ± 6 years, body fat 17 ± 5 %) completed three 53 h trials: a control (CON: 436 min/night sleep), SDEP (0 min sleep), and sleep deprivation and energy restriction (SDEP + ER: 0 min sleep and 10% daily energy requirements). Exhaustive exercise was completed after 5 and 29 h. After 53 h participants completed a semi-nude seated cold air test (CAT, 0 °C), for 4 h or until rectal core temperature (T re) reached 36 °C. Two nights of sleep and energy restriction did not impair the thermal response to cold (T re, CON 36.15 ± 0.20 °C, SDEP 36.30 ± 0.15 °C, SDEP + ER 36.25 ± 0.20 °C, P = 0.25). Rewarming was also similar as indicated by 1 h post-CAT T re (P = 0.78). In contrast, perceived thermal discomfort during the initial hour of the CAT tended to be greater after SDEP and SDEP + ER (P ≤ 0.1). Sleep and energy restriction, at least as evaluated within this experiment, should be considered minimal risk factors for hypothermia. The greater perception of cold discomfort at the same body temperature suggests that sleep and energy restriction may actually reduce cold injury risk, as people are likely to engage earlier in normal behavioral cold adaptation.

  9. Effects of Sleep Deprivation on Cognitive Ability and Skills of Pediatrics Residents.

    ERIC Educational Resources Information Center

    Storer, James S.; And Others

    1989-01-01

    The cognitive and skills performances of sleep-deprived pediatrics residents were measured by using questions like those on the pediatrics board certification examination and using tasks that required coordination and dexterity. Implications of findings are discussed in the context of the controversy over the structure and process of medical…

  10. Advice for the Sleep-Deprived

    ERIC Educational Resources Information Center

    Wolfe, Pat

    2005-01-01

    A research has uncovered that adolescent sleep patterns are influenced not so much by the activities of the young adults as by the changes taking place in the biological timing system of their brains. It is evident that teenagers are not getting the amount of sleep they require and suggestions are presented to help diminish if not entirely avoid…

  11. Sleep disturbances and resistant hypertension: association or causality?

    PubMed

    Genta-Pereira, Daniel Castanho; Pedrosa, Rodrigo P; Lorenzi-Filho, Geraldo; Drager, Luciano F

    2014-08-01

    Two main sleep disturbances, namely obstructive sleep apnea (OSA) and sleep deprivation, have gained growing interest in the field of hypertension research. This fact is supported not only by evidence that both disturbances are quite common in modern societies but also that OSA and sleep deprivation are associated with several pathways that may contribute to a predisposition to hypertension or even exacerbate blood pressure levels in hypertensive patients. In the present review, we will discuss current evidence supporting a potential role of these sleep disturbances in the resistant hypertension scenario.

  12. Pupillographic assessment of sleepiness in sleep-deprived healthy subjects.

    PubMed

    Wilhelm, B; Wilhelm, H; Lüdtke, H; Streicher, P; Adler, M

    1998-05-01

    Spontaneous pupillary-behavior in darkness provides information about a subject's level of sleepiness. In the present work, pupil measurements in complete darkness and quiet have been recorded continuously over 11-minute period with infrared video pupillography at 25 Hz. The data have been analyzed to yield three parameters describing pupil behavior; the power of diameter variation at frequencies below 0.8 Hz (slow changes in pupil size), the pupillary unrest index, and the average pupil size. To investigate the changes of these parameters in sleep deprivation, spontaneous pupillary behavior in darkness was recorded every 2 hours in 13 healthy subjects from 19:00 to 07:00 during forced wakefulness. On each occasion, comparative subjective sleepiness was assessed with a self-rating scale (Stanford Sleepiness Scale, SSS). The power of slow pupillary oscillations (< or = 0.8 Hz) increased significantly and so did the values of SSS, while basic pupil diameter decreased significantly. Slow pupillary oscillations and SSS did not correlate well in general but high values of pupil parameters were always associated with high values in subjective rating. Our results demonstrate a strong relationship between ongoing sleep deprivation and typical changes in the frequency profiles of spontaneous pupillary oscillations and the tendency to instability in pupil size in normals. These findings suggest that the results of pupil data analysis permit an objective measurement of sleepiness.

  13. Chronic social stress leads to altered sleep homeostasis in mice.

    PubMed

    Olini, Nadja; Rothfuchs, Iru; Azzinnari, Damiano; Pryce, Christopher R; Kurth, Salome; Huber, Reto

    2017-06-01

    Disturbed sleep and altered sleep homeostasis are core features of many psychiatric disorders such as depression. Chronic uncontrollable stress is considered an important factor in the development of depression, but little is known on how chronic stress affects sleep regulation and sleep homeostasis. We therefore examined the effects of chronic social stress (CSS) on sleep regulation in mice. Adult male C57BL/6 mice were implanted for electrocortical recordings (ECoG) and underwent either a 10-day CSS protocol or control handling (CON). Subsequently, ECoG was assessed across a 24-h post-stress baseline, followed by a 4-h sleep deprivation, and then a 20-h recovery period. After sleep deprivation, CSS mice showed a blunted increase in sleep pressure compared to CON mice, as measured using slow wave activity (SWA, electroencephalographic power between 1-4Hz) during non-rapid eye movement (NREM) sleep. Vigilance states did not differ between CSS and CON mice during post-stress baseline, sleep deprivation or recovery, with the exception of CSS mice exhibiting increased REM sleep during recovery sleep. Behavior during sleep deprivation was not affected by CSS. Our data provide evidence that CSS alters the homeostatic regulation of sleep SWA in mice. In contrast to acute social stress, which results in a faster SWA build-up, CSS decelerates the homeostatic build up. These findings are discussed in relation to the causal contribution of stress-induced sleep disturbance to depression. Copyright © 2017 Elsevier B.V. All rights reserved.

  14. Sleeping difficulties and health-related quality of life in Parkinson's disease.

    PubMed

    Ylikoski, A; Martikainen, K; Sieminski, M; Partinen, M

    2017-04-01

    Various sleep-related symptoms occur in Parkinson's disease (PD). Their occurrence with health-related quality of life (HRQL), comorbid sleep disorders, and other comorbidities was studied. Altogether, 1447 randomly selected patients with Parkinson's disease, aged 43-89 years, participated in a questionnaire study. A structured questionnaire with 207 items was based on the Basic Nordic Sleep Questionnaire. Questions on demographics, PD, sleep disorders, and comorbidities were included. The response rate was 59.0%, and of these, 80% had answered to all questions that were used in the analyses (N=684). Occurrence of long sleep was found in 26.2% of the subjects, short sleep in 32.5%, poor sleep in 21.2%, sleep deprivation in 33.8%, disrupted sleep in 47.4%, and difficulties to fall asleep in 12.2%, respectively. Poor self-rated health and poor quality of life occurred in 44.4% and in 43.3% of all participants. In the logistic regression, age and gender differentially predicted long sleep and sleep deprivation, such that older age and being male were positively associated with long sleep but negatively associated with the report of sleep deprivation. Depression, subjective negative stress, and fatigue occurred with long sleep. On the other hand, poor sleep and excessive daytime sleepiness occurred with short sleep and sleep deprivation. The sleep difficulties in PD are frequent. The long sleeping patients have depression, stress, and fatigue. © 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

  15. Mammalian sleep

    NASA Astrophysics Data System (ADS)

    Staunton, Hugh

    2005-05-01

    This review examines the biological background to the development of ideas on rapid eye movement sleep (REM sleep), so-called paradoxical sleep (PS), and its relation to dreaming. Aspects of the phenomenon which are discussed include physiological changes and their anatomical location, the effects of total and selective sleep deprivation in the human and animal, and REM sleep behavior disorder, the latter with its clinical manifestations in the human. Although dreaming also occurs in other sleep phases (non-REM or NREM sleep), in the human, there is a contingent relation between REM sleep and dreaming. Thus, REM is taken as a marker for dreaming and as REM is distributed ubiquitously throughout the mammalian class, it is suggested that other mammals also dream. It is suggested that the overall function of REM sleep/dreaming is more important than the content of the individual dream; its function is to place the dreamer protagonist/observer on the topographical world. This has importance for the developing infant who needs to develop a sense of self and separateness from the world which it requires to navigate and from which it is separated for long periods in sleep. Dreaming may also serve to maintain a sense of ‘I’ness or “self” in the adult, in whom a fragility of this faculty is revealed in neurological disorders.

  16. The Degree of Radiation-Induced DNA Strand Breaks Is Altered by Acute Sleep Deprivation and Psychological Stress and Is Associated with Cognitive Performance in Humans.

    PubMed

    Moreno-Villanueva, Maria; von Scheven, Gudrun; Feiveson, Alan; Bürkle, Alexander; Wu, Honglu; Goel, Namni

    2018-03-27

    Sleep deprivation is associated with impaired immune responses, cancer, and morbidity and mortality, and can degrade cognitive performance, although individual differences exist in such responses. Sleep deprivation induces DNA strand breaks and DNA base oxidation in animals, and psychological stress is associated with increased DNA damage in humans. It remains unknown whether sleep deprivation or psychological stress in humans affects DNA damage response from environmental stressors, and whether these responses predict cognitive performance during sleep deprivation. Sixteen healthy adults (ages 29-52;mean age±SD, 36.4±7.1 years;7 women) participated in a 5-day experiment involving two 8 hour time-in-bed [TIB] baseline nights, followed by 39 hours total sleep deprivation (TSD), and two 8-10 hour TIB recovery nights. A modified Trier Social Stress Test was conducted on the day after TSD. Psychomotor Vigilance Tests measured behavioral attention. DNA damage was assessed in blood cells collected at 5 time points, and blood cells were irradiated ex-vivo. TSD, alone or in combination with psychological stress, did not induce significant increases in DNA damage. By contrast, radiation-induced DNA damage decreased significantly in response to TSD, but increased back to baseline when combined with psychological stress. Cognitively-vulnerable individuals had more radiation-induced DNA strand breaks before TSD, indicating their greater sensitivity to DNA damage from environmental stressors. Our results provide novel insights into the molecular consequences of sleep deprivation, psychological stress, and performance vulnerability. They are important for situations involving sleep loss, radiation exposure and cognitive deficits, including cancer therapy, environmental toxicology, and space medicine.

  17. The effects of one night of partial sleep deprivation on executive functions in individuals reporting chronic insomnia and good sleepers.

    PubMed

    Ballesio, Andrea; Cerolini, Silvia; Ferlazzo, Fabio; Cellini, Nicola; Lombardo, Caterina

    2018-02-15

    The aim of the present study was to investigate the effects of a partial sleep deprivation night on executive functions in participants reporting chronic insomnia and good sleepers using a Task Switching paradigm. Sixteen participants reporting symptoms of chronic insomnia and sixteen good sleepers were tested after a night of habitual sleep and after a night of partial sleep deprivation (5 h of sleep allowed). The Switch Cost (SC) and the Backward Inhibition (BI) were computed as measures of switching attention and response inhibition, respectively. We observed a marginally significant interaction Night × Group on SC (F (1,29)  = 4.06, p = 0.053), η 2  = 0.123. Fisher's least significant difference (LSD) post-hoc revealed a smaller SC after the sleep deprived night relative to the habitual night for the good sleepers (p = 0.027; M = 192.23 ± 201.81 vs M = 98.99 ± 141.16). Differently, participants with insomnia did not show any change after the two nights. Several limitations must be acknowledged including the use of a convenient sample of university students and the use of a single task of cognitive performance. We found that SC was smaller in the good sleepers after a night of partial sleep deprivation compared to a habitual night, indicating a better switching performance. The insomnia group showed no differences in performance after the two experimental nights. Several factors may account for these results, including increased levels of arousal and cognitive effort during task execution. Copyright © 2018 Elsevier Ltd. All rights reserved.

  18. Effect of caffeine on simulator flight performance in sleep-deprived military pilot students.

    PubMed

    Lohi, Jouni J; Huttunen, Kerttu H; Lahtinen, Taija M M; Kilpeläinen, Airi A; Muhli, Arto A; Leino, Tuomo K

    2007-09-01

    Caffeine has been suggested to act as a countermeasure against fatigue in military operations. In this randomized, double-blind, placebo-controlled study, the effect of caffeine on simulator flight performance was examined in 13 military pilots during 37 hours of sleep deprivation. Each subject performed a flight mission in simulator four times. The subjects received either a placebo (six subjects) or 200 mg of caffeine (seven subjects) 1 hour before the simulated flights. A moderate 200 mg intake of caffeine was associated with higher axillary temperatures, but it did not affect subjectively assessed sleepiness. Flight performance was similar in both groups during the four rounds flown under sleep deprivation. However, subjective evaluation of overall flight performance in the caffeine group tended to be too optimistic, indicating a potential flight safety problem. Based on our results, we do not recommend using caffeine pills in military flight operations.

  19. Perceived Sleepiness, Sleep Habits and Sleep Concerns of Public School Teachers, Administrators and Other Personnel

    ERIC Educational Resources Information Center

    Amschler, Denise H.; McKenzie, James F.

    2010-01-01

    Background: Sleep deprivation is a world-wide health concern. Few studies have examined the sleep behaviors of those employed in the education field. Purpose: To describe the sleep habits and concerns of school personnel in a Midwest school corporation. Methods: A cross-sectional survey design was used to collect data about demographics, the…

  20. Sleep enhances false memories depending on general memory performance.

    PubMed

    Diekelmann, Susanne; Born, Jan; Wagner, Ullrich

    2010-04-02

    Memory is subject to dynamic changes, sometimes giving rise to the formation of false memories due to biased processes of consolidation or retrieval. Sleep is known to benefit memory consolidation through an active reorganization of representations whereas acute sleep deprivation impairs retrieval functions. Here, we investigated whether sleep after learning and sleep deprivation at retrieval enhance the generation of false memories in a free recall test. According to the Deese, Roediger, McDermott (DRM) false memory paradigm, subjects learned lists of semantically associated words (e.g., "night", "dark", "coal", etc.), lacking the strongest common associate or theme word (here: "black"). Free recall was tested after 9h following a night of sleep, a night of wakefulness (sleep deprivation) or daytime wakefulness. Compared with memory performance after a retention period of daytime wakefulness, both post-learning nocturnal sleep as well as acute sleep deprivation at retrieval significantly enhanced false recall of theme words. However, these effects were only observed in subjects with low general memory performance. These data point to two different ways in which sleep affects false memory generation through semantic generalization: one acts during consolidation on the memory trace per se, presumably by active reorganization of the trace in the post-learning sleep period. The other is related to the recovery function of sleep and affects cognitive control processes of retrieval. Both effects are unmasked when the material is relatively weakly encoded. Crown Copyright 2009. Published by Elsevier B.V. All rights reserved.

  1. Genes involved in the astrocyte-neuron lactate shuttle (ANLS) are specifically regulated in cortical astrocytes following sleep deprivation in mice.

    PubMed

    Petit, Jean-Marie; Gyger, Joël; Burlet-Godinot, Sophie; Fiumelli, Hubert; Martin, Jean-Luc; Magistretti, Pierre J

    2013-10-01

    There is growing evidence indicating that in order to meet the neuronal energy demands, astrocytes provide lactate as an energy substrate for neurons through a mechanism called "astrocyte-neuron lactate shuttle" (ANLS). Since neuronal activity changes dramatically during vigilance states, we hypothesized that the ANLS may be regulated during the sleep-wake cycle. To test this hypothesis we investigated the expression of genes associated with the ANLS specifically in astrocytes following sleep deprivation. Astrocytes were purified by fluorescence-activated cell sorting from transgenic mice expressing the green fluorescent protein (GFP) under the control of the human astrocytic GFAP-promoter. 6-hour instrumental sleep deprivation (TSD). Animal sleep research laboratory. Young (P23-P27) FVB/N-Tg (GFAP-GFP) 14Mes/J (Tg) mice of both sexes and 7-8 week male Tg and FVB/Nj mice. Basal sleep recordings and sleep deprivation achieved using a modified cage where animals were gently forced to move. Since Tg and FVB/Nj mice displayed a similar sleep-wake pattern, we performed a TSD in young Tg mice. Total RNA was extracted from the GFP-positive and GFP-negative cells sorted from cerebral cortex. Quantitative RT-PCR analysis showed that levels of Glut1, α-2-Na/K pump, Glt1, and Ldha mRNAs were significantly increased following TSD in GFP-positive cells. In GFP-negative cells, a tendency to increase, although not significant, was observed for Ldha, Mct2, and α-3-Na/K pump mRNAs. This study shows that TSD induces the expression of genes associated with ANLS specifically in astrocytes, underlying the important role of astrocytes in the maintenance of the neuro-metabolic coupling across the sleep-wake cycle.

  2. Enhancing Slow Wave Sleep with Sodium Oxybate Reduces the Behavioral and Physiological Impact of Sleep Loss

    PubMed Central

    Walsh, James K.; Hall-Porter, Janine M.; Griffin, Kara S.; Dodson, Ehren R.; Forst, Elizabeth H.; Curry, Denise T.; Eisenstein, Rhody D.; Schweitzer, Paula K.

    2010-01-01

    Study Objectives: To investigate whether enhancement of slow wave sleep (SWS) with sodium oxybate reduces the impact of sleep deprivation. Design: Double-blind, parallel group, placebo-controlled design Setting: Sleep research laboratory Participants: Fifty-eight healthy adults (28 placebo, 30 sodium oxybate), ages 18-50 years. Interventions: A 5-day protocol included 2 screening/baseline nights and days, 2 sleep deprivation nights, each followed by a 3-h daytime (08:00-11:00) sleep opportunity and a recovery night. Sodium oxybate or placebo was administered prior to each daytime sleep period. Multiple sleep latency test (MSLT), psychomotor vigilance test (PVT), Karolinska Sleepiness Scale (KSS), and Profile of Mood States were administered during waking hours. Measurements and Results: During daytime sleep, the sodium oxybate group had more SWS, more EEG spectral power in the 1-9 Hz range, and less REM. Mean MSLT latency was longer for the sodium oxybate group on the night following the first daytime sleep period and on the day following the second day sleep period. Median PVT reaction time was faster in the sodium oxybate group following the second day sleep period. The change from baseline in SWS was positively correlated with the change in MSLT and KSS. During recovery sleep the sodium oxybate group had less TST, SWS, REM, and slow wave activity (SWA) than the placebo group. Conclusions: Pharmacological enhancement of SWS with sodium oxybate resulted in a reduced response to sleep loss on measures of alertness and attention. In addition, SWS enhancement during sleep restriction appears to result in a reduced homeostatic response to sleep loss. Citation: Walsh JK; Hall-Porter JM; Griffin KS; Dodson ER; Forst EH; Curry DT; Eisenstein RD; Schweitzer PK. Enhancing slow wave sleep with sodium oxybate reduces the behavioral and physiological impact of sleep loss. SLEEP 2010;33(9):1217-1225. PMID:20857869

  3. Differences in sensory reweighting due to loss of visual and proprioceptive cues in postural stability support among sleep-deprived cadet pilots.

    PubMed

    Cheng, Shan; Ma, Jin; Sun, Jicheng; Wang, Jian; Xiao, Xiao; Wang, Yihan; Hu, Wendong

    2018-04-26

    Sleep deprivation is known to diminish postural control. We investigated whether sleep deprivation affects sensory reweighting for postural control due to loss of visual and proprioceptive cues. Two cohorts of cadet pilots were deprived of sleep for 40 h. Variabilty in force-platform center of pressure was analyzed based on the whole path length (WPL); circumference area (CA); mean of displacement along x and y axes and corresponding standard deviations (SDx, SDy); and frequency of body-sway intensity, all of which were recorded while the cadets stood with eyes open (NEO), eyes closed (NEC), and eyes closed on a foam platform base (FEC) A sleepiness index (SUBI) based on principal component analysis of selected Cohort 1 data (n = 37) was used to compare Cohort 2 data (n = 29) with scores for the Stanford Sleepiness Scale (SSS) and Pittsburg Sleep Quality Index (PSQI). Balance began to deteriorate at 16 h for NEO and at 28 h for NEC and FEC (p < 0.05). At 40 h, WPL, CA, and SDy of COP for NEO indicated balance deteriorated further while WPL and SDy for NEC and WPL, CA, SDx, and SDy for FEC indicated balance incrementally improved. Frequency bias of body-sway differed between NEO, NEC, and FEC. In Cohort 2, the SUBI correlated significantly with SSS (p < 0.05), but not with PSQI. Effects of sleep deprivation were mitigated over time, suggesting that compensatory mechanisms influenced sensory reweighting for NEC and FEC between 28 and 40 h of sleep deprivation, but not for NEO. Frequency bias of body-sway suggested that sensory reweighting in the absence of visual cues differed from that in the absence of both visual and proprioceptive cues. Copyright © 2018 Elsevier B.V. All rights reserved.

  4. Morin hydrate mitigates rapid eye movement sleep deprivation-induced neurobehavioural impairments and loss of viable neurons in the hippocampus of mice.

    PubMed

    Olonode, Elizabeth T; Aderibigbe, Adegbuyi O; Adeoluwa, Olusegun A; Eduviere, Anthony T; Ben-Azu, Benneth

    2017-12-25

    Rapid eye movement sleep deprivation distorts the body's homeostasis and results in oxidative breakdown which may be responsible for a variety of neurological disorders. Some naturally occurring compounds of plant origin with antioxidant and neuroprotective properties are known to attenuate the detrimental effects of REM sleep deprivation. Morin hydrate, a flavonoid from Mulberry has demonstrated antioxidant and neuroprotective activities but its effect in sleep disturbed mice is unknown. The study was designed to explore the neuroprotective effect of Morin hydrate on 48 h. REM sleep deprivation-induced behavioural impairments and neuronal damage in mice. Mice were allotted into six treatment groups (n = 6): groups 1 and 2 received vehicle (10 ml/kg normal saline), groups 3-5 received Morin hydrate (5, 10, 20 mg/kg i.p) while group 6 received ginseng (25 mg/kg) which served as the reference drug. Treatment was performed daily for 5 days and animals were sleep-deprived on the last 48 h. Various behavioural tests (Elevated plus maze, Y-maze, locomotor activity) followed by oxidative parameters (malondialdehyde, nitric oxide, reduced glutathione) and histolopathological changes in the Cornu ammonis 1 (CA1) region of the hippocampus were assessed. Data were analysed using ANOVA at α 0.05 . Morin hydrate (5, 10, 20 mg/kg) significantly enhanced memory performance, improves anxiolytic-like behaviour, reverses hyperlocomotion, restored depleted reduced glutathione, attenuated raised malondialdehyde and nitric oxide levels as compared to control animals and protects against loss of hippocampal neurons. Results of this present study suggest that Morin hydrate possess neuroprotective effects against sleep deprivation-induced behavioural impairments, oxidative stress and neuronal damage. Copyright © 2017 Elsevier B.V. All rights reserved.

  5. Age-Related Reduction of Recovery Sleep and Arousal Threshold in Drosophila.

    PubMed

    Vienne, Julie; Spann, Ryanne; Guo, Fang; Rosbash, Michael

    2016-08-01

    Physiological studies show that aging affects both sleep quality and quantity in humans, and sleep complaints increase with age. Along with knowledge about the negative effects of poor sleep on health, understanding the enigmatic relationship between sleep and aging is important. Because human sleep is similar to Drosophila (fruit fly) sleep in many ways, we addressed the effects of aging on sleep in this model organism. Baseline sleep was recorded in five different Drosophila genotypes raised at either 21°C or 25°C. The amount of sleep recovered was then investigated after a nighttime of sleep deprivation (12 h) and after chronic sleep deprivation (3 h every night for multiple nights). Finally, the effects of aging on arousal, namely, sensitivity to neuronal and mechanical stimuli, were studied. We show that fly sleep is affected by age in a manner similar to that of humans and other mammals. Not only do older flies of several genotypes have more fragmented sleep and reduced total sleep time compared to young flies, but older flies also fail to recover as much sleep after sleep deprivation. This suggests either lower sleep homeostasis and/or a failure to properly recover sleep. Older flies also show a decreased arousal threshold, i.e., an increased response to neuronal and mechanical wake-promoting stimuli. The reduced threshold may either reflect or cause the reduced recovery sleep of older flies compared to young flies after sleep deprivation. Further studies are certainly needed, but we suggest that the lower homeostatic sleep drive of older flies causes their decreased arousal threshold. © 2016 Associated Professional Sleep Societies, LLC.

  6. [Sleep disorders among physicians on shift work].

    PubMed

    Schlafer, O; Wenzel, V; Högl, B

    2014-11-01

    Sleep disorders in physicians who perform shift work can result in increased risks of health problems that negatively impact performance and patient safety. Even those who cope well with shift work are likely to suffer from sleep disorders. The aim of this manuscript is to discuss possible causes, contributing factors and consequences of sleep disorders in physicians and to identify measures that can improve adaptation to shift work and treatment strategies for shift work-associated sleep disorders. The risk factors that influence the development of sleep disorders in physicians are numerous and include genetic factors (15 % of the population), age (> 50 years), undiagnosed sleep apnea,, alcohol abuse as well as multiple stress factors inherent in clinical duties (including shift work), research, teaching and family obligations. Several studies have reported an increased risk for medical errors in sleep-deprived physicians. Shift workers have an increased risk for psychiatric and cardiovascular diseases and shift work may also be a contributing factor to cancer. A relationship has been reported not only with sleep deprivation and changes in food intake but also with diabetes mellitus, obesity, hypertension and coronary heart disease. Nicotine and alcohol consumption are more frequent among shift workers. Increased sickness and accident rates among physicians when commuting (especially after night shifts) have a socioeconomic impact. In order to reduce fatigue and to improve performance, short naps during shiftwork or naps plus caffeine, have been proposed as coping strategies; however, napping during adverse circadian phases is less effective, if not impossible when unable to fall asleep. Bright and blue light supports alertness during a night shift. After shiftwork, direct sunlight exposure to the retina can be avoided by using dark sunglasses or glasses with orange lenses for commuting home. The home environment for daytime sleeping after a night shift should be

  7. Age-Related Reduction of Recovery Sleep and Arousal Threshold in Drosophila

    PubMed Central

    Vienne, Julie; Spann, Ryanne; Guo, Fang; Rosbash, Michael

    2016-01-01

    Study Objectives: Physiological studies show that aging affects both sleep quality and quantity in humans, and sleep complaints increase with age. Along with knowledge about the negative effects of poor sleep on health, understanding the enigmatic relationship between sleep and aging is important. Because human sleep is similar to Drosophila (fruit fly) sleep in many ways, we addressed the effects of aging on sleep in this model organism. Methods: Baseline sleep was recorded in five different Drosophila genotypes raised at either 21°C or 25°C. The amount of sleep recovered was then investigated after a nighttime of sleep deprivation (12 h) and after chronic sleep deprivation (3 h every night for multiple nights). Finally, the effects of aging on arousal, namely, sensitivity to neuronal and mechanical stimuli, were studied. Results: We show that fly sleep is affected by age in a manner similar to that of humans and other mammals. Not only do older flies of several genotypes have more fragmented sleep and reduced total sleep time compared to young flies, but older flies also fail to recover as much sleep after sleep deprivation. This suggests either lower sleep homeostasis and/or a failure to properly recover sleep. Older flies also show a decreased arousal threshold, i.e., an increased response to neuronal and mechanical wake-promoting stimuli. The reduced threshold may either reflect or cause the reduced recovery sleep of older flies compared to young flies after sleep deprivation. Conclusions: Further studies are certainly needed, but we suggest that the lower homeostatic sleep drive of older flies causes their decreased arousal threshold. Citation: Vienne J, Spann R, Guo F, Rosbash M. Age-related reduction of recovery sleep and arousal threshold in Drosophila. SLEEP 2016;39(8):1613–1624. PMID:27306274

  8. MicroRNAs Regulate Sleep and Sleep Homeostasis in Drosophila.

    PubMed

    Goodwin, Patricia R; Meng, Alice; Moore, Jessie; Hobin, Michael; Fulga, Tudor A; Van Vactor, David; Griffith, Leslie C

    2018-06-26

    To discover microRNAs that regulate sleep, we performed a genetic screen using a library of miRNA sponge-expressing flies. We identified 25 miRNAs that regulate baseline sleep; 17 were sleep-promoting and 8 promoted wake. We identified one miRNA that is required for recovery sleep after deprivation and 8 miRNAs that limit the extent of recovery sleep. 65% of the hits belong to human-conserved families. Interestingly, the majority (75%), but not all, of the baseline sleep-regulating miRNAs are required in neurons. Sponges that target miRNAs in the same family, including the miR-92a/92b/310 family and the miR-263a/263b family, have similar effects. Finally, mutation of one of the screen's strongest hits, let-7, using CRISPR/Cas-9, phenocopies sponge-mediated let-7 inhibition. Cell-type-specific and temporally restricted let-7 sponge expression experiments suggest that let-7 is required in the mushroom body both during development and in adulthood. This screen sets the stage for understanding the role of miRNAs in sleep. Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.

  9. The brain functional connectome is robustly altered by lack of sleep.

    PubMed

    Kaufmann, Tobias; Elvsåshagen, Torbjørn; Alnæs, Dag; Zak, Nathalia; Pedersen, Per Ø; Norbom, Linn B; Quraishi, Sophia H; Tagliazucchi, Enzo; Laufs, Helmut; Bjørnerud, Atle; Malt, Ulrik F; Andreassen, Ole A; Roussos, Evangelos; Duff, Eugene P; Smith, Stephen M; Groote, Inge R; Westlye, Lars T

    2016-02-15

    Sleep is a universal phenomenon necessary for maintaining homeostasis and function across a range of organs. Lack of sleep has severe health-related consequences affecting whole-body functioning, yet no other organ is as severely affected as the brain. The neurophysiological mechanisms underlying these deficits are poorly understood. Here, we characterize the dynamic changes in brain connectivity profiles inflicted by sleep deprivation and how they deviate from regular daily variability. To this end, we obtained functional magnetic resonance imaging data from 60 young, adult male participants, scanned in the morning and evening of the same day and again the following morning. 41 participants underwent total sleep deprivation before the third scan, whereas the remainder had another night of regular sleep. Sleep deprivation strongly altered the connectivity of several resting-state networks, including dorsal attention, default mode, and hippocampal networks. Multivariate classification based on connectivity profiles predicted deprivation state with high accuracy, corroborating the robustness of the findings on an individual level. Finally, correlation analysis suggested that morning-to-evening connectivity changes were reverted by sleep (control group)-a pattern which did not occur after deprivation. We conclude that both, a day of waking and a night of sleep deprivation dynamically alter the brain functional connectome. Copyright © 2015 Elsevier Inc. All rights reserved.

  10. Voluntary Sleep Loss in Rats.

    PubMed

    Oonk, Marcella; Krueger, James M; Davis, Christopher J

    2016-07-01

    Animal sleep deprivation (SDEP), in contrast to human SDEP, is involuntary and involves repeated exposure to aversive stimuli including the inability of the animal to control the waking stimulus. Therefore, we explored intracranial self-stimulation (ICSS), an operant behavior, as a method for voluntary SDEP in rodents. Male Sprague-Dawley rats were implanted with electroencephalography/electromyography (EEG/EMG) recording electrodes and a unilateral bipolar electrode into the lateral hypothalamus. Rats were allowed to self-stimulate, or underwent gentle handling-induced SDEP (GH-SDEP), during the first 6 h of the light phase, after which they were allowed to sleep. Other rats performed the 6 h ICSS and 1 w later were subjected to 6 h of noncontingent stimulation (NCS). During NCS the individual stimulation patterns recorded during ICSS were replayed. After GH-SDEP, ICSS, or NCS, time in nonrapid eye movement (NREM) sleep and rapid eye movement (REM) sleep increased. Further, in the 24 h after SDEP, rats recovered all of the REM sleep lost during SDEP, but only 75% to 80% of the NREM sleep lost, regardless of the SDEP method. The magnitude of EEG slow wave responses occurring during NREM sleep also increased after SDEP treatments. However, NREM sleep EEG slow wave activity (SWA) responses were attenuated following ICSS, compared to GH-SDEP and NCS. We conclude that ICSS and NCS can be used to sleep deprive rats. Changes in rebound NREM sleep EEG SWA occurring after ICSS, NCS, and GH-SDEP suggest that nonspecific effects of the SDEP procedure differentially affect recovery sleep phenotypes. © 2016 Associated Professional Sleep Societies, LLC.

  11. Sleep Deprivation Impairs and Caffeine Enhances My Performance, but Not Always Our Performance

    PubMed Central

    Faber, Nadira S.; Häusser, Jan A.; Kerr, Norbert L.

    2016-01-01

    What effects do factors that impair or enhance performance in individuals have when these individuals act in groups? We provide a framework, called the GIE ("Effects of Grouping on Impairments and Enhancements”) framework, for investigating this question. As prominent examples for individual-level impairments and enhancements, we discuss sleep deprivation and caffeine. Based on previous research, we derive hypotheses on how they influence performance in groups, specifically process gains and losses in motivation, individual capability, and coordination. We conclude that the effect an impairment or enhancement has on individual-level performance is not necessarily mirrored in group performance: grouping can help or hurt. We provide recommendations on how to estimate empirically the effects individual-level performance impairments and enhancements have in groups. By comparing sleep deprivation to stress and caffeine to pharmacological cognitive enhancement, we illustrate that we cannot readily generalize from group results on one impairment or enhancement to another, even if they have similar effects on individual-level performance. PMID:26468077

  12. Sleep Deprivation Impairs and Caffeine Enhances My Performance, but Not Always Our Performance.

    PubMed

    Faber, Nadira S; Häusser, Jan A; Kerr, Norbert L

    2017-02-01

    What effects do factors that impair or enhance performance in individuals have when these individuals act in groups? We provide a framework, called the GIE ("Effects of Grouping on Impairments and Enhancements") framework, for investigating this question. As prominent examples for individual-level impairments and enhancements, we discuss sleep deprivation and caffeine. Based on previous research, we derive hypotheses on how they influence performance in groups, specifically process gains and losses in motivation, individual capability, and coordination. We conclude that the effect an impairment or enhancement has on individual-level performance is not necessarily mirrored in group performance: grouping can help or hurt. We provide recommendations on how to estimate empirically the effects individual-level performance impairments and enhancements have in groups. By comparing sleep deprivation to stress and caffeine to pharmacological cognitive enhancement, we illustrate that we cannot readily generalize from group results on one impairment or enhancement to another, even if they have similar effects on individual-level performance.

  13. Why Sleep Matters—The Economic Costs of Insufficient Sleep

    PubMed Central

    Hafner, Marco; Stepanek, Martin; Taylor, Jirka; Troxel, Wendy M.; van Stolk, Christian

    2017-01-01

    Abstract The Centers for Disease Control and Prevention (CDC) in the United States has declared insufficient sleep a “public health problem.” Indeed, according to a recent CDC study, more than a third of American adults are not getting enough sleep on a regular basis. However, insufficient sleep is not exclusively a US problem, and equally concerns other industrialised countries such as the United Kingdom, Japan, Germany, or Canada. According to some evidence, the proportion of people sleeping less than the recommended hours of sleep is rising and associated with lifestyle factors related to a modern 24/7 society, such as psychosocial stress, alcohol consumption, smoking, lack of physical activity and excessive electronic media use, among others. This is alarming as insufficient sleep has been found to be associated with a range of negative health and social outcomes, including success at school and in the labour market. Over the last few decades, for example, there has been growing evidence suggesting a strong association between short sleep duration and elevated mortality risks. Given the potential adverse effects of insufficient sleep on health, well-being and productivity, the consequences of sleep-deprivation have far-reaching economic consequences. Hence, in order to raise awareness of the scale of insufficient sleep as a public-health issue, comparative quantitative figures need to be provided for policy- and decision-makers, as well as recommendations and potential solutions that can help tackling the problem. PMID:28983434

  14. Voluntary Sleep Loss in Rats

    PubMed Central

    Oonk, Marcella; Krueger, James M.; Davis, Christopher J.

    2016-01-01

    Study Objectives: Animal sleep deprivation (SDEP), in contrast to human SDEP, is involuntary and involves repeated exposure to aversive stimuli including the inability of the animal to control the waking stimulus. Therefore, we explored intracranial self-stimulation (ICSS), an operant behavior, as a method for voluntary SDEP in rodents. Methods: Male Sprague-Dawley rats were implanted with electroencephalography/electromyography (EEG/EMG) recording electrodes and a unilateral bipolar electrode into the lateral hypothalamus. Rats were allowed to self-stimulate, or underwent gentle handling-induced SDEP (GH-SDEP), during the first 6 h of the light phase, after which they were allowed to sleep. Other rats performed the 6 h ICSS and 1 w later were subjected to 6 h of noncontingent stimulation (NCS). During NCS the individual stimulation patterns recorded during ICSS were replayed. Results: After GH-SDEP, ICSS, or NCS, time in nonrapid eye movement (NREM) sleep and rapid eye movement (REM) sleep increased. Further, in the 24 h after SDEP, rats recovered all of the REM sleep lost during SDEP, but only 75% to 80% of the NREM sleep lost, regardless of the SDEP method. The magnitude of EEG slow wave responses occurring during NREM sleep also increased after SDEP treatments. However, NREM sleep EEG slow wave activity (SWA) responses were attenuated following ICSS, compared to GH-SDEP and NCS. Conclusions: We conclude that ICSS and NCS can be used to sleep deprive rats. Changes in rebound NREM sleep EEG SWA occurring after ICSS, NCS, and GH-SDEP suggest that nonspecific effects of the SDEP procedure differentially affect recovery sleep phenotypes. Citation: Oonk M, Krueger JM, Davis CJ. Voluntary sleep loss in rats. SLEEP 2016;39(7):1467–1479. PMID:27166236

  15. Preemptive Caffeine Administration Blocks the Increase in Postoperative Pain Caused by Previous Sleep Loss in the Rat: A Potential Role for Preoptic Adenosine A2A Receptors in Sleep-Pain Interactions.

    PubMed

    Hambrecht-Wiedbusch, Viviane S; Gabel, Maya; Liu, Linda J; Imperial, John P; Colmenero, Angelo V; Vanini, Giancarlo

    2017-09-01

    Sleep and pain are reciprocally related, but the precise mechanisms underlying this relationship are poorly understood. This study used a rat model of surgical pain to examine the effect of previous sleep loss on postoperative pain and tested the hypothesis that preoptic adenosinergic mechanisms regulate sleep-pain interactions. Relative to ad libitum sleep, 6 hours of total sleep deprivation prior to a surgical incision significantly enhanced postoperative mechanical hypersensitivity in the affected paw and prolonged the time to recovery from surgery. There were no sex-specific differences in these measures. There were also no changes in adrenocorticotropic hormone and corticosterone levels after sleep deprivation, suggesting that this effect was not mediated by the stress associated with the sleep perturbation. Systemic administration of the nonselective adenosine receptor antagonist caffeine at the onset of sleep deprivation prevented the sleep deprivation-induced increase in postoperative hypersensitivity. Microinjection of the adenosine A2A receptor antagonist ZM 241385 into the median preoptic nucleus (MnPO) blocked the increase in surgical pain levels and duration caused by prior sleep deprivation and eliminated the thermal hyperalgesia induced by sleep deprivation in a group of nonoperated (i.e., without surgical incision) rats. These data show that even a brief sleep disturbance prior to surgery worsens postoperative pain and are consistent with our hypothesis that adenosine A2A receptors in the MnPO contribute to regulate these sleep-pain interactions. © Sleep Research Society 2017. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.

  16. How acute total sleep loss affects the attending brain: a meta-analysis of neuroimaging studies.

    PubMed

    Ma, Ning; Dinges, David F; Basner, Mathias; Rao, Hengyi

    2015-02-01

    Attention is a cognitive domain that can be severely affected by sleep deprivation. Previous neuroimaging studies have used different attention paradigms and reported both increased and reduced brain activation after sleep deprivation. However, due to large variability in sleep deprivation protocols, task paradigms, experimental designs, characteristics of subject populations, and imaging techniques, there is no consensus regarding the effects of sleep loss on the attending brain. The aim of this meta-analysis was to identify brain activations that are commonly altered by acute total sleep deprivation across different attention tasks. Coordinate-based meta-analysis of neuroimaging studies of performance on attention tasks during experimental sleep deprivation. The current version of the activation likelihood estimation (ALE) approach was used for meta-analysis. The authors searched published articles and identified 11 sleep deprivation neuroimaging studies using different attention tasks with a total of 185 participants, equaling 81 foci for ALE analysis. The meta-analysis revealed significantly reduced brain activation in multiple regions following sleep deprivation compared to rested wakefulness, including bilateral intraparietal sulcus, bilateral insula, right prefrontal cortex, medial frontal cortex, and right parahippocampal gyrus. Increased activation was found only in bilateral thalamus after sleep deprivation compared to rested wakefulness. Acute total sleep deprivation decreases brain activation in the fronto-parietal attention network (prefrontal cortex and intraparietal sulcus) and in the salience network (insula and medial frontal cortex). Increased thalamic activation after sleep deprivation may reflect a complex interaction between the de-arousing effects of sleep loss and the arousing effects of task performance on thalamic activity. © 2015 Associated Professional Sleep Societies, LLC.

  17. Sleep, Torpor and Memory Impairment

    NASA Astrophysics Data System (ADS)

    Palchykova, S.; Tobler, I.

    It is now well known that daily torpor induces a sleep deficit. Djungarian hamsters emerging from this hypometabolic state spend most of the time in sleep. This sleep is characterized by high initial values of EEG slow-wave activity (SWA) that monotonically decline during recovery sleep. These features resemble the changes seen in numerous species during recovery after prolonged wakefulness or sleep deprivation (SD). When hamsters are totally or partially sleep deprived immediately after emerging from torpor, an additional increase in SWA can be induced. It has been therefore postulated, that these slow- waves are homeostatically regulated, as predicted by the two-process model of sleep regulation, and that during daily torpor a sleep deficit is accumulated as it is during prolonged waking. The predominance of SWA in the frontal EEG observed both after SD and daily torpor provides further evidence for the similarity of these conditions. It has been shown in several animal and human studies that sleep can enhance memory consolidation, and that SD leads to memory impairment. Preliminary data obtained in the Djungarian hamster showed that both SD and daily torpor result in object recognition deficits. Thus, animals subjected to SD immediately after learning, or if they underwent an episode of daily torpor between learning and retention, displayed impaired recognition memory for complex object scenes. The investigation of daily torpor can reveal mechanisms that could have important implications for hypometabolic state induction in other mammalian species, including humans.

  18. Dual-Tasking Alleviated Sleep Deprivation Disruption in Visuomotor Tracking: An fMRI Study

    ERIC Educational Resources Information Center

    Gazes, Yunglin; Rakitin, Brian C.; Steffener, Jason; Habeck, Christian; Butterfield, Brady; Basner, Robert C.; Ghez, Claude; Stern, Yaakov

    2012-01-01

    Effects of dual-responding on tracking performance after 49-h of sleep deprivation (SD) were evaluated behaviorally and with functional magnetic resonance imaging (fMRI). Continuous visuomotor tracking was performed simultaneously with an intermittent color-matching visual detection task in which a pair of color-matched stimuli constituted a…

  19. Sleep and moral awareness.

    PubMed

    Barnes, Christopher M; Gunia, Brian C; Wagner, David T

    2015-04-01

    The implications of sleep for morality are only starting to be explored. Extending the ethics literature, we contend that because bringing morality to conscious attention requires effort, a lack of sleep leads to low moral awareness. We test this prediction with three studies. A laboratory study with a manipulation of sleep across 90 participants judging a scenario for moral content indicates that a lack of sleep leads to low moral awareness. An archival study of Google Trends data across 6 years highlights a national dip in Web searches for moral topics (but not other topics) on the Monday after the Spring time change, which tends to deprive people of sleep. Finally, a diary study of 127 participants indicates that (within participants) nights with a lack of sleep are associated with low moral awareness the next day. Together, these three studies suggest that a lack of sleep leaves people less morally aware, with important implications for the recognition of morality in others. © 2014 European Sleep Research Society.

  20. Sleep Interacts with Aβ to Modulate Intrinsic Neuronal Excitability

    PubMed Central

    Tabuchi, Masashi; Lone, Shahnaz R.; Liu, Sha; Liu, Qili; Zhang, Julia; Spira, Adam P.; Wu, Mark N.

    2015-01-01

    SUMMARY Background Emerging data suggest an important relationship between sleep and Alzheimer’s Disease (AD), but how poor sleep promotes the development of AD remains unclear. Results Here, using a Drosophila model of AD, we provide evidence suggesting that changes in neuronal excitability underlie the effects of sleep loss on AD pathogenesis. β-amyloid (Aβ) accumulation leads to reduced and fragmented sleep, while chronic sleep deprivation increases Aβ burden. Moreover, enhancing sleep reduces Aβ deposition. Increasing neuronal excitability phenocopies the effects of reducing sleep on Aβ, and decreasing neuronal activity blocks the elevated Aβ accumulation induced by sleep deprivation. At the single neuron level, we find that chronic sleep deprivation, as well as Aβ expression, enhances intrinsic neuronal excitability. Importantly, these data reveal that sleep loss exacerbates Aβ–induced hyperexcitability and suggest that defects in specific K+ currents underlie the hyperexcitability caused by sleep loss and Aβ expression. Finally, we show that feeding levetiracetam, an anti-epileptic medication, to Aβ-expressing flies suppresses neuronal excitability and significantly prolongs their lifespan. Conclusions Our findings directly link sleep loss to changes in neuronal excitability and Aβ accumulation and further suggest that neuronal hyperexcitability is an important mediator of Aβ toxicity. Taken together, these data provide a mechanistic framework for a positive feedback loop, whereby sleep loss and neuronal excitation accelerate the accumulation of Aβ, a key pathogenic step in the development of AD. PMID:25754641