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Sample records for sleep sleep deprivation

  1. Sleep

    MedlinePlus

    ... sleep deprivation? What are sleep myths? What are sleep disorders? Can certain diseases/conditions disrupt sleep? What is ... sleep deprivation? What are sleep myths? What are sleep disorders? Can certain diseases/conditions disrupt sleep? What is ...

  2. Total sleep deprivation, chronic sleep restriction and sleep disruption.

    PubMed

    Reynolds, Amy C; Banks, Siobhan

    2010-01-01

    Sleep loss may result from total sleep deprivation (such as a shift worker might experience), chronic sleep restriction (due to work, medical conditions or lifestyle) or sleep disruption (which is common in sleep disorders such as sleep apnea or restless legs syndrome). Total sleep deprivation has been widely researched, and its effects have been well described. Chronic sleep restriction and sleep disruption (also known as sleep fragmentation) have received less experimental attention. Recently, there has been increasing interest in sleep restriction and disruption as it has been recognized that they have a similar impact on cognitive functioning as a period of total sleep deprivation. Sleep loss causes impairments in cognitive performance and simulated driving and induces sleepiness, fatigue and mood changes. This review examines recent research on the effects of sleep deprivation, restriction and disruption on cognition and neurophysiologic functioning in healthy adults, and contrasts the similarities and differences between these three modalities of sleep loss.

  3. Sleep deprivation and false memories.

    PubMed

    Frenda, Steven J; Patihis, Lawrence; Loftus, Elizabeth F; Lewis, Holly C; Fenn, Kimberly M

    2014-09-01

    Many studies have investigated factors that affect susceptibility to false memories. However, few have investigated the role of sleep deprivation in the formation of false memories, despite overwhelming evidence that sleep deprivation impairs cognitive function. We examined the relationship between self-reported sleep duration and false memories and the effect of 24 hr of total sleep deprivation on susceptibility to false memories. We found that under certain conditions, sleep deprivation can increase the risk of developing false memories. Specifically, sleep deprivation increased false memories in a misinformation task when participants were sleep deprived during event encoding, but did not have a significant effect when the deprivation occurred after event encoding. These experiments are the first to investigate the effect of sleep deprivation on susceptibility to false memories, which can have dire consequences.

  4. Neurobiological consequences of sleep deprivation.

    PubMed

    Alkadhi, Karim; Zagaar, Munder; Alhaider, Ibrahim; Salim, Samina; Aleisa, Abdulaziz

    2013-05-01

    Although the physiological function of sleep is not completely understood, it is well documented that it contributes significantly to the process of learning and memory. Ample evidence suggests that adequate sleep is essential for fostering connections among neuronal networks for memory consolidation in the hippocampus. Sleep deprivation studies are extremely valuable in understanding why we sleep and what are the consequences of sleep loss. Experimental sleep deprivation in animals allows us to gain insight into the mechanism of sleep at levels not possible to study in human subjects. Many useful approaches have been utilized to evaluate the effect of sleep loss on cognitive function, each with relative advantages and disadvantages. In this review we discuss sleep and the detrimental effects of sleep deprivation mostly in experimental animals. The negative effects of sleep deprivation on various aspects of brain function including learning and memory, synaptic plasticity and the state of cognition-related signaling molecules are discussed.

  5. Neurobiological Consequences of Sleep Deprivation

    PubMed Central

    Alkadhi, Karim; Zagaar, Munder; Alhaider, Ibrahim; Salim, Samina; Aleisa, Abdulaziz

    2013-01-01

    Although the physiological function of sleep is not completely understood, it is well documented that it contributes significantly to the process of learning and memory. Ample evidence suggests that adequate sleep is essential for fostering connections among neuronal networks for memory consolidation in the hippocampus. Sleep deprivation studies are extremely valuable in understanding why we sleep and what are the consequences of sleep loss. Experimental sleep deprivation in animals allows us to gain insight into the mechanism of sleep at levels not possible to study in human subjects. Many useful approaches have been utilized to evaluate the effect of sleep loss on cognitive function, each with relative advantages and disadvantages. In this review we discuss sleep and the detrimental effects of sleep deprivation mostly in experimental animals. The negative effects of sleep deprivation on various aspects of brain function including learning and memory, synaptic plasticity and the state of cognition-related signaling molecules are discussed. PMID:24179461

  6. Energy expenditure during sleep, sleep deprivation and sleep following sleep deprivation in adult humans.

    PubMed

    Jung, Christopher M; Melanson, Edward L; Frydendall, Emily J; Perreault, Leigh; Eckel, Robert H; Wright, Kenneth P

    2011-01-01

    Sleep has been proposed to be a physiological adaptation to conserve energy, but little research has examined this proposed function of sleep in humans. We quantified effects of sleep, sleep deprivation and recovery sleep on whole-body total daily energy expenditure (EE) and on EE during the habitual day and nighttime. We also determined effects of sleep stage during baseline and recovery sleep on EE. Seven healthy participants aged 22 ± 5 years (mean ± s.d.) maintained ∼8 h per night sleep schedules for 1 week before the study and consumed a weight-maintenance diet for 3 days prior to and during the laboratory protocol. Following a habituation night, subjects lived in a whole-room indirect calorimeter for 3 days. The first 24 h served as baseline – 16 h wakefulness, 8 h scheduled sleep – and this was followed by 40 h sleep deprivation and 8 h scheduled recovery sleep. Findings show that, compared to baseline, 24 h EE was significantly increased by ∼7% during the first 24 h of sleep deprivation and was significantly decreased by ∼5% during recovery, which included hours awake 25-40 and 8 h recovery sleep. During the night time, EE was significantly increased by ∼32% on the sleep deprivation night and significantly decreased by ∼4% during recovery sleep compared to baseline. Small differences in EE were observed among sleep stages, but wakefulness during the sleep episode was associated with increased energy expenditure. These findings provide support for the hypothesis that sleep conserves energy and that sleep deprivation increases total daily EE in humans.

  7. Sleep deprivation in honey bees.

    PubMed

    Sauer, Stefan; Herrmann, Eva; Kaiser, Walter

    2004-06-01

    Rest at night in forager honey bees (Apis mellifera) meets essential criteria of sleep. This paper reports the effect of a 12-h total sleep deprivation (SD) by forced activity on the behaviour of these animals. The behaviour of sleep-deprived animals is compared with that of control animals under LD [periodic alternation between light (L) and darkness (D)] 12 : 12 hours. SD for 12 h during the first D period resulted in a significant difference with respect to the parameter 'hourly amount of antennal immobility' between sleep-deprived and control animals during the remaining L and D periods. This difference did not occur in the L period following the deprivation night, but rather it became obvious at the beginning of the following D period. The increase of the amount of antennal immobility in sleep-deprived bees was accompanied by an increase of the duration of episodes of antennal immobility. Moreover, the latency from 'lights off' to the first episode of antennal immobility lasting 20 s or longer ('deep sleep latency') tended to be shorter in sleep-deprived than in control animals. Disturbing the bees during the day (L period) did not result in such differences between disturbed and control animals. Highest reaction thresholds in sleeping honey bees occur during long episodes of antennal immobility. We therefore conclude that honey bees compensate a sleep deficit by intensification (deepening) of the sleep process and thus that sleep in honey bees, like that in other arthropods and mammals, is controlled by regulatory mechanisms.

  8. Sleep Deprivation and Advice Taking

    PubMed Central

    Häusser, Jan Alexander; Leder, Johannes; Ketturat, Charlene; Dresler, Martin; Faber, Nadira Sophie

    2016-01-01

    Judgements and decisions in many political, economic or medical contexts are often made while sleep deprived. Furthermore, in such contexts individuals are required to integrate information provided by – more or less qualified – advisors. We asked if sleep deprivation affects advice taking. We conducted a 2 (sleep deprivation: yes vs. no) ×2 (competency of advisor: medium vs. high) experimental study to examine the effects of sleep deprivation on advice taking in an estimation task. We compared participants with one night of total sleep deprivation to participants with a night of regular sleep. Competency of advisor was manipulated within subjects. We found that sleep deprived participants show increased advice taking. An interaction of condition and competency of advisor and further post-hoc analyses revealed that this effect was more pronounced for the medium competency advisor compared to the high competency advisor. Furthermore, sleep deprived participants benefited more from an advisor of high competency in terms of stronger improvement in judgmental accuracy than well-rested participants. PMID:27109507

  9. Sleep Deprivation and Advice Taking.

    PubMed

    Häusser, Jan Alexander; Leder, Johannes; Ketturat, Charlene; Dresler, Martin; Faber, Nadira Sophie

    2016-01-01

    Judgements and decisions in many political, economic or medical contexts are often made while sleep deprived. Furthermore, in such contexts individuals are required to integrate information provided by - more or less qualified - advisors. We asked if sleep deprivation affects advice taking. We conducted a 2 (sleep deprivation: yes vs. no) ×2 (competency of advisor: medium vs. high) experimental study to examine the effects of sleep deprivation on advice taking in an estimation task. We compared participants with one night of total sleep deprivation to participants with a night of regular sleep. Competency of advisor was manipulated within subjects. We found that sleep deprived participants show increased advice taking. An interaction of condition and competency of advisor and further post-hoc analyses revealed that this effect was more pronounced for the medium competency advisor compared to the high competency advisor. Furthermore, sleep deprived participants benefited more from an advisor of high competency in terms of stronger improvement in judgmental accuracy than well-rested participants. PMID:27109507

  10. 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

  11. Sleep deprivation in honey bees.

    PubMed

    Sauer, Stefan; Herrmann, Eva; Kaiser, Walter

    2004-06-01

    Rest at night in forager honey bees (Apis mellifera) meets essential criteria of sleep. This paper reports the effect of a 12-h total sleep deprivation (SD) by forced activity on the behaviour of these animals. The behaviour of sleep-deprived animals is compared with that of control animals under LD [periodic alternation between light (L) and darkness (D)] 12 : 12 hours. SD for 12 h during the first D period resulted in a significant difference with respect to the parameter 'hourly amount of antennal immobility' between sleep-deprived and control animals during the remaining L and D periods. This difference did not occur in the L period following the deprivation night, but rather it became obvious at the beginning of the following D period. The increase of the amount of antennal immobility in sleep-deprived bees was accompanied by an increase of the duration of episodes of antennal immobility. Moreover, the latency from 'lights off' to the first episode of antennal immobility lasting 20 s or longer ('deep sleep latency') tended to be shorter in sleep-deprived than in control animals. Disturbing the bees during the day (L period) did not result in such differences between disturbed and control animals. Highest reaction thresholds in sleeping honey bees occur during long episodes of antennal immobility. We therefore conclude that honey bees compensate a sleep deficit by intensification (deepening) of the sleep process and thus that sleep in honey bees, like that in other arthropods and mammals, is controlled by regulatory mechanisms. PMID:15175094

  12. 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. PMID:26758201

  13. Sleep deprivation: consequences for students.

    PubMed

    Marhefka, Julie King

    2011-09-01

    During the adolescent years, a delayed pattern of the sleep-wake cycle occurs. Many parents and health care providers are not aware that once established, these poor sleep habits can continue into adulthood. Early school hours start a pattern of sleep loss that begins a cycle of daytime sleepiness, which may affect mood, behavior, and increase risk for accidents or injury. These sleep-deprived habits established in adolescence can often lead to problems during college years. Sleep hygiene can be initiated to help break the cycle, along with education and implementation of a strict regimen. Monitoring all adolescents and college-aged students for sleep insufficiency is imperative to improve both academic and emotional well-being. PMID:21846079

  14. Sleep Deprivation and Deficiency

    MedlinePlus

    ... August 19, 2014 Gary H. Gibbons Why Do Fruit Flies Take Naps? NHLBI Investigator Studies Connections Between Sleep Patterns and Gene Networks in Fruit Flies Read all Director's Messages Twitter Facebook YouTube Google+ ...

  15. 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

  16. Effects of sleep deprivation on prospective memory.

    PubMed

    Grundgeiger, Tobias; Bayen, Ute J; Horn, Sebastian S

    2014-01-01

    Sleep deprivation reduces cognitive performance; however, its effects on prospective memory (remembering to perform intended actions) are unknown. One view suggests that effects of sleep deprivation are limited to tasks associated with prefrontal functioning. An alternative view suggests a global, unspecific effect on human cognition, which should affect a variety of cognitive tasks. We investigated the impact of sleep deprivation (25 hours of sleep deprivation vs. no sleep deprivation) on prospective-memory performance in more resource-demanding and less resource-demanding prospective-memory tasks. Performance was lower after sleep deprivation and with a more resource-demanding prospective-memory task, but these factors did not interact. These results support the view that sleep deprivation affects cognition more globally and demonstrate that sleep deprivation increases failures to carry out intended actions, which may have severe consequences in safety-critical situations.

  17. 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

  18. Sleep deprivation suppresses aggression in Drosophila.

    PubMed

    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.

  19. Sleep deprivation suppresses aggression in Drosophila.

    PubMed

    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. PMID:26216041

  20. Sleep Deprivation Induced Anxiety and Anaerobic Performance

    PubMed Central

    Vardar, Selma Arzu; Öztürk, Levent; Kurt, Cem; Bulut, Erdogan; Sut, Necdet; Vardar, Erdal

    2007-01-01

    The aim of this study was to investigate the effects of sleep deprivation induced anxiety on anaerobic performance. Thirteen volunteer male physical education students completed the Turkish version of State Anxiety Inventory and performed Wingate anaerobic test for three times: (1) following a full-night of habitual sleep (baseline measurements), (2) following 30 hours of sleep deprivation, and (3) following partial-night sleep deprivation. Baseline measurements were performed the day before total sleep deprivation. Measurements following partial sleep deprivation were made 2 weeks later than total sleep deprivation measurements. State anxiety was measured prior to each Wingate test. The mean state anxiety following total sleep deprivation was higher than the baseline measurement (44.9 ± 12.9 vs. 27.6 ± 4.2, respectively, p = 0.02) whereas anaerobic performance parameters remained unchanged. Neither anaerobic parameters nor state anxiety levels were affected by one night partial sleep deprivation. Our results suggest that 30 hours continuous wakefulness may increase anxiety level without impairing anaerobic performance, whereas one night of partial sleep deprivation was ineffective on both state anxiety and anaerobic performance. Key pointsShort time total sleep deprivation (30 hours) increases state anxiety without any competition stress.Anaerobic performance parameters such as peak power, mean power and minimum power may not show a distinctive difference from anaerobic performance in a normal sleep day despite the high anxiety level induced by short time sleep deprivation.Partial sleep deprivation does not affect anxiety level and anaerobic performance of the next day. PMID:24149488

  1. Sleep deprivation and false confessions.

    PubMed

    Frenda, Steven J; Berkowitz, Shari R; Loftus, Elizabeth F; Fenn, Kimberly M

    2016-02-23

    False confession is a major contributor to the problem of wrongful convictions in the United States. Here, we provide direct evidence linking sleep deprivation and false confessions. In a procedure adapted from Kassin and Kiechel [(1996) Psychol Sci 7(3):125-128], participants completed computer tasks across multiple sessions and repeatedly received warnings that pressing the "Escape" key on their keyboard would cause the loss of study data. In their final session, participants either slept all night in laboratory bedrooms or remained awake all night. In the morning, all participants were asked to sign a statement, which summarized their activities in the laboratory and falsely alleged that they pressed the Escape key during an earlier session. After a single request, the odds of signing were 4.5 times higher for the sleep-deprived participants than for the rested participants. These findings have important implications and highlight the need for further research on factors affecting true and false confessions. PMID:26858426

  2. Sleep deprivation and false confessions.

    PubMed

    Frenda, Steven J; Berkowitz, Shari R; Loftus, Elizabeth F; Fenn, Kimberly M

    2016-02-23

    False confession is a major contributor to the problem of wrongful convictions in the United States. Here, we provide direct evidence linking sleep deprivation and false confessions. In a procedure adapted from Kassin and Kiechel [(1996) Psychol Sci 7(3):125-128], participants completed computer tasks across multiple sessions and repeatedly received warnings that pressing the "Escape" key on their keyboard would cause the loss of study data. In their final session, participants either slept all night in laboratory bedrooms or remained awake all night. In the morning, all participants were asked to sign a statement, which summarized their activities in the laboratory and falsely alleged that they pressed the Escape key during an earlier session. After a single request, the odds of signing were 4.5 times higher for the sleep-deprived participants than for the rested participants. These findings have important implications and highlight the need for further research on factors affecting true and false confessions.

  3. Selective REM sleep deprivation in narcolepsy.

    PubMed

    Vu, Manh Hoang; Hurni, Christoph; Mathis, Johannes; Roth, Corinne; Bassetti, Claudio L

    2011-03-01

    Narcolepsy is characterized by excessive daytime sleepiness and rapid eye movement (REM) sleep abnormalities, including cataplexy. The aim of this study was to assess REM sleep pressure and homeostasis in narcolepsy. Six patients with narcolepsy and six healthy controls underwent a REM sleep deprivation protocol, including one habituation, one baseline, two deprivation nights (D1, D2) and one recovery night. Multiple sleep latency tests (MSLTs) were performed during the day after baseline and after D2. During D1 and D2 REM sleep was prevented by awakening the subjects at the first polysomnographic signs of REM sleep for 2 min. Mean sleep latency and number of sleep-onset REM periods (SOREMs) were determined on all MSLT. More interventions were required to prevent REM sleep in narcoleptics compared with control subjects during D1 (57 ± 16 versus 24 ± 10) and D2 (87 ± 22 versus 35 ± 8, P = 0.004). Interventions increased from D1 to D2 by 46% in controls and by 53% in narcoleptics (P < 0.03). Selective REM sleep deprivation was successful in both controls (mean reduction of REM to 6% of baseline) and narcoleptics (11%). Both groups had a reduction of total sleep time during the deprivation nights (P = 0.03). Neither group had REM sleep rebound in the recovery night. Narcoleptics had, however, an increase in the number of SOREMs on MSLT (P = 0.005). There was no increase in the number of cataplexies after selective REM sleep deprivation. We conclude that: (i) REM sleep pressure is higher in narcoleptics; (ii) REM sleep homeostasis is similar in narcoleptics and controls; (iii) in narcoleptics selective REM sleep deprivation may have an effect on sleep propensity but not on cataplexy.

  4. Sleep deprivation in mood disorders.

    PubMed

    Benedetti, Francesco; Colombo, Cristina

    2011-01-01

    Growing clinical evidence in support of the efficacy and safety of sleep deprivation (SD), and its biological mechanisms of action suggest that this technique can now be included among the first-line antidepressant treatment strategies for mood disorders. SD targets the broadly defined depressive syndrome, and can be administered according to several different treatment schedules: total versus partial, single versus repeated, alone or combined with antidepressant drugs, mood stabilizers, or other chronotherapeutic techniques, such as light therapy and sleep phase advance. The present review focuses on clinical evidence about the place of SD in therapy, its indications, dosage and timing of the therapeutic wake, interactions with other treatments, precautions and contraindications, adverse reactions, mechanism of action, and comparative efficacy, with the aim of providing the clinical psychiatrist with an updated, concise guide to its application.

  5. Role of corticosterone on sleep homeostasis induced by REM sleep deprivation in rats.

    PubMed

    Machado, Ricardo Borges; Tufik, Sergio; Suchecki, Deborah

    2013-01-01

    Sleep is regulated by humoral and homeostatic processes. If on one hand chronic elevation of stress hormones impair sleep, on the other hand, rapid eye movement (REM) sleep deprivation induces elevation of glucocorticoids and time of REM sleep during the recovery period. In the present study we sought to examine whether manipulations of corticosterone levels during REM sleep deprivation would alter the subsequent sleep rebound. Adult male Wistar rats were fit with electrodes for sleep monitoring and submitted to four days of REM sleep deprivation under repeated corticosterone or metyrapone (an inhibitor of corticosterone synthesis) administration. Sleep parameters were continuously recorded throughout the sleep deprivation period and during 3 days of sleep recovery. Plasma levels of adrenocorticotropic hormone and corticosterone were also evaluated. Metyrapone treatment prevented the elevation of corticosterone plasma levels induced by REM sleep deprivation, whereas corticosterone administration to REM sleep-deprived rats resulted in lower corticosterone levels than in non-sleep deprived rats. Nonetheless, both corticosterone and metyrapone administration led to several alterations on sleep homeostasis, including reductions in the amount of non-REM and REM sleep during the recovery period, although corticosterone increased delta activity (1.0-4.0 Hz) during REM sleep deprivation. Metyrapone treatment of REM sleep-deprived rats reduced the number of REM sleep episodes. In conclusion, reduction of corticosterone levels during REM sleep deprivation resulted in impairment of sleep rebound, suggesting that physiological elevation of corticosterone levels resulting from REM sleep deprivation is necessary for plentiful recovery of sleep after this stressful event.

  6. 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…

  7. Sleep deprivation and false confessions

    PubMed Central

    Frenda, Steven J.; Berkowitz, Shari R.; Loftus, Elizabeth F.; Fenn, Kimberly M.

    2016-01-01

    False confession is a major contributor to the problem of wrongful convictions in the United States. Here, we provide direct evidence linking sleep deprivation and false confessions. In a procedure adapted from Kassin and Kiechel [(1996) Psychol Sci 7(3):125–128], participants completed computer tasks across multiple sessions and repeatedly received warnings that pressing the “Escape” key on their keyboard would cause the loss of study data. In their final session, participants either slept all night in laboratory bedrooms or remained awake all night. In the morning, all participants were asked to sign a statement, which summarized their activities in the laboratory and falsely alleged that they pressed the Escape key during an earlier session. After a single request, the odds of signing were 4.5 times higher for the sleep-deprived participants than for the rested participants. These findings have important implications and highlight the need for further research on factors affecting true and false confessions. PMID:26858426

  8. Immediate error correction process following sleep deprivation.

    PubMed

    Hsieh, Shulan; Cheng, I-Chen; Tsai, Ling-Ling

    2007-06-01

    Previous studies have suggested that one night of sleep deprivation decreases frontal lobe metabolic activity, particularly in the anterior cingulated cortex (ACC), resulting in decreased performance in various executive function tasks. This study thus attempted to address whether sleep deprivation impaired the executive function of error detection and error correction. Sixteen young healthy college students (seven women, nine men, with ages ranging from 18 to 23 years) participated in this study. Participants performed a modified letter flanker task and were instructed to make immediate error corrections on detecting performance errors. Event-related potentials (ERPs) during the flanker task were obtained using a within-subject, repeated-measure design. The error negativity or error-related negativity (Ne/ERN) and the error positivity (Pe) seen immediately after errors were analyzed. The results show that the amplitude of the Ne/ERN was reduced significantly following sleep deprivation. Reduction also occurred for error trials with subsequent correction, indicating that sleep deprivation influenced error correction ability. This study further demonstrated that the impairment in immediate error correction following sleep deprivation was confined to specific stimulus types, with both Ne/ERN and behavioral correction rates being reduced only for trials in which flanker stimuli were incongruent with the target stimulus, while the response to the target was compatible with that of the flanker stimuli following sleep deprivation. The results thus warrant future systematic investigation of the interaction between stimulus type and error correction following sleep deprivation. PMID:17542943

  9. Habitual sleep length and patterns of recovery sleep after 24 hour and 36 hour sleep deprivation.

    PubMed

    Benoit, O; Foret, J; Bouard, G; Merle, B; Landau, J; Marc, M E

    1980-12-01

    Five long sleepers (LS) and 5 short sleepers (SS) were selected from 310 medical students. Nine regular sleepers (RS) were used as a control. The sleep was recorded during 3 reference nights, one recovery night after a 36 h sleep deprivation (R2), one morning sleep after a 24 h sleep deprivation (D1) and the night following D1(R1). According to previous data slow wave sleep (SWS) amounts were the same in the 3 groups while stage 2 and paradoxical sleep (PS) amounts increased with the sleep duration. The hourly distribution of intervening wakefulness and SWS were similar for all groups. When compared to RS or SS the hourly distribution in LS of PS was lower until the sixth hour. As a function of experimental conditions, sleep patterns of LS were the most affected. In R2 the sleep of LS more closely resembled that of RS or SS than in reference nights, while in R1 LS' sleep was the most disturbed. Morning sleep durations were very similar for all groups, but in LS intervening wakefulness was increased and PS was decreased when compared to RS and SS. Negative correlations (Spearman rank test) were found between the morning increase of body temperature after a sleep-deprived night and both TST and PS durations. In all recorded sleep periods, SWS amounts were positively correlated with prior wakefulness duration and the PS amount with TST. PMID:6160990

  10. 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

  11. 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

  12. 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.

  13. 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

  14. Degradation of Binocular Coordination during Sleep Deprivation.

    PubMed

    Tong, Jianliang; Maruta, Jun; Heaton, Kristin J; Maule, Alexis L; Rajashekar, Umesh; Spielman, Lisa A; Ghajar, Jamshid

    2016-01-01

    To aid a clear and unified visual perception while tracking a moving target, both eyes must be coordinated, so the image of the target falls on approximately corresponding areas of the fovea of each eye. The movements of the two eyes are decoupled during sleep, suggesting a role of arousal in regulating binocular coordination. While the absence of visual input during sleep may also contribute to binocular decoupling, sleepiness is a state of reduced arousal that still allows for visual input, providing a context within which the role of arousal in binocular coordination can be studied. We examined the effects of sleep deprivation on binocular coordination using a test paradigm that we previously showed to be sensitive to sleep deprivation. We quantified binocular coordination with the SD of the distance between left and right gaze positions on the screen. We also quantified the stability of conjugate gaze on the target, i.e., gaze-target synchronization, with the SD of the distance between the binocular average gaze and the target. Sleep deprivation degraded the stability of both binocular coordination and gaze-target synchronization, but between these two forms of gaze control the horizontal and vertical components were affected differently, suggesting that disconjugate and conjugate eye movements are under different regulation of attentional arousal. The prominent association found between sleep deprivation and degradation of binocular coordination in the horizontal direction may be used for a fit-for-duty assessment. PMID:27379009

  15. Degradation of Binocular Coordination during Sleep Deprivation

    PubMed Central

    Tong, Jianliang; Maruta, Jun; Heaton, Kristin J.; Maule, Alexis L.; Rajashekar, Umesh; Spielman, Lisa A.; Ghajar, Jamshid

    2016-01-01

    To aid a clear and unified visual perception while tracking a moving target, both eyes must be coordinated, so the image of the target falls on approximately corresponding areas of the fovea of each eye. The movements of the two eyes are decoupled during sleep, suggesting a role of arousal in regulating binocular coordination. While the absence of visual input during sleep may also contribute to binocular decoupling, sleepiness is a state of reduced arousal that still allows for visual input, providing a context within which the role of arousal in binocular coordination can be studied. We examined the effects of sleep deprivation on binocular coordination using a test paradigm that we previously showed to be sensitive to sleep deprivation. We quantified binocular coordination with the SD of the distance between left and right gaze positions on the screen. We also quantified the stability of conjugate gaze on the target, i.e., gaze–target synchronization, with the SD of the distance between the binocular average gaze and the target. Sleep deprivation degraded the stability of both binocular coordination and gaze–target synchronization, but between these two forms of gaze control the horizontal and vertical components were affected differently, suggesting that disconjugate and conjugate eye movements are under different regulation of attentional arousal. The prominent association found between sleep deprivation and degradation of binocular coordination in the horizontal direction may be used for a fit-for-duty assessment. PMID:27379009

  16. Degradation of Binocular Coordination during Sleep Deprivation.

    PubMed

    Tong, Jianliang; Maruta, Jun; Heaton, Kristin J; Maule, Alexis L; Rajashekar, Umesh; Spielman, Lisa A; Ghajar, Jamshid

    2016-01-01

    To aid a clear and unified visual perception while tracking a moving target, both eyes must be coordinated, so the image of the target falls on approximately corresponding areas of the fovea of each eye. The movements of the two eyes are decoupled during sleep, suggesting a role of arousal in regulating binocular coordination. While the absence of visual input during sleep may also contribute to binocular decoupling, sleepiness is a state of reduced arousal that still allows for visual input, providing a context within which the role of arousal in binocular coordination can be studied. We examined the effects of sleep deprivation on binocular coordination using a test paradigm that we previously showed to be sensitive to sleep deprivation. We quantified binocular coordination with the SD of the distance between left and right gaze positions on the screen. We also quantified the stability of conjugate gaze on the target, i.e., gaze-target synchronization, with the SD of the distance between the binocular average gaze and the target. Sleep deprivation degraded the stability of both binocular coordination and gaze-target synchronization, but between these two forms of gaze control the horizontal and vertical components were affected differently, suggesting that disconjugate and conjugate eye movements are under different regulation of attentional arousal. The prominent association found between sleep deprivation and degradation of binocular coordination in the horizontal direction may be used for a fit-for-duty assessment.

  17. Sleep deprivation due to shift work.

    PubMed

    Costa, Giovanni

    2015-01-01

    Sleep deprivation due to shift work is related to perturbation of the sleep/wake cycle, associated with the modified activity/rest pattern. This may cause a significant disruption of circadian rhythms of biologic functions, driven by the body clock located in the suprachiasmatic nuclei of the hypothalamus. Shift and night workers have to change sleep times and strategies according to their duty periods; consequently, both sleep length and quality can be considerably affected depending on the variable start and finish times on different shifts. About 10% of night and rotating shift workers, aged between 18 and 65 years, have been estimated to have a diagnosable "shift-work sleep disorder," according to the International Classification of Sleep Disorders, version 2 (ICSD-2). In the long run, this may lead to persistent and severe disturbances of sleep, chronic fatigue and psychoneurotic syndromes, besides being a risk or aggravating factor for accidents, gastrointestinal, cardiovascular, and reproductive disorders, as well as, probably, for cancer. Preventive and corrective actions deal with the organization of shift schedules according to ergonomic criteria, careful health surveillance, appropriate education and training on effective countermeasures, in particular, sleep hygiene and napping. PMID:26563802

  18. Sleep and Women

    MedlinePlus

    ... Benefits Side Effects Variations Tips Healthy Sleep Habits Sleep Disorders by Category Insomnias Insomnia Child Insomnia Short Sleeper ... Work SIDS Sleep apnea Sleep Debt Sleep Deprivation Sleep Disorders Sleep history Sleep hygiene sleep length Sleep Need ...

  19. 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

  20. Biperiden administration during REM sleep deprivation diminished the frequency of REM sleep attempts.

    PubMed

    Salin-Pascual, R J; Grandos-Fuentes, D; Galicia-Polo, L; Nieves, E; Roehrs, T A; Roth, T

    1992-06-01

    Sixteen subjects were assigned to a group using either placebo or biperiden, with eight subjects in each group. Both groups were studied for one acclimatization night, one baseline night, four nights of rapid eye movement (REM) sleep deprivation and two recovery nights. All the subjects received either placebo or 4 mg biperiden 1 hour before sleep during the four nights of REM sleep deprivation. During the baseline and the recovery nights both groups received placebo capsules. The results showed that REM sleep time during the REM sleep deprivation was reduced by 70-75% below the baseline night in both groups. The number of attempts to enter REM sleep was significantly reduced by biperiden as compared to placebo for each of the four REM sleep deprivation nights. Because the total sleep time in the biperiden group was reduced, the number of REM sleep attempts was corrected by the total sleep time. The adjusted number of REM sleep attempts was also significantly reduced in the biperiden group. REM sleep latency showed a reduction in the placebo group, whereas in the biperiden group REM sleep latency was unchanged throughout the deprivation nights. In the recovery night REM sleep time was increased in both groups, with no differences between the groups. The REM sleep latency showed a reduction in the first recovery night in both groups that persisted through the second recovery night. The above findings support the role of biperiden as a REM sleep suppressive drug.

  1. Are You Sleep Deprived? | NIH MedlinePlus the Magazine

    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 ...

  2. Adverse effects of sleep deprivation in the ICU.

    PubMed

    Salas, Rachel E; Gamaldo, Charlene E

    2008-07-01

    The hospital is not conducive to sleep. Patients in the ICU are particularly susceptible to sleep disruption secondary to environmental and medical issues. Despite the frequency of sleep disruption in the ICU, the quality of critically ill patients' sleep is often overlooked. This article discusses the following issues essential to understanding the factors associated with sleep loss in the ICU: (1) core elements to consider from the baseline sleep history, (2) impact of the ICU environment on the ICU patient's sleep pattern, and (3) overall systematic impact of sleep deprivation on the ICU patient.

  3. 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

  4. Sleep deprivation lowers reactive aggression and testosterone in men.

    PubMed

    Cote, Kimberly A; McCormick, Cheryl M; Geniole, Shawn N; Renn, Ryan P; MacAulay, Stacey D

    2013-02-01

    The role of sleep deprivation in aggressive behavior has not been systematically investigated, despite a great deal of evidence to suggest a relationship. We investigated the impact of 33 h of sleep loss on endocrine function and reactive aggression using the Point Subtraction Aggression Paradigm (PSAP) task. PSAP performance was assessed in 24 young men and 25 women who were randomly assigned to a sleep deprivation or control condition. Sleep deprivation lowered reactive aggression and testosterone (but not cortisol) in men, and disrupted the positive relationship between a pre-post PSAP increase in testosterone and aggression that was evident in rested control men. While women increased aggression following provocation as expected, no influence of sleep deprivation was found. This is the first experimental study to demonstrate that sleep deprivation lowers reactive aggression in men. Testosterone, but not cortisol, played a role in the relationship between sleep and reactive aggression in men.

  5. Sleep deprivation produces feelings of vicarious agency.

    PubMed

    Hon, Nicholas; Poh, Jia-Hou

    2016-02-01

    A variety of self-related psychological constructs are supported by the fundamental ability to accurately sense either self-agency or lack of agency in some action or outcome. Agency judgments are typically studied in individuals who are well-rested and mentally-fresh; however, in our increasingly fast-paced world, such judgments often need to be made while in less optimal states. Here, we studied the effect of being in one such non-optimal state - when sleep-deprived - on judgments of agency. We found that 24h of total sleep deprivation elevated agency ratings on trials designed to produce a strong sense of non-agency. These data provide the first evidence that physiological state variables can affect agency processing in the normal population.

  6. Sleep deprivation produces feelings of vicarious agency.

    PubMed

    Hon, Nicholas; Poh, Jia-Hou

    2016-02-01

    A variety of self-related psychological constructs are supported by the fundamental ability to accurately sense either self-agency or lack of agency in some action or outcome. Agency judgments are typically studied in individuals who are well-rested and mentally-fresh; however, in our increasingly fast-paced world, such judgments often need to be made while in less optimal states. Here, we studied the effect of being in one such non-optimal state - when sleep-deprived - on judgments of agency. We found that 24h of total sleep deprivation elevated agency ratings on trials designed to produce a strong sense of non-agency. These data provide the first evidence that physiological state variables can affect agency processing in the normal population. PMID:26773604

  7. 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. PMID:27413249

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

    PubMed Central

    Gao, Yanxia

    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. PMID:27413249

  9. 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.

  10. 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. PMID:19864296

  11. 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.

  12. 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. PMID:26780802

  13. Functional connectivity during rested wakefulness predicts vulnerability to sleep deprivation.

    PubMed

    Yeo, B T Thomas; Tandi, Jesisca; Chee, Michael W L

    2015-05-01

    Significant inter-individual differences in vigilance decline following sleep deprivation exist. We characterized functional connectivity in 68 healthy young adult participants in rested wakefulness and following a night of total sleep deprivation. After whole brain signal regression, functionally connected cortical networks during the well-rested state exhibited reduced correlation following sleep deprivation, suggesting that highly integrated brain regions become less integrated during sleep deprivation. In contrast, anti-correlations in the well-rested state became less so following sleep deprivation, suggesting that highly segregated networks become less segregated during sleep deprivation. Subjects more resilient to vigilance decline following sleep deprivation showed stronger anti-correlations among several networks. The weaker anti-correlations overlapped with connectivity alterations following sleep deprivation. Resilient individuals thus evidence clearer separation of highly segregated cortical networks in the well-rested state. In contrast to corticocortical connectivity, subcortical-cortical connectivity was comparable across resilient and vulnerable groups despite prominent state-related changes in both groups. Because sleep deprivation results in a significant elevation of whole brain signal amplitude, the aforesaid signal changes and group contrasts may be masked in analyses omitting their regression, suggesting possible value in regressing whole brain signal in certain experimental contexts.

  14. 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

  15. 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.

  16. Manipulating REM sleep in older adults by selective REM sleep deprivation and physiological as well as pharmacological REM sleep augmentation methods.

    PubMed

    Hornung, Orla P; Regen, Francesca; Schredl, Michael; Heuser, Isabella; Danker-Hopfe, Heidi

    2006-02-01

    Experimental approaches to manipulate REM sleep within the cognitive neuroscience of sleep are usually based on sleep deprivation paradigms and focus on younger adults. In the present study, a traditional selective REM sleep deprivation paradigm as well as two alternative manipulation paradigms targeting REM sleep augmentation were investigated in healthy older adults. The study sample consisted of 107 participants, male and female, between the ages of 60 and 82 years, who had been randomly assigned to five experimental groups. During the study night, a first group was deprived of REM sleep by selective REM sleep awakenings, while a second group was woken during stage 2 NREM sleep in matched frequency. Physiological REM sleep augmentation was realized by REM sleep rebound after selective REM sleep deprivation, pharmacological REM sleep augmentation by administering an acetylcholinesterase inhibitor in a double-blind, placebo-controlled design. Deprivation and augmentation paradigms manipulated REM sleep significantly, the former affecting more global measures such as REM sleep minutes and percentage, the latter more organizational aspects such as stage shifts to REM sleep, REM latency, REM density (only pharmacological augmentation) and phasic REM sleep duration. According to our findings, selective REM sleep deprivation seems to be an efficient method of REM sleep manipulation in healthy older adults. While physiological rebound-based and pharmacological cholinergic REM sleep augmentation methods both failed to affect global measures of REM sleep, their efficiency in manipulating organizational aspects of REM sleep extends the traditional scope of REM sleep manipulation methods within the cognitive neuroscience of sleep.

  17. 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.

  18. 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

  19. Effects of sleep deprivation on brain bioenergetics, sleep, and cognitive performance in cocaine-dependent individuals.

    PubMed

    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 ³¹P magnetic resonance spectroscopy (MRS) brain imaging, polysomnography, Continuous Performance Task, and Digit Symbol Substitution Task. Following recovery sleep, ³¹P 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. 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

  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. Effect of sleep and sleep deprivation on ventilatory response to bronchoconstriction.

    PubMed

    Ballard, R D; Tan, W C; Kelly, P L; Pak, J; Pandey, R; Martin, R J

    1990-08-01

    To characterize ventilatory responses to bronchoconstriction during sleep and to assess the effect of prior sleep deprivation on ventilatory and arousal responses to bronchoconstriction, bronchoconstriction was induced in eight asthmatic subjects while they were awake, during normal sleep, and during sleep after a 36-h period of sleep deprivation. Each subject was bronchoconstricted with increasing concentrations of aerosolized methacholine while ventilatory patterns and lower airway resistance (Rla) were continually monitored. The asthmatic patients maintained their minute ventilation as Rla increased under all conditions, demonstrating a stable tidal volume with a mild increase in respiratory frequency. Inspiratory drive, as measured by occlusion pressure (P0.1), increased progressively and significantly as Rla increased under all conditions (slopes of P0.1 vs. Rla = 0.249, 0.112, and 0.154 for awake, normal sleep, and sleep after sleep deprivation, respectively, P less than 0.0006). Chemostimuli did not appear to contribute significantly to the observed increases in P0.1. Prior sleep deprivation had no effect on ventilatory and P0.1 responses to bronchoconstriction but did significantly raise the arousal threshold to induced bronchoconstriction. We conclude that ventilatory responses to bronchoconstriction, unlike extrinsic loading, are not imparied by the presence of sleep, nor are they chemically mediated. However, prior sleep deprivation does increase the subsequent arousal threshold.

  3. Short-term homeostasis of REM sleep assessed in an intermittent REM sleep deprivation protocol in the rat.

    PubMed

    Ocampo-Garcés, Adrián; Vivaldi, Ennio A

    2002-03-01

    An intermittent rapid eye movement (REM) sleep deprivation protocol was applied to determine whether an increase in REM sleep propensity occurs throughout an interval without REM sleep comparable with the spontaneous sleep cycle of the rat. Seven chronically implanted rats under a 12 : 12 light-dark schedule were subjected to an intermittent REM sleep deprivation protocol that started at hour 6 after lights-on and lasted for 3 h. It consisted of six instances of a 10-min REM sleep permission window alternating with a 20-min REM sleep deprivation window. REM sleep increased throughout the protocol, so that total REM sleep in the two REM sleep permission windows of the third hour became comparable with that expected in the corresponding baseline hour. Attempted REM sleep transitions were already increased in the second deprivation window. Attempted transitions to REM sleep were more frequent in the second than in the first half of any 20-min deprivation window. From one deprivation window to the next, transitions to REM sleep changed in correspondence to the amount of REM sleep in the permission window in-between. Our results suggest that: (i) REM sleep pressure increases throughout a time segment similar in duration to a spontaneous interval without REM sleep; (ii) it diminishes during REM sleep occurrence; and (iii) that drop is proportional to the intervening amount of REM sleep. These results are consistent with a homeostatic REM sleep regulatory mechanism that operates in the time scale of spontaneous sleep cycle.

  4. Tempol prevents chronic sleep-deprivation induced memory impairment.

    PubMed

    Alzoubi, Karem H; Khabour, Omar F; Albawaana, Amal S; Alhashimi, Farah H; Athamneh, Rabaa Y

    2016-01-01

    Sleep deprivation is associated with oxidative stress that causes learning and memory impairment. Tempol is a nitroxide compound that promotes the metabolism of many reactive oxygen species (ROS) and has antioxidant and neuroprotective effect. The current study investigated whether chronic administration of tempol can overcome oxidative stress and prevent learning and memory impairment induced by sleep deprivation. Sleep deprivation was induced in rats using multiple platform model. Tempol was administered to rats via oral gavages. Behavioral studies were conducted to test the spatial learning and memory using radial arm water maze. The hippocampus was dissected; antioxidant biomarkers (GSH, GSSG, GSH/GSSG ratio, GPx, SOD, and catalase) were assessed. The result of this project revealed that chronic sleep deprivation impaired both short and long term memory (P<0.05), while tempol treatment prevented such effect. Furthermore, tempol normalized chronic sleep deprivation induced reduction in the hippocampus activity of catalase, GPx, and SOD (P<0.05). Tempol also enhanced the ratio of GSH/GSSG in chronically sleep deprived rats treated with tempol as compared with only sleep deprived rats (P<0.05). In conclusion chronic sleep deprivation induced memory impairment, and treatment with tempol prevented this impairment probably through normalizing antioxidant mechanisms in the hippocampus.

  5. 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…

  6. Tempol prevents chronic sleep-deprivation induced memory impairment.

    PubMed

    Alzoubi, Karem H; Khabour, Omar F; Albawaana, Amal S; Alhashimi, Farah H; Athamneh, Rabaa Y

    2016-01-01

    Sleep deprivation is associated with oxidative stress that causes learning and memory impairment. Tempol is a nitroxide compound that promotes the metabolism of many reactive oxygen species (ROS) and has antioxidant and neuroprotective effect. The current study investigated whether chronic administration of tempol can overcome oxidative stress and prevent learning and memory impairment induced by sleep deprivation. Sleep deprivation was induced in rats using multiple platform model. Tempol was administered to rats via oral gavages. Behavioral studies were conducted to test the spatial learning and memory using radial arm water maze. The hippocampus was dissected; antioxidant biomarkers (GSH, GSSG, GSH/GSSG ratio, GPx, SOD, and catalase) were assessed. The result of this project revealed that chronic sleep deprivation impaired both short and long term memory (P<0.05), while tempol treatment prevented such effect. Furthermore, tempol normalized chronic sleep deprivation induced reduction in the hippocampus activity of catalase, GPx, and SOD (P<0.05). Tempol also enhanced the ratio of GSH/GSSG in chronically sleep deprived rats treated with tempol as compared with only sleep deprived rats (P<0.05). In conclusion chronic sleep deprivation induced memory impairment, and treatment with tempol prevented this impairment probably through normalizing antioxidant mechanisms in the hippocampus. PMID:26616531

  7. Are seizures in the setting of sleep deprivation provoked?

    PubMed

    Lawn, Nicholas; Lieblich, Sam; Lee, Judy; Dunne, John

    2014-04-01

    It is generally accepted that sleep deprivation contributes to seizures. However, it is unclear whether a seizure occurring in the setting of sleep deprivation should be considered as provoked or not and whether this is influenced by seizure type and etiology. This information may have an important impact on epilepsy diagnosis and management. We prospectively analyzed the influence of sleep deprivation on the risk of seizure recurrence in patients with first-ever unprovoked seizures and compared the findings with patients with first-ever provoked seizures. Of 1026 patients with first-ever unprovoked seizures, 204 (20%) were associated with sleep deprivation. While the overall likelihood of seizure recurrence was slightly lower in sleep-deprived patients with first-ever seizures (log-rank p=0.03), sleep deprivation was not an independent predictor of seizure recurrence on multivariate analysis. Seizure recurrence following a first-ever unprovoked seizure associated with sleep deprivation was far more likely than for 174 patients with a provoked first-ever seizure (log-rank p<0.0001). Our findings support the International League Against Epilepsy recommendation that seizures occurring in the setting of sleep deprivation should not be regarded as provoked.

  8. 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. PMID:16920372

  9. Sleep Deprived and Sweating It Out: The Effects of Total Sleep Deprivation on Skin Conductance Reactivity to Psychosocial Stress

    PubMed Central

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

    2015-01-01

    Study Objectives: We examined how sleep deprivation alters physiological responses to psychosocial stress by evaluating changes in skin conductance. Design: Between-subjects design with one group allocated to 24 h of total sleep deprivation and the other to rested wakefulness. Setting: The study took place in a research laboratory. Participants: Participants were 40 healthy young adults recruited from a university. Interventions: Sleep deprivation and feedback. Measurements and Results: 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. Conclusions: 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. Citation: Liu JC, Verhulst S, Massar SA, Chee MW. Sleep deprived and sweating it out: the effects of total sleep deprivation on skin conductance reactivity to psychosocial stress. SLEEP 2015;38(1):155–159. PMID:25325448

  10. Night shifts, sleep deprivation, and attention performance in medical students

    PubMed Central

    Ibanez-Pinilla, Milciades

    2014-01-01

    Objectives To determine attention performance of medical students after sleep deprivation due to night shift work. Methods Prospective cohort design. All seventh, eighth and ninth semester students were invited to participate (n= 209). The effectiveness and concentration indices (d2 Test for attention, dependent variable) from 180 students at 3 evaluations during the semester were compared. Eighth and ninth semester students underwent their second evaluation after a night shift. The independent variables were nocturnal sleep measurements. Results No differences in nocturnal sleep hours during the previous week (p=0.966), sleep deprivation (p=0.703) or effectiveness in the d2 Test (p=0.428) were found between the groups at the beginning of the semester. At the beginning and the end of the semester, the d2 Test results were not different between groups (p=0.410, p=0.394) respectively. The second evaluation showed greater sleep deprivation in students with night shift work (p<0.001). The sleep deprived students had lower concentration indices (p<0.001).The differences were associated with the magnitude of sleep deprivation (p=0.008). Multivariate regression analysis showed that attention performance was explained by sleep deprivation due to night shift work, adjusting for age and gender. Students with sleep deprivation had worse concentration than those without. Conclusions Sleep deprivation due to night shift work in medical students had a negative impact on their attention performance. Medical educators should address these potential negative learning and patient care consequences of sleep deprivation in medical students due to night shifts. PMID:25341213

  11. Sleep deprivation in adolescents and adults: changes in affect.

    PubMed

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

    2010-12-01

    The present study investigated the impact of sleep deprivation on several aspects of affective functioning in healthy participants selected from three different developmental periods: early adolescence (ages 10-13), midadolescence (ages 13-16), and adulthood (ages 30-60). Participants completed an affective functioning battery under conditions of sleep deprivation (a maximum of 6.5 hours total sleep time on the first night followed by a maximum of 2 hours total sleep time on the second night) and rest (approximately 7-8 hours total sleep time each night for two consecutive nights). Less positive affect was observed in the sleep-deprived, compared to rested, condition. This effect held for 9 of the 12 positive affect items on the PANAS-C. Participants also reported a greater increase in anxiety during a catastrophizing task and rated the likelihood of potential catastrophes as higher when sleep deprived, relative to when rested. Early adolescents appraised their main worry as more threatening when sleep deprived, relative to when rested. These results support and extend previous research underscoring the adverse affective consequences of sleep deprivation. PMID:21058849

  12. Melatonin improves experimental colitis with sleep deprivation

    PubMed Central

    PARK, YOUNG-SOOK; CHUNG, SOOK-HEE; LEE, SEONG-KYU; KIM, JA-HYUN; KIM, JUN-BONG; KIM, TAE-KYUN; KIM, DONG-SHIN; BAIK, HAING-WOON

    2015-01-01

    Sleep deprivation (SD) is an epidemic phenomenon in modern countries, and its harmful effects are well known. SD acts as an aggravating factor in inflammatory bowel disease. Melatonin is a sleep-related neurohormone, also known to have antioxidant and anti-inflammatory effects in the gastrointestinal tract; however, the effects of melatonin on colitis have been poorly characterized. Thus, in this study, we assessed the measurable effects of SD on experimental colitis and the protective effects of melatonin. For this purpose, male imprinting control region (ICR) mice (n=24) were used; the mice were divided into 4 experimental groups as follows: the control, colitis, colitis with SD and colitis with SD and melatonin groups. Colitis was induced by the administration of 5% dextran sulfate sodium (DSS) in the drinking water for 6 days. The mice were sleep-deprived for 3 days. Changes in body weight, histological analyses of colon tissues and the expression levels of pro-inflammatory cytokines and genes were evaluated. SD aggravated inflammation and these effects were reversed by melatonin in the mice with colitis. In addition, weight loss in the mice with colitis with SD was significantly reduced by the injection of melatonin. Treatment with melatonin led to high survival rates in the mice, in spite of colitis with SD. The levels of pro-inflammatory cytokines, such as interleukin (IL)-1β, IL-6, IL-17, interferon-γ and tumor necrosis factor-α, in the serum of mice were significantly increased by SD and reduced by melatonin treatment. The melatonin-treated group showed a histological improvement of inflammation. Upon gene analysis, the expression of the inflammatory genes, protein kinase Cζ (PKCζ) and calmodulin 3 (CALM3), was increased by SD, and the levels decreased following treatment with melatonin. The expression levels of the apoptosis-related inducible nitric oxide synthase (iNOS) and wingless-type MMTV integration site family, member 5A (Wnt5a) genes was

  13. Sleep deprivation attenuates inflammatory responses and ischemic cell death.

    PubMed

    Weil, Zachary M; Norman, Greg J; Karelina, Kate; Morris, John S; Barker, Jacqueline M; Su, Alan J; Walton, James C; Bohinc, Steven; Nelson, Randy J; DeVries, A Courtney

    2009-07-01

    Although the biological function of sleep remains uncertain, the consequences of sleep deprivation are well-described and are reported to be detrimental to cognitive function and affective well-being. Sleep deprivation also is strongly associated with elevated risk factors for cardiovascular disease. We used a mouse model of cardiac arrest/cardiopulmonary resuscitation to test the hypothesis that acute sleep deprivation would exacerbate neuroinflammation and neurodegeneration after global ischemia. The resulting data led to a rejection of our hypothesis that sleep deprivation is necessarily detrimental. Indeed, acute sleep deprivation (ASD) was associated with a reduction in ischemia-induced interleukin 1beta (IL-1beta) gene expression and attenuation of neuronal damage in the hippocampus. Further, sleep deprivation increased gene expression of two anti-inflammatory cytokines, IL-6 and IL-10 that are associated with improved ischemic outcome. To determine whether the anti-inflammatory properties of ASD were specific to ischemia, mice were treated systemically with lipopolysaccharide (LPS), a potent inflammogen. Acute sleep deprivation attenuated the central and peripheral increase in tumor necrosis factor-alpha (TNFalpha) and increased IL-10 expression. Together, the ischemia and LPS data suggest that, ASD produces an anti-inflammatory bias that could be exploited to improve medical procedures that are compromised by inflammation. PMID:19409382

  14. 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

  15. 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

  16. 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

  17. 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.

  18. 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

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

    PubMed Central

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

    2015-01-01

    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 1H 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. PMID:26450397

  20. 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.

  1. Sleep Deprivation and Time-Based Prospective Memory

    PubMed Central

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

    2015-01-01

    Study Objectives: 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). Design: 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. Settings: Laboratory. Participants: Fifty healthy young adults (mean age 22 ± 2.1, 31 female). Interventions: 24 h of total sleep deprivation. Measurements and Results: 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. Conclusions: 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. Citation: Esposito MJ, Occhionero M, Cicogna P. Sleep deprivation and time-based prospective memory. SLEEP 2015;38(11):1823–1826. PMID:26085303

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

    PubMed Central

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

    2010-01-01

    Objective To investigate whether sleep deprived people are perceived as less healthy, less attractive, and more tired than after a normal night’s sleep. Design Experimental study. Setting Sleep laboratory in Stockholm, Sweden. Participants 23 healthy, sleep deprived adults (age 18-31) who were photographed and 65 untrained observers (age 18-61) who rated the photographs. Intervention 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. Main outcome measure Difference in observer ratings of perceived health, attractiveness, and tiredness between sleep deprived and well rested participants using a visual analogue scale (100 mm). Results 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. Conclusion 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. PMID:21156746

  3. Sleep Deficiency and Deprivation Leading to Cardiovascular Disease

    PubMed Central

    Kohansieh, Michelle; Makaryus, Amgad N.

    2015-01-01

    Sleep plays a vital role in an individual's mental, emotional, and physiological well-being. Not only does sleep deficiency lead to neurological and psychological disorders, but also the literature has explored the adverse effects of sleep deficiency on the cardiovascular system. Decreased quantity and quality of sleep have been linked to cardiovascular disease (CVD) risk factors, such as hypertension, obesity, diabetes, and dyslipidemia. We explore the literature correlating primary sleep deficiency and deprivation as a cause for cardiovascular disease and cite endothelial dysfunction as a common underlying mechanism. PMID:26495139

  4. Gene expression in the rat brain during sleep deprivation and recovery sleep: an Affymetrix GeneChip study.

    PubMed

    Terao, A; Wisor, J P; Peyron, C; Apte-Deshpande, A; Wurts, S W; Edgar, D M; Kilduff, T S

    2006-01-01

    Previous studies have demonstrated that macromolecular synthesis in the brain is modulated in association with the occurrence of sleep and wakefulness. Similarly, the spectral composition of electroencephalographic activity that occurs during sleep is dependent on the duration of prior wakefulness. Since this homeostatic relationship between wake and sleep is highly conserved across mammalian species, genes that are truly involved in the electroencephalographic response to sleep deprivation might be expected to be conserved across mammalian species. Therefore, in the rat cerebral cortex, we have studied the effects of sleep deprivation on the expression of immediate early gene and heat shock protein mRNAs previously shown to be upregulated in the mouse brain in sleep deprivation and in recovery sleep after sleep deprivation. We find that the molecular response to sleep deprivation and recovery sleep in the brain is highly conserved between these two mammalian species, at least in terms of expression of immediate early gene and heat shock protein family members. Using Affymetrix Neurobiology U34 GeneChips , we also screened the rat cerebral cortex, basal forebrain, and hypothalamus for other genes whose expression may be modulated by sleep deprivation or recovery sleep. We find that the response of the basal forebrain to sleep deprivation is more similar to that of the cerebral cortex than to the hypothalamus. Together, these results suggest that sleep-dependent changes in gene expression in the cerebral cortex are similar across rodent species and therefore may underlie sleep history-dependent changes in sleep electroencephalographic activity.

  5. 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.

  6. Estradiol suppresses recovery of REM sleep following sleep deprivation in ovariectomized female rats.

    PubMed

    Schwartz, Michael D; Mong, Jessica A

    2011-10-24

    Sleep complaints such as insufficient sleep and insomnia are twice as prevalent in women. Symptoms of sleep disruption are often coincident with changes in the gonadal hormone profile across a women's lifespan. Data from a number of different species, including humans, non-human primates and rodents strongly implicate a role for gonadal hormones in the modulation of sleep. In female rats, increased levels of circulating estradiol increase wakefulness and reduce sleep in the dark phase. In this study, we asked whether this reduction in sleep is driven by estradiol-dependent reduction in sleep need during the dark phase by assessing sleep before and after sleep deprivation (SD). Ovariectomized rats implanted with EEG telemetry transmitters were given Silastic capsules containing either 17-β estradiol in sesame oil (E2) or sesame oil alone. After a 24-hour baseline, animals were sleep-deprived via gentle handling for the entire 12-hour light phase, and then allowed to recover. E2 treatment suppressed baseline REM sleep duration in the dark phase, but not NREM or Wake duration, within three days. While SD induced a compensatory increase in REM duration in both groups, this increase was smaller in E2-treated rats compared to oils, as measured in absolute duration as well as by relative increase over baseline. Thus, E2 suppressed REM sleep in the dark phase both before and after SD. E2 also suppressed NREM and increased waking in the early- to mid-dark phase on the day after SD. NREM delta power tracked NREM sleep before and after SD, with small hormone-dependent reductions in delta power in recovery, but not spontaneous sleep. These results demonstrate that E2 powerfully and specifically suppresses spontaneous and recovery REM sleep in the dark phase, and suggest that ovarian steroids may consolidate circadian sleep-wake rhythms.

  7. REM sleep deprivation and food intake.

    PubMed

    Bhanot, J L; Chhina, G S; Singh, B; Sachdeva, U; Kumar, V M

    1989-01-01

    The effect of REM-sleep deprivation (REM-SD) on diet preference was studied in rats. REM-SD for a period of 72 hrs produced an increase in day, night and 24 hrs (day plus night) intakes of Carbohydrate Rich diet (CRD) and Total diet (TD). Body weight (BWt) was also increased. The maximum increase in the above parameters were recorded on the 2nd day of REM-SD. During recovery period the intakes of TD fully recovered, but the BWt and consumption of CRD remained high. Intakes of Balanced diet (BD) remained significantly on the lower side when compared to the pre REM-SD mean values. During REM-SD, the rats preferred CRD than BD. The body temperature did not show any change. The increase in TD intake and BWt could be the result of an increase in insulin level and the change appears to be mediated by the activation of hypothalamic feeding centre.

  8. 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)

  9. 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

  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 deprivation in junior doctors--house officers in Singapore.

    PubMed

    Puvanendran, K; Venkatramani, Jayant; Jain, Amit; Farid, Mohamad

    2005-01-01

    House officers are known to endure marked levels of sleep deprivation in administration of their duties. We aim to establish sleep patterns of local house officers while on the job and the impact it might have on their mood and sleepiness state. We also studied their sleep during their final year of medical school and pre-university for identification of any prior sleep deprivation. Questionnaires were used to assess sleep and mood change. Sleepiness levels on the day after call were assessed using the Stamford Sleepiness Scale. Subjects were found to sleep a median of only 1.0 (+/- 2.0) h per night on call and 6.0 h (+/- 1.0) per non-call night. They suffered median of 5 interruptions (+/- 5) during sleep on one night call. Night call was found to adversely affect mood in 89.5% of the subjects while daytime sleepiness levels following call were found to increase the more the time spent at work after call. Subjects were found to have had 6.5 h (+/- 1.0) of sleep per night during final year of medical school and 8.0 h (+/- 1.0) in final year of pre-university. House officers enter the profession chronically sleep-deprived. The call schedule and general work regime further add to the existent sleep deprivation and may have adverse consequences on patient care and doctor's health. This calls for measures to be instituted for provision of proper sleep and work hours for them. PMID:15732315

  12. 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.

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

    PubMed Central

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

    2015-01-01

    Study Objectives: 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. Design: 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. Setting: Chronobiology and Sleep Laboratory, Duke-NUS Graduate Medical School. Participants: Healthy ethnic-Chinese males aged 21–28 y (n = 20). Interventions: Subjects were kept awake for 40 consecutive hours. Measurements and Results: 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. Conclusions: 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. Citation: Chua EC, Shui G, Cazenave-Gassiot A, Wenk MR, Gooley JJ. Changes in plasma lipids during exposure to total sleep

  14. 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

  15. 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.

  16. The molecular neurobiology of the sleep-deprived, fuzzy brain.

    PubMed

    Sweatt, J David; Hawkins, Kimberly E

    2016-01-01

    Sleep deprivation is well established to cause diminution of cognitive function, including disruption of both minute-to-minute working memory and decrements in the stabilization of long-term memories. Moreover, "replay" during sleep of episodes and sequences of events that were experienced during wakefulness has been implicated in consolidation of long-term memories. However, the molecular mechanisms underlying the role of sleep in memory function are just starting to be defined. In this issue of Science Signaling, Tudor et al identify one molecular component underlying the effects of sleep on memory function: dynamic experience-dependent regulation of protein synthesis in the hippocampus. PMID:27117249

  17. 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

  18. 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

  19. 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

  20. Sleep deprivation, pain and prematurity: a review study.

    PubMed

    Bonan, Kelly Cristina Santos de Carvalho; Pimentel Filho, João da Costa; Tristão, Rosana Maria; Jesus, José Alfredo Lacerda de; Campos Junior, Dioclécio

    2015-02-01

    The aim was to describe current reports in the scientific literature on sleep in the intensive care environment and sleep deprivation associated with painful experiences in premature infant. A systematic search was conducted for studies on sleep, pain, premature birth and care of the newborn. Web of Knowledge, MEDLINE, LILACS, Cochrane Library, PubMed, EMBASE, Scopus, VHL and SciELO databases were consulted. The association between sleep deprivation and pain generates effects that are observed in the brain and the behavioral and physiological activity of preterm infants. Polysomnography in intensive care units and pain management in neonates allow comparison with the first year of life and term infants. We have found few references and evidence that neonatal care programs can influence sleep development and reduce the negative impact of the environment. This evidence is discussed from the perspective of how hospital intervention can improve the development of premature infants.

  1. Effects of sleep deprivation on naval seamen: II. Short recovery sleep on performance.

    PubMed

    Foo, S C; How, J; Siew, M G; Wong, T M; Vijayan, A; Kanapathy, R

    1994-09-01

    Twenty male naval volunteers, aged 18 to 20 years, with 12 to 14 years of education, underwent a total sleep deprivation experiment on board a Republic of Singapore Navy landing ship in the South China Sea for a period of 42-102 hours. The sleep group comprised eight volunteers who dropped out at the 44th-46th h of the experiment and were randomly assigned to a 2 or 4 h sleep regime. The rest served as sleep-deprived controls. Neurobehavioural performance tests, profile of mood state and the Stanford Sleepiness Scale were applied 6 hourly starting from 6.00 am on the first experimental day. No thresholds were observed in the performance of tests related to manual tasks and subjective feeling, including naval tasks, mood and sleepiness scale during the sleep deprivation experiment. However, thresholds were observed in the performance of tests requiring cognitive and perceptive skills, including the grooved peg board, trail making, sea-shore rhythm, addition, digit span, digit symbol, flicker fusion and dynamometer tests. Performances in these tests were observed to deteriorate only after approximately 30 h of sleep deprivation. The Z score for the non-threshold tests (Z-N) deteriorated from -0.01 at the start of the experiment to 1.25 at the 42nd h of the experiment just before the imposed sleep and improved to 0.81 at the 48th h of the experiment just after the imposed sleep; and the Z score for the threshold tests (Z-T) varied from -0.07 at the start to 0.49 just before sleep (at the 42nd h) and to continuously deteriorate to 0.83 just after sleep (at the 48th h).(ABSTRACT TRUNCATED AT 250 WORDS)

  2. 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. PMID:27560704

  3. [Effects of sleep deprivation on human performance].

    PubMed

    Fu, Z J; Ma, R S

    2000-08-01

    Objective. To investigate the effects of sleep deprivation (SD) on human performance. Method. 8 healthy male college students participated the test. During 26 h of continuous awakeness (from 6:00 to 8:00 the next day), the volunteers were demanded to perform a battery of tests at 9 different time (7:00, 12:00, 16:00, 20:00, 0:00, 2:00, 4:00, 6:00, 8:00). The tests include: (1) single task: aural Oddball response, the response time (RT1) and correct rate (CR1) were recorded; (2) dual tasks: manual tracking and aural Oddball response, the response time (RT2), tracking error (ER) and correct rate (CR2) were recorded; (3) The Stanford sleepiness scale and subjective ratings of task difficulty access. Result. SD had significant effects on CT1, CT2 and ER (P=0.0001, P=0.00001, P=0.0004 respectively); SD increased RT1, RT2, ER at night time. SD had significant effects on SR, SSS score (P=0.0001, P=0.0000 respectively); SD increased SR, SSS score at night time. Since the subjects changed their response strategy, CR1 and CR2 were not influenced by SD at night time. Conclusion. SD has significant effects on response time, tracking error, subjective difficulty of cognitive tasks and subjective sleepiness. PMID:11892744

  4. 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

  5. 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.

  6. 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

  7. Detrimental role of prolonged sleep deprivation on adult neurogenesis

    PubMed Central

    Fernandes, Carina; Rocha, Nuno Barbosa F.; Rocha, Susana; Herrera-Solís, Andrea; Salas-Pacheco, José; García-García, Fabio; Murillo-Rodríguez, Eric; Yuan, Ti-Fei; Machado, Sergio; Arias-Carrión, Oscar

    2015-01-01

    Adult mammalian brains continuously generate new neurons, a phenomenon called adult neurogenesis. Both environmental stimuli and endogenous factors are important regulators of adult neurogenesis. Sleep has an important role in normal brain physiology and its disturbance causes very stressful conditions, which disrupt normal brain physiology. Recently, an influence of sleep in adult neurogenesis has been established, mainly based on sleep deprivation studies. This review provides an overview on how rhythms and sleep cycles regulate hippocampal and subventricular zone neurogenesis, discussing some potential underlying mechanisms. In addition, our review highlights some interacting points between sleep and adult neurogenesis in brain function, such as learning, memory, and mood states, and provides some insights on the effects of antidepressants and hypnotic drugs on adult neurogenesis. PMID:25926773

  8. Detrimental role of prolonged sleep deprivation on adult neurogenesis.

    PubMed

    Fernandes, Carina; Rocha, Nuno Barbosa F; Rocha, Susana; Herrera-Solís, Andrea; Salas-Pacheco, José; García-García, Fabio; Murillo-Rodríguez, Eric; Yuan, Ti-Fei; Machado, Sergio; Arias-Carrión, Oscar

    2015-01-01

    Adult mammalian brains continuously generate new neurons, a phenomenon called adult neurogenesis. Both environmental stimuli and endogenous factors are important regulators of adult neurogenesis. Sleep has an important role in normal brain physiology and its disturbance causes very stressful conditions, which disrupt normal brain physiology. Recently, an influence of sleep in adult neurogenesis has been established, mainly based on sleep deprivation studies. This review provides an overview on how rhythms and sleep cycles regulate hippocampal and subventricular zone neurogenesis, discussing some potential underlying mechanisms. In addition, our review highlights some interacting points between sleep and adult neurogenesis in brain function, such as learning, memory, and mood states, and provides some insights on the effects of antidepressants and hypnotic drugs on adult neurogenesis. PMID:25926773

  9. Gambling when sleep deprived: don't bet on stimulants.

    PubMed

    Killgore, William D S; Grugle, Nancy L; Balkin, Thomas J

    2012-02-01

    Recent evidence suggests that sleep deprivation leads to suboptimal decision-making on the Iowa Gambling Task (IGT), a pattern that appears to be unaffected by moderate doses of caffeine. It is not known whether impaired decision-making could be reversed by higher doses of caffeine or by other stimulant countermeasures, such as dextroamphetamine or modafinil. Fifty-four diurnally active healthy subjects completed alternate versions of the IGT at rested baseline, at 23 and 46 h awake, and following a night of recovery sleep. After 44 h awake, participants received a double-blind dose of caffeine (600 mg), dextroamphetamine (20 mg), modafinil (400 mg), or placebo. At baseline, participants showed a normal pattern of advantageous performance, whereas both sleep-deprived sessions were associated with suboptimal decision-making on the IGT. Following stimulant administration on the second night of sleep deprivation, groups receiving caffeine, dextroamphetamine, or modafinil showed significant reduction in subjective sleepiness and improvement in psychomotor vigilance, but decision-making on the IGT remained impaired for all stimulants and did not differ from placebo. Decision-making returned to normal following recovery sleep. These findings are consistent with prior research showing that sleep deprivation leads to suboptimal decision-making on some types of tasks, particularly those that rely heavily on emotion processing regions of the brain, such as the ventromedial prefrontal cortex. Moreover, the deficits in decision-making were not reversed by commonly used stimulant countermeasures, despite restoration of psychomotor vigilance and alertness. These three stimulants may restore some, but not all, aspects of cognitive functioning during sleep deprivation.

  10. 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. PMID:26087833

  11. 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.

  12. Comparison of the effects of sleep deprivation, alcohol and obstructive sleep apnoea (OSA) on simulated steering performance.

    PubMed

    Hack, M A; Choi, S J; Vijayapalan, P; Davies, R J; Stradling, J R

    2001-07-01

    Patients with obstructive sleep apnoea (OSA) are reported to have an increased risk of road traffic accidents. This study examines the nature of the impairment during simulated steering in patients with OSA, compared to normal subjects following either sleep deprivation or alcohol ingestion. Twenty-six patients with OSA and 12 normal subjects, either deprived of one night's sleep or following alcohol ingestion [mean (SD) alcohol blood level 71.6 mg dl(-1) (19.6)], performed a simulated steering task for a total of 90 min. Performance was measured using the tendency to wander (SD), deterioration across the task, number of 'off-road' events and the reaction time to peripheral events. Control data for OSA, sleep deprivation and alcohol were obtained following treatment with nasal continuous positive airway pressure (nCPAP), after a normal night of sleep, and following no alcohol, respectively. Patients with untreated OSA, and sleep-deprived or alcohol-intoxicated normal subjects performed significantly less well, compared to their respective controls (P<0.01 for all tests), with untreated OSA lying between that of alcohol intoxication and sleep deprivation. Alcohol impaired steering error equally throughout the whole drive, whilst sleep deprivation caused progressive deterioration through the drive, but not initially. Untreated OSA was more like sleep deprivation than alcohol, although there was a wide spread of data. This suggests that the driving impairment in patients with OSA is more compatible with sleep deprivation or fragmentation as the cause, rather than abnormal cognitive or motor skills.

  13. 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…

  14. Neuronal activity in the preoptic hypothalamus during sleep deprivation and recovery sleep

    PubMed Central

    Alam, Md. Aftab; Kumar, Sunil; McGinty, Dennis; Alam, Md. Noor

    2013-01-01

    The preoptic hypothalamus is implicated in sleep regulation. Neurons in the median preoptic nucleus (MnPO) and the ventrolateral preoptic area (VLPO) have been identified as potential sleep regulatory elements. However, the extent to which MnPO and VLPO neurons are activated in response to changing homeostatic sleep regulatory demands is unresolved. To address this question, we continuously recorded the extracellular activity of neurons in the rat MnPO, VLPO and dorsal lateral preoptic area (LPO) during baseline sleep and waking, during 2 h of sleep deprivation (SD) and during 2 h of recovery sleep (RS). Sleep-active neurons in the MnPO (n = 11) and VLPO (n = 13) were activated in response to SD, such that waking discharge rates increased by 95.8 ± 29.5% and 59.4 ± 17.3%, respectively, above waking baseline values. During RS, non-rapid eye movement (REM) sleep discharge rates of MnPO neurons initially increased to 65.6 ± 15.2% above baseline values, then declined to baseline levels in association with decreases in EEG delta power. Increase in non-REM sleep discharge rates in VLPO neurons during RS averaged 40.5 ± 7.6% above baseline. REM-active neurons (n = 16) in the LPO also exhibited increased waking discharge during SD and an increase in non-REM discharge during RS. Infusion of A2A adenosine receptor antagonist into the VLPO attenuated SD-induced increases in neuronal discharge. Populations of LPO wake/REM-active and state-indifferent neurons and dorsal LPO sleep-active neurons were unresponsive to SD. These findings support the hypothesis that sleep-active neurons in the MnPO and VLPO, and REM-active neurons in the LPO, are components of neuronal circuits that mediate homeostatic responses to sustained wakefulness. PMID:24174649

  15. Neuronal activity in the preoptic hypothalamus during sleep deprivation and recovery sleep.

    PubMed

    Alam, Md Aftab; Kumar, Sunil; McGinty, Dennis; Alam, Md Noor; Szymusiak, Ronald

    2014-01-01

    The preoptic hypothalamus is implicated in sleep regulation. Neurons in the median preoptic nucleus (MnPO) and the ventrolateral preoptic area (VLPO) have been identified as potential sleep regulatory elements. However, the extent to which MnPO and VLPO neurons are activated in response to changing homeostatic sleep regulatory demands is unresolved. To address this question, we continuously recorded the extracellular activity of neurons in the rat MnPO, VLPO and dorsal lateral preoptic area (LPO) during baseline sleep and waking, during 2 h of sleep deprivation (SD) and during 2 h of recovery sleep (RS). Sleep-active neurons in the MnPO (n = 11) and VLPO (n = 13) were activated in response to SD, such that waking discharge rates increased by 95.8 ± 29.5% and 59.4 ± 17.3%, respectively, above waking baseline values. During RS, non-rapid eye movement (REM) sleep discharge rates of MnPO neurons initially increased to 65.6 ± 15.2% above baseline values, then declined to baseline levels in association with decreases in EEG delta power. Increase in non-REM sleep discharge rates in VLPO neurons during RS averaged 40.5 ± 7.6% above baseline. REM-active neurons (n = 16) in the LPO also exhibited increased waking discharge during SD and an increase in non-REM discharge during RS. Infusion of A2A adenosine receptor antagonist into the VLPO attenuated SD-induced increases in neuronal discharge. Populations of LPO wake/REM-active and state-indifferent neurons and dorsal LPO sleep-active neurons were unresponsive to SD. These findings support the hypothesis that sleep-active neurons in the MnPO and VLPO, and REM-active neurons in the LPO, are components of neuronal circuits that mediate homeostatic responses to sustained wakefulness.

  16. 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. PMID:26953626

  17. Decreased attentional responsivity during sleep deprivation: orienting response latency, amplitude, and habituation.

    PubMed

    McCarthy, M E; Waters, W F

    1997-02-01

    Ever increasing societal demands for uninterrupted work are causing unparalleled amounts of sleep deprivation among workers. Sleep deprivation has been linked to safety problems ranging from medical misdiagnosis to industrial and vehicular accidents. Microsleeps (very brief intrusions of sleep into wakefulness) are usually cited as the cause of the performance decrements during sleep deprivation. Changes in a more basic physiological phenomenon, attentional shift, were hypothesized to be additional factors in performance declines. The current study examined the effects of 36 hours of sleep deprivation on the electrodermal-orienting response (OR), a measure of attentional shift or capture. Subjects were 71 male undergraduate students, who were divided into sleep deprivation and control (non-sleep deprivation) groups. The expected negative effects of sleep deprivation on performance were noted in increased reaction times and increased variability in the sleep-deprived group on attention-demanding cognitive tasks. OR latency was found to be significantly delayed after sleep deprivation, OR amplitude was significantly decreased, and habituation of the OR was significantly faster during sleep deprivation. These findings indicate impaired attention, the first revealing slowed shift of attention to novel stimuli, the second indicating decreased attentional allocation to stimuli, and the third revealing more rapid loss of attention to repeated stimuli. These phenomena may be factors in the impaired cognitive performance seen during sleep deprivation. PMID:9143071

  18. Altered salience network connectivity predicts macronutrient intake after sleep deprivation

    PubMed Central

    Fang, Zhuo; Spaeth, Andrea M.; Ma, Ning; Zhu, Senhua; Hu, Siyuan; Goel, Namni; Detre, John A.; Dinges, David F.; Rao, Hengyi

    2015-01-01

    Although insufficient sleep is a well-recognized risk factor for overeating and weight gain, the neural mechanisms underlying increased caloric (particularly fat) intake after sleep deprivation remain unclear. Here we used resting-state functional magnetic resonance imaging and examined brain connectivity changes associated with macronutrient intake after one night of total sleep deprivation (TSD). Compared to the day following baseline sleep, healthy adults consumed a greater percentage of calories from fat and a lower percentage of calories from carbohydrates during the day following TSD. Subjects also exhibited increased brain connectivity in the salience network from the dorsal anterior cingulate cortex (dACC) to bilateral putamen and bilateral anterior insula (aINS) after TSD. Moreover, dACC-putamen and dACC-aINS connectivity correlated with increased fat and decreased carbohydrate intake during the day following TSD, but not during the day following baseline sleep. These findings provide a potential neural mechanism by which sleep loss leads to increased fat intake. PMID:25645575

  19. 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

  20. 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.

  1. Effects of Extreme Sleep Deprivation on Human Performance

    SciTech Connect

    Tuan Tran; Kimberly R. Raddatz; Elizabeth T. Cady; Bradford Amstutz; Pete D. Elgin; Christopher Vowels; Gerald Deehan

    2007-04-01

    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, a 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.

  2. 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.

  3. 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

  4. 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. PMID:27555235

  5. 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.

  6. Effects of one night of sleep deprivation on hormone profiles and performance efficiency.

    PubMed

    Goh, V H; Tong, T Y; Lim, C L; Low, E C; Lee, L K

    2001-05-01

    This study examined the effects of one night of sleep deprivation on melatonin and cortisol profiles, as well as performance efficiency of military service members. Sleep intervention consisted of total lack of sleep (N = 7) or 8 hours of sleep (control group; N = 7) during the night. All parameters were measured at selected time intervals before (day 1), during (only in sleep-deprived individuals), and after (day 2) sleep intervention. Rotary pursuit scores and handgrip strength data were used as indices of psychomotor and physical performance, respectively. In sleep-deprived individuals, more salivary melatonin, but not cortisol, was secreted than in subjects who slept adequately. Significant increases in melatonin and cortisol were noted, especially at 1:30 p.m. on the day after nighttime sleep deprivation. In contrast, the tracking scores for rotary pursuit and grip strength among sleep-deprived and rested individuals were comparable. Across a normal working day (day 1), all parameters studied revealed time-specific fluctuations in both control and sleep-deprived groups. Irrespective of nighttime sleep schedule, the patterns of performance on day 2 differed from those on day 1. The tracking performance improved on day 2, whereas grip strength worsened, which may reflect inherent learning and muscle fatigue, respectively. During the night of sleep deprivation, performance declined. In conclusion, the present study showed that one night of sleep deprivation (8 hours) resulted in significant hormonal changes on the next afternoon but did not modify tracking and muscular strength performance.

  7. Antidepressant effects of sleep deprivation require astrocyte-dependent adenosine mediated signaling.

    PubMed

    Hines, D J; Schmitt, L I; Hines, R M; Moss, S J; Haydon, P G

    2013-01-01

    Major depressive disorder is a debilitating condition with a lifetime risk of ten percent. Most treatments take several weeks to achieve clinical efficacy, limiting the ability to bring instant relief needed in psychiatric emergencies. One intervention that rapidly alleviates depressive symptoms is sleep deprivation; however, its mechanism of action is unknown. Astrocytes regulate responses to sleep deprivation, raising the possibility that glial signaling mediates antidepressive-like actions of sleep deprivation. Here, we found that astrocytic signaling to adenosine (A1) receptors was required for the robust reduction of depressive-like behaviors following 12 hours of sleep deprivation. As sleep deprivation activates synaptic A1 receptors, we mimicked the effect of sleep deprivation on depression phenotypes by administration of the A1 agonist CCPA. These results provide the first mechanistic insight into how sleep deprivation impacts mood, and provide a novel pathway for rapid antidepressant development by modulation of glial signaling in the brain. PMID:23321809

  8. Antidepressant effects of sleep deprivation require astrocyte-dependent adenosine mediated signaling

    PubMed Central

    Hines, D J; Schmitt, L I; Hines, R M; Moss, S J; Haydon, P G

    2013-01-01

    Major depressive disorder is a debilitating condition with a lifetime risk of ten percent. Most treatments take several weeks to achieve clinical efficacy, limiting the ability to bring instant relief needed in psychiatric emergencies. One intervention that rapidly alleviates depressive symptoms is sleep deprivation; however, its mechanism of action is unknown. Astrocytes regulate responses to sleep deprivation, raising the possibility that glial signaling mediates antidepressive-like actions of sleep deprivation. Here, we found that astrocytic signaling to adenosine (A1) receptors was required for the robust reduction of depressive-like behaviors following 12 hours of sleep deprivation. As sleep deprivation activates synaptic A1 receptors, we mimicked the effect of sleep deprivation on depression phenotypes by administration of the A1 agonist CCPA. These results provide the first mechanistic insight into how sleep deprivation impacts mood, and provide a novel pathway for rapid antidepressant development by modulation of glial signaling in the brain. PMID:23321809

  9. Mutual relations between sleep deprivation, sleep stealers and risk behaviours in adolescents

    PubMed Central

    Paiva, Teresa; Gaspar, Tania; Matos, Margarida Gaspar

    2016-01-01

    Objectives The aim is to evaluate the mutual influences between sleep duration/sleep deprivation (SD) and the sleep stealers/adolescent risk behaviours. Methods The national survey is a component of the Health Behaviour in School-Aged Children (HBSC) study, it is based on a school-based self-completed questionnaire; 3476 students were randomly selected from 139 randomly chosen Portuguese schools using as an unit the class, 53.8% were girls; 45.9% attended the 8th grade and 54.1% the 10th grade; the mean age was 14.9 years. The measured variables were: 1) gender and age; 2) sociodemographics; 3) sleep duration during the week and during weekends and computed SD; 4) screen time (computer use during the week and during the week end (PC use); watching TV and mobile phone use; 5) earlier sexual behaviour; 6) violent behaviours: fights, use of weapons; 7) use of tobacco, alcohol and drugs. The statistical analysis included Pearson chi-square tests and logistic regression. Results Excessive use of mobile phone, of computer use during weekdays, and internet facilities; substance use; violence and earlier sexual relations had significantly higher prevalence in sleep deprived adolescents. By logistic regression only using PC during weekdays, tobacco, drugs and weapons were associated to SD, while SD was associated to PC use during weekdays, tobacco use and drugs’ use. Computer uses tend to be associated among themselves. Mobile phone is associated with computer practices and with alcohol and tobacco use. Tobacco is associated with most risk behaviours. Alcohol use is associated with other substance use, computer use and violent behaviours. Violence behaviours, earlier sex and drugs use tend to be associated among themselves. Conclusions Sleep stealers use and risk behaviours are more prevalent in sleep deprived adolescents, but, in spite of significant individual associations, models of risk behaviours are still lacking. PMID:27226817

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

    PubMed Central

    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

    2016-01-01

    AIM To determine adiponectin expression in colonic tissue of murine colitis and systemic cytokine expression after melatonin treatments and sleep deprivation. METHODS 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. RESULTS 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. CONCLUSION 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.

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

    PubMed Central

    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

    2016-01-01

    AIM To determine adiponectin expression in colonic tissue of murine colitis and systemic cytokine expression after melatonin treatments and sleep deprivation. METHODS 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. RESULTS 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. CONCLUSION 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. PMID:27672276

  12. 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.

  13. Grooming analysis algorithm: use in the relationship between sleep deprivation and anxiety-like behavior.

    PubMed

    Pires, Gabriel N; Tufik, Sergio; Andersen, Monica L

    2013-03-01

    Increased anxiety is a classic effect of sleep deprivation. However, results regarding sleep deprivation-induced anxiety-like behavior are contradictory in rodent models. The grooming analysis algorithm is a method developed to examine anxiety-like behavior and stress in rodents, based on grooming characteristics and microstructure. This study evaluated the applicability of the grooming analysis algorithm to distinguish sleep-deprived and control rats in comparison to traditional grooming analysis. Forty-six animals were distributed into three groups: control (n=22), paradoxical sleep-deprived (96 h, n=10) and total sleep deprived (6 h, n=14). Immediately after the sleep deprivation protocol, grooming was evaluated using both the grooming analysis algorithm and traditional measures (grooming latency, frequency and duration). Results showed that both paradoxical sleep-deprived and total sleep-deprived groups displayed grooming in a fragmented framework when compared to control animals. Variables from the grooming analysis algorithm were successful in distinguishing sleep-deprived and normal sleep animals regarding anxiety-like behavior. The grooming analysis algorithm and traditional measures were strongly correlated. In conclusion, the grooming analysis algorithm is a reliable method to assess the relationship between anxiety-like behavior and sleep deprivation.

  14. Sleepless in adolescence: prospective data on sleep deprivation, health and functioning.

    PubMed

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

    2009-10-01

    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 6h or less per night during the past 4 weeks. Weighted logistic regression procedures were employed to calculate prevalence, incidence, persistence/chronicity, and odds ratios. Prevalence rates and rates of persistence suggest sleep deprivation is highly prevalent and chronic. Multivariate analyses indicate that short sleep increases risk across multiple domains of dysfunction, suggesting pervasive deleterious effects. The broad impact of sleep deprivation and its pervasiveness suggests interventions will need to focus on multilevel changes to increase sleep time and reduce the negative impact of sleep deprivation among adolescents.

  15. 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).

  16. One night of sleep deprivation decreases treadmill endurance performance.

    PubMed

    Oliver, Samuel J; Costa, Ricardo J S; Laing, Stewart J; Bilzon, James L J; Walsh, Neil P

    2009-09-01

    The aim was to test the hypothesis that one night of sleep deprivation will impair pre-loaded 30 min endurance performance and alter the cardio-respiratory, thermoregulatory and perceptual responses to exercise. Eleven males completed two randomised trials separated by 7 days: once after normal sleep (496 (18) min: CON) and once following 30 h without sleep (SDEP). After 30 h participants performed a 30 min pre-load at 60% [VO(2 max) followed by a 30 min self-paced treadmill distance test. Speed, RPE, core temperature (T(re)), mean skin temperature (T(sk)), heart rate (HR) and respiratory parameters VO(2 max), VCO(2), VE, RER pre-load only) were measured. Less distance (P = 0.016, d = 0.23) was covered in the distance test after SDEP (6037 (759) 95%CI 5527 to 6547 m) compared with CON (6224 (818) 95%CI 5674 to 6773 m). SDEP did not significantly alter T(re) at rest or thermoregulatory responses during the pre-load including heat storage (0.8 degrees C) and T(sk). With the exception of raised VO(2) at 30 min on the pre-load, cardio-respiratory parameters, RPE and speed were not different between trials during the pre-load or distance test (distance test mean HR, CON 174 (12), SDEP 170 (13) beats min(-1): mean RPE, CON 14.8 (2.7), SDEP 14.9 (2.6)). In conclusion, one night of sleep deprivation decreased endurance performance with limited effect on pacing, cardio-respiratory or thermoregulatory function. Despite running less distance after sleep deprivation compared with control, participants' perception of effort was similar indicating that altered perception of effort may account for decreased endurance performance after a night without sleep.

  17. 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…

  18. 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…

  19. How sleep deprivation affects psychological variables related to college students' cognitive performance.

    PubMed

    Pilcher, J J; Walters, A S

    1997-11-01

    The effects of sleep deprivation on cognitive performance psychological variables related to cognitive performance were studied in 44 college students. Participants completed the Watson-Glaser Critical Thinking Appraisal after either 24 hours of sleep deprivation or approximately 8 hours of sleep. After completing the cognitive task, the participants completed 2 questionnaires, one assessing self-reported effort, concentration, and estimated performance, the other assessing off-task cognitions. As expected, sleep-deprived participants performed significantly worse than the nondeprived participants on the cognitive task. However, the sleep-deprived participants rated their concentration and effort higher than the nondeprived participants did. In addition, the sleep-deprived participants rated their estimated performance significantly higher than the nondeprived participants did. The findings indicate that college students are not aware of the extent to which sleep deprivation negatively affects their ability to complete cognitive tasks. PMID:9394089

  20. The dual effect of paradoxical sleep deprivation on murine immune functions.

    PubMed

    Sá-Nunes, Anderson; Bizzarro, Bruna; Egydio, Flávia; Barros, Michele S; Sesti-Costa, Renata; Soares, Elyara M; Pina, Adriana; Russo, Momtchilo; Faccioli, Lúcia H; Tufik, Sergio; Andersen, Monica L

    2016-01-15

    We aimed to evaluate the effect of paradoxical sleep deprivation on the cellular migration during inflammation, the peritoneal macrophage phenotype and the infectious stimulus outcomes. A/J mice were inoculated with thioglycollate and exposed to paradoxical sleep deprivation. Sleep-deprived animals presented decreased cell migration compared to controls. Nitric oxide production was reduced in macrophages from sleep-deprived mice compared to controls. Cell surface analysis showed that sleep deprivation reduced F4/80(+)/CD80(low) peritoneal cell population induced by thioglycollate injection. Sleep-deprived mice were not more susceptible to infection than control mice. Our findings challenge the general perception that sleep loss always increases infection susceptibility. PMID:26711562

  1. Exercise‐Induced growth hormone during acute sleep deprivation

    PubMed Central

    Ritsche, Kevin; Nindl, Bradly C.; Wideman, Laurie

    2014-01-01

    Abstract The effect of acute (24‐h) sleep deprivation on exercise‐induced growth hormone (GH) and insulin‐like growth factor‐1 (IGF‐1) was examined. Ten men (20.6 ± 1.4 years) completed two randomized 24‐h sessions including a brief, high‐intensity exercise bout following either a night of sleep (SLEEP) or (24‐h) sleep deprivation (SLD). Anaerobic performance (mean power [MP], peak power [PP], minimum power [MinP], time to peak power [TTPP], fatigue index, [FI]) and total work per sprint [TWPS]) was determined from four maximal 30‐sec Wingate sprints on a cycle ergometer. Self‐reported sleep 7 days prior to each session was similar between SLEEP and SLD sessions (7.92 ± 0.33 vs. 7.98 ± 0.39 h, P =0.656, respectively) and during the actual SLEEP session in the lab, the total amount of sleep was similar to the 7 days leading up to the lab session (7.72 ± 0.14 h vs. 7.92 ± 0.33 h, respectively) (P =0.166). No differences existed in MP, PP, MinP, TTPP, FI, TWPS, resting GH concentrations, time to reach exercise‐induced peak GH concentration (TTP), or free IGF‐1 between sessions. GH area under the curve (AUC) (825.0 ± 199.8 vs. 2212.9 ± 441.9 μg/L*min, P <0.01), exercise‐induced peak GH concentration (17.8 ± 3.7 vs. 39.6 ± 7.1 μg/L, P <0.01) and ΔGH (peak GH – resting GH) (17.2 ± 3.7 vs. 38.2 ± 7.3 μg/L, P <0.01) were significantly lower during the SLEEP versus SLD session. Our results indicate that the exercise‐induced GH response was significantly augmented in sleep‐deprived individuals. PMID:25281616

  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. 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…

  4. Age-related changes in sleep spindles characteristics during daytime recovery following a 25-hour sleep deprivation

    PubMed Central

    Rosinvil, T.; Lafortune, M.; Sekerovic, Z.; Bouchard, M.; Dubé, J.; Latulipe-Loiselle, A.; Martin, N.; Lina, J. M.; Carrier, J.

    2015-01-01

    Objectives: The mechanisms underlying sleep spindles (~11–15 Hz; >0.5 s) help to protect sleep. With age, it becomes increasingly difficult to maintain sleep at a challenging time (e.g., daytime), even after sleep loss. This study compared spindle characteristics during daytime recovery and nocturnal sleep in young and middle-aged adults. In addition, we explored whether spindles characteristics in baseline nocturnal sleep were associated with the ability to maintain sleep during daytime recovery periods in both age groups. Methods: Twenty-nine young (15 women and 14 men; 27.3 y ± 5.0) and 31 middle-aged (19 women and 13 men; 51.6 y ± 5.1) healthy subjects participated in a baseline nocturnal sleep and a daytime recovery sleep after 25 hours of sleep deprivation. Spindles were detected on artifact-free Non-rapid eye movement (NREM) sleep epochs. Spindle density (nb/min), amplitude (μV), frequency (Hz), and duration (s) were analyzed on parasagittal (linked-ears) derivations. Results: In young subjects, spindle frequency increased during daytime recovery sleep as compared to baseline nocturnal sleep in all derivations, whereas middle-aged subjects showed spindle frequency enhancement only in the prefrontal derivation. No other significant interaction between age group and sleep condition was observed. Spindle density for all derivations and centro-occipital spindle amplitude decreased whereas prefrontal spindle amplitude increased from baseline to daytime recovery sleep in both age groups. Finally, no significant correlation was found between spindle characteristics during baseline nocturnal sleep and the marked reduction in sleep efficiency during daytime recovery sleep in both young and middle-aged subjects. Conclusion: These results suggest that the interaction between homeostatic and circadian pressure modulates spindle frequency differently in aging. Spindle characteristics do not seem to be linked with the ability to maintain daytime recovery sleep. PMID

  5. 5'-Ectonucleotidase-knockout mice lack non-REM sleep responses to sleep deprivation.

    PubMed

    Zielinski, Mark R; Taishi, Ping; Clinton, James M; Krueger, James M

    2012-06-01

    Adenosine and extracellular adenosine triphosphate (ATP) have multiple physiological central nervous system actions including regulation of cerebral blood flow, inflammation and sleep. However, their exact sleep regulatory mechanisms remain unknown. Extracellular ATP and adenosine diphosphate are converted to adenosine monophosphate (AMP) by the enzyme ectonucleoside triphosphate diphosphohydrolase 1, also known as CD39, and extracellular AMP is in turn converted to adenosine by the 5'-ectonuleotidase enzyme CD73. We investigated the role of CD73 in sleep regulation. Duration of spontaneous non-rapid eye movement sleep (NREMS) was greater in CD73-knockout (KO) mice than in C57BL/6 controls whether determined in our laboratory or by others. After sleep deprivation (SD), NREMS was enhanced in controls but not CD73-KO mice. Interleukin-1 beta (IL1β) enhanced NREMS in both strains, indicating that the CD73-KO mice were capable of sleep responses. Electroencephalographic power spectra during NREMS in the 1.0-2.5 Hz frequency range was significantly enhanced after SD in both CD73-KO and WT mice; the increases were significantly greater in the WT mice than in the CD73-KO mice. Rapid eye movement sleep did not differ between strains in any of the experimental conditions. With the exception of CD73 mRNA, the effects of SD on various adenosine-related mRNAs were small and similar in the two strains. These data suggest that sleep is regulated, in part, by extracellular adenosine derived from the actions of CD73.

  6. 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). PMID:26911684

  7. 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).

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

    SciTech Connect

    Volkow N. D.; Fowler J.; Volkow, N.D.; Tomasi, D.; Wang, G.-J.; Fowler, J.S.; Logan, J.; Benveniste, H.; Kin, R.; Thanos, P.K.; Sergi F.

    2012-03-23

    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, dopamine 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.

  9. 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

  10. Sleep deprivation, allergy symptoms, and negatively reinforced problem behavior.

    PubMed

    Kennedy, C H; Meyer, K A

    1996-01-01

    We studied the relation between the presence versus the absence of sleep deprivation or allergy symptoms and the rate and function of problem behavior. Three students whose problem behavior was negatively reinforced by escape form instruction were studied across several weeks using analogue functional analyses. Our results indicated that the extraexperimental events were associated with (a) termination of instruction functioning as a negative reinforcer, (b) increased rates of negatively reinforced problem behavior, or (c) increased rates of problem behavior across all conditions.

  11. 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.

  12. REM sleep deprivation inhibits LTP in vivo in area CA1 of rat hippocampus.

    PubMed

    Kim, Eun Young; Mahmoud, Ghada S; Grover, Lawrence M

    2005-11-18

    Rapid eye movement (REM) sleep deprivation has previously been shown to interfere with normal learning and memory and to inhibit long-term potentiation (LTP) in vitro. Previous studies on REM sleep deprivation and LTP have relied on in vitro analysis in isolated brain slices taken from animals following several days of sleep deprivation. LTP in the hippocampus in situ may differ from LTP in vitro due to modulatory inputs from other brain regions, which are altered after REM sleep deprivation. Here, we examined LTP in unanesthetized, behaving animals on the first and second recovery days following REM sleep deprivation to determine if similar effects are seen in vivo as previously reported in vitro. We found that LTP was significantly impaired in REM sleep-deprived animals on the second recovery day but not the first recovery day. Our results extend previous findings by showing that REM sleep deprivation continues to affect hippocampal function for more than 24h following the end of deprivation. Our results also suggest the presence of a modulatory process not present in vitro. Our findings are not explained by stress during REM sleep deprivation because equivalent circulating corticosterone levels (an index of stress) were found during both REM sleep deprivation and control treatment.

  13. 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.

  14. Predicting vulnerability to sleep deprivation using diffusion model parameters.

    PubMed

    Patanaik, Amiya; Zagorodnov, Vitali; Kwoh, Chee Keong; Chee, Michael W L

    2014-10-01

    We used diffusion modelling to predict vulnerability to decline in psychomotor vigilance task (PVT) performance following a night of total sleep deprivation (SD). A total of 135 healthy young adults (69 women, age = 21.9 ± 1.7 years) participated in several within-subject cross-over design studies that incorporated the PVT. Participants were classified as vulnerable (lower tertile) or non-vulnerable (upper tertile) according to their change in lapse rate [lapse = reaction time (RT) ≥ 500 ms] between the evening before (ESD) and the morning after SD. RT data were fitted using Ratcliff's diffusion model. Although both groups showed significant change in RT during SD, there was no significant group difference in RT during the ESD session. In contrast, during ESD, the mean diffusion drift of vulnerable subjects was significantly lower than for non-vulnerable subjects. Mean drift and non-decision times were both adversely affected by sleep deprivation. Both mean drift and non-decision time showed significant state × vulnerability interaction. Diffusion modelling appears to have promise in predicting vulnerability to vigilance decline induced by a night of total sleep deprivation.

  15. The spectrum of the non-rapid eye movement sleep electroencephalogram following total sleep deprivation is trait-like.

    PubMed

    Tarokh, Leila; Rusterholz, Thomas; Achermann, Peter; Van Dongen, Hans P A

    2015-08-01

    The sleep electroencephalogram (EEG) spectrum is unique to an individual and stable across multiple baseline recordings. The aim of this study was to examine whether the sleep EEG spectrum exhibits the same stable characteristics after acute total sleep deprivation. Polysomnography (PSG) was recorded in 20 healthy adults across consecutive sleep periods. Three nights of baseline sleep [12 h time in bed (TIB)] following 12 h of wakefulness were interleaved with three nights of recovery sleep (12 h TIB) following 36 h of sustained wakefulness. Spectral analysis of the non-rapid eye movement (NREM) sleep EEG (C3LM derivation) was used to calculate power in 0.25 Hz frequency bins between 0.75 and 16.0 Hz. Intraclass correlation coefficients (ICCs) were calculated to assess stable individual differences for baseline and recovery night spectra separately and combined. ICCs were high across all frequencies for baseline and recovery and for baseline and recovery combined. These results show that the spectrum of the NREM sleep EEG is substantially different among individuals, highly stable within individuals and robust to an experimental challenge (i.e. sleep deprivation) known to have considerable impact on the NREM sleep EEG. These findings indicate that the NREM sleep EEG represents a trait.

  16. 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

  17. 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. PMID:24587073

  18. 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.

  19. The effects of sleep deprivation in humans: topographical electroencephalogram changes in non-rapid eye movement (NREM) sleep versus REM sleep.

    PubMed

    Marzano, Cristina; Ferrara, Michele; Curcio, Giuseppe; De Gennaro, Luigi

    2010-06-01

    Studies on homeostatic aspects of sleep regulation have been focussed upon non-rapid eye movement (NREM) sleep, and direct comparisons with regional changes in rapid eye movement (REM) sleep are sparse. To this end, evaluation of electroencephalogram (EEG) changes in recovery sleep after extended waking is the classical approach for increasing homeostatic need. Here, we studied a large sample of 40 healthy subjects, considering a full-scalp EEG topography during baseline (BSL) and recovery sleep following 40 h of wakefulness (REC). In NREM sleep, the statistical maps of REC versus BSL differences revealed significant fronto-central increases of power from 0.5 to 11 Hz and decreases from 13 to 15 Hz. In REM sleep, REC versus BSL differences pointed to significant fronto-central increases in the 0.5-7 Hz and decreases in the 8-11 Hz bands. Moreover, the 12-15 Hz band showed a fronto-parietal increase and that at 22-24 Hz exhibited a fronto-central decrease. Hence, the 1-7 Hz range showed significant increases in both NREM sleep and REM sleep, with similar topography. The parallel change of NREM sleep and REM sleep EEG power is related, as confirmed by a correlational analysis, indicating that the increase in frequency of 2-7 Hz possibly subtends a state-aspecific homeostatic response. On the contrary, sleep deprivation has opposite effects on alpha and sigma activity in both states. In particular, this analysis points to the presence of state-specific homeostatic mechanisms for NREM sleep, limited to <2 Hz frequencies. In conclusion, REM sleep and NREM sleep seem to share some homeostatic mechanisms in response to sleep deprivation, as indicated mainly by the similar direction and topography of changes in low-frequency activity.

  20. Impact of Monetary Incentives on Cognitive Performance and Error Monitoring following Sleep Deprivation

    PubMed Central

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

    2010-01-01

    Study Objectives: 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. Design: 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. Results: 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. Conclusions: 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. Citation: Hsieh S; Li TH; Tsai LL. Impact of monetary incentives on cognitive performance and

  1. Sleep deprivation induces excess diuresis and natriuresis in healthy children.

    PubMed

    Mahler, B; Kamperis, K; Schroeder, M; Frøkiær, J; Djurhuus, J C; Rittig, S

    2012-01-15

    Urine production is reduced at night, allowing undisturbed sleep. This study was undertaken to show the effect of sleep deprivation (SD) on urine production in healthy children. Special focus was on gender and children at an age where enuresis is still prominent. Twenty healthy children (10 girls) underwent two 24-h studies, randomly assigned to either sleep or SD on the first study night. Diet and fluid intake were standardized. Blood samples were drawn every 4 h during daytime and every 2 h at night. Urine was fractionally collected. Blood pressure and heart rate were noninvasively monitored. Blood was analyzed for plasma antidiuretic hormone (AVP), atrial natriuretic peptide (ANP), angiotensin II, aldosterone, and renin. Urine was analyzed for aquaporin-2 and PGE(2). Successful SD was achieved in all participants with a minimum of 4 h 50 min, and full-night SD was obtained in 50% of the participants. During SD, both boys and girls produced markedly larger amounts of urine than during normal sleep (477 ± 145 vs. 291 ± 86 ml, P < 0.01). SD increased urinary excretion of sodium (0.17 ± 0.05 vs. 0.10 ± 0.03 mmol·kg(-1)·h(-1)) whereas solute-free water reabsorption remained unchanged. SD induced a significant fall in nighttime plasma AVP (P < 0.01), renin (P < 0.05), angiotensin II (P < 0.001), and aldosterone (P < 0.05) whereas plasma ANP levels remained uninfluenced (P = 0.807). Nighttime blood pressure and heart rate were significantly higher during SD (mean arterial pressure: 78.5 ± 8.0 vs. 74.7 ± 8.7 mmHg, P < 0.001). SD leads to natriuresis and excess diuresis in healthy children. The underlying mechanism could be a reduced nighttime dip in blood pressure and a decrease in renin-angiotensin-aldosterone system levels during sleep deprivation.

  2. 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.

  3. Circadian rhythms (temperature, heart rate, vigilance, mood) of short and long sleepers: effects of sleep deprivation.

    PubMed

    Benoit, O; Foret, J; Merle, B; Reinberg, A

    1981-01-01

    Seven long sleepers (LS) (sleep greater than or equal to 9 h) and seven short sleepers (SS) (sleep less than or equal to 7 h), aged 20 to 23 years, were selected among medical students. They measured their axillary temperature (T), heart rate (HR) and self-estimated their vigilance (V) and mood (M) every 4 h from awakening to bed time during a ten-day control span and during the two sleep deprived nights. Polygraphic sleep recordings were performed on 3 control days and recovery from 24 h (day sleep) or 36 h (night sleep) sleep deprivations. For the 4 variables (T, HR, V and M), group circadian patterns were analyzed by means of the cosinor method for the control span and after both types of sleep deprivation. The acrophases of the 4 variables clustered more in LS than in SS. The acrophases of V and M were found to be more closely related to the sleep/wake rhythm than those of T and HR. Sleep deprivation resulted in a large change of the circadian rhythms in LS but had little effect in SS as indicated by the non detection of most acrophases in LS and the persistence of such acrophases in SS. This difference might be explained by the large interindividual variability of changes induced by the sleep deprivation in LS. Moreover, day sleep recovery was more disturbed in LS than in SS. PMID:7327054

  4. Partial sleep deprivation and energy balance in adults: an emerging issue for consideration by dietetics practitioners.

    PubMed

    Shlisky, Julie D; Hartman, Terryl J; Kris-Etherton, Penny M; Rogers, Connie J; Sharkey, Neil A; Nickols-Richardson, Sharon M

    2012-11-01

    During the past 30 years, rates of partial sleep deprivation and obesity have increased in the United States. Evidence linking partial sleep deprivation, defined as sleeping <6 hours per night, to energy imbalance is relevant to weight gain prevention and weight loss promotion. With a majority of Americans overweight or obese, weight loss is a recommended strategy for reducing comorbid conditions. Our purpose was to review the literature regarding the role of partial sleep deprivation on energy balance and weight regulation. An inverse relationship between obesity and sleep duration has been demonstrated in cross-sectional and prospective studies. Several intervention studies have tested mechanisms by which partial sleep deprivation affects energy balance. Reduced sleep may disrupt appetitive hormone regulation, specifically increasing ghrelin and decreasing leptin and, thereby, influence energy intake. Increased wakefulness also may promote food intake episodes and energy imbalance. Energy expenditure may not be greatly affected by partial sleep deprivation, although additional and more accurate methods of measurements may be necessary to detect subtle changes in energy expenditure. Body weight loss achieved by reduced energy intake and/or increased energy expenditure combined with partial sleep deprivation may contribute to undesirable body composition change with proportionately more fat-free soft tissue mass lost compared with fat mass. Evaluating sleep patterns and recommending regular, sufficient sleep for individuals striving to manage weight may be prudent.

  5. MCH levels in the CSF, brain preproMCH and MCHR1 gene expression during paradoxical sleep deprivation, sleep rebound and chronic sleep restriction.

    PubMed

    Dias Abdo Agamme, Ana Luiza; Aguilar Calegare, Bruno Frederico; Fernandes, Leandro; Costa, Alicia; Lagos, Patricia; Torterolo, Pablo; D'Almeida, Vânia

    2015-12-01

    Neurons that utilize melanin-concentrating hormone (MCH) as neuromodulator are located in the lateral hypothalamus and incerto-hypothalamic area. These neurons project throughout the central nervous system and play a role in sleep regulation. With the hypothesis that the MCHergic system function would be modified by the time of the day as well as by disruptions of the sleep-wake cycle, we quantified in rats the concentration of MCH in the cerebrospinal fluid (CSF), the expression of the MCH precursor (Pmch) gene in the hypothalamus, and the expression of the MCH receptor 1 (Mchr1) gene in the frontal cortex and hippocampus. These analyses were performed during paradoxical sleep deprivation (by a modified multiple platform technique), paradoxical sleep rebound and chronic sleep restriction, both at the end of the active (dark) phase (lights were turned on at Zeitgeber time zero, ZT0) and during the inactive (light) phase (ZT8). We observed that in control condition (waking and sleep ad libitum), Mchr1 gene expression was larger at ZT8 (when sleep predominates) than at ZT0, both in frontal cortex and hippocampus. In addition, compared to control, disturbances of the sleep-wake cycle produced the following effects: paradoxical sleep deprivation for 96 and 120 h reduced the expression of Mchr1 gene in frontal cortex at ZT0. Sleep rebound that followed 96 h of paradoxical sleep deprivation increased the MCH concentration in the CSF also at ZT0. Twenty-one days of sleep restriction produced a significant increment in MCH CSF levels at ZT8. Finally, sleep disruptions unveiled day/night differences in MCH CSF levels and in Pmch gene expression that were not observed in control (undisturbed) conditions. In conclusion, the time of the day and sleep disruptions produced subtle modifications in the physiology of the MCHergic system.

  6. 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.

  7. Sleep deprivation inhibits adult neurogenesis in the hippocampus by elevating glucocorticoids.

    PubMed

    Mirescu, Christian; Peters, Jennifer D; Noiman, Liron; Gould, Elizabeth

    2006-12-12

    Prolonged sleep deprivation is stressful and has been associated with adverse consequences for health and cognitive performance. Here, we show that sleep deprivation inhibits adult neurogenesis at a time when circulating levels of corticosterone are elevated. Moreover, clamping levels of this hormone prevents the sleep deprivation-induced reduction of cell proliferation. The recovery of normal levels of adult neurogenesis after chronic sleep deprivation occurs over a 2-wk period and involves a temporary increase in new neuron formation. This compensatory increase is dissociated from glucocorticoid levels as well as from the restoration of normal sleep patterns. Collectively, these findings suggest that, although sleep deprivation inhibits adult neurogenesis by acting as a stressor, its compensatory aftereffects involve glucocorticoid-independent factors.

  8. Activation of c-fos in GABAergic neurones in the preoptic area during sleep and in response to sleep deprivation.

    PubMed

    Gong, Hui; McGinty, Dennis; Guzman-Marin, Ruben; Chew, Keng-Tee; Stewart, Darya; Szymusiak, Ronald

    2004-05-01

    Neurones in the median preoptic nucleus (MnPN) and the ventrolateral preoptic area (vlPOA) express immunoreactivity for c-Fos protein following sustained sleep, and display elevated discharge rates during both non-REM and REM sleep compared to waking. We evaluated the hypothesis that MnPN and vlPOA sleep-active neurones are GABAergic by combining staining for c-Fos protein with staining for glutamic acid decarboxylase (GAD). In a group of six rats exhibiting spontaneous total sleep times averaging 82.2 +/- 5.1% of the 2 h immediately prior to death, >75% of MnPN neurones that were Fos-immunoreactive (IR) were also GAD-IR. Similar results were obtained in the vlPOA. In a group of 11 rats exhibiting spontaneous sleep times ranging from 20 to 92%, the number of Fos + GAD-IR neurones in MnPN and vlPOA was positively correlated with total sleep time. Compared to control animals, Fos + GAD-IR cell counts in the MnPN were significantly elevated in rats that were sleep deprived for 24 h and permitted 2 h of recovery sleep. These findings demonstrate that a majority of MnPN and vlPOA neurones that express Fos-IR during sustained spontaneous sleep are GABAergic. They also demonstrate that sleep deprivation is associated with increased activation of GABAergic neurones in the MnPN and vlPOA.

  9. Sleep deprivation attenuates experimental stroke severity in rats.

    PubMed

    Moldovan, Mihai; Constantinescu, Alexandra Oana; Balseanu, Adrian; Oprescu, Nicoleta; Zagrean, Leon; Popa-Wagner, Aurel

    2010-03-01

    Indirect epidemiological and experimental evidence suggest that the severity of injury during stroke is influenced by prior sleep history. The aim of our study was to test the effect of acute sleep deprivation on early outcome following experimental stroke. Young male Sprague-Dawley rats (n=20) were subjected to focal cerebral ischemia by reversible right middle cerebral artery occlusion (MCAO) for 90 min. In 10 rats, MCAO was performed just after 6-h of total sleep deprivation (TSD) by "gentle handling", whereas the other rats served as controls. Neurological function during the first week after stroke was monitored using a battery of behavioral tests investigating the asymmetry of sensorimotor deficit (tape removal test and cylinder test), bilateral sensorimotor coordination (rotor-rod and Inclined plane) and memory (T-maze and radial maze). Following MCAO, control rats had impaired behavioral performance in all tests. The largest impairment was noted in the tape test where the tape removal time from the left forelimb (contralateral to MCAO) was increased by approximately 10 fold (p<0.01). In contrast, rats subjected to TSD had complete recovery of sensorimotor performance consistent with a 2.5 fold smaller infarct volume and reduced morphological signs of neuronal injury at day 7 after MCAO. Our data suggest that brief TSD induces a neuroprotective response that limits the severity of a subsequent stroke, similar to rapid ischemic preconditioning. PMID:20045410

  10. Changes in direct current potentials during sleep deprivation.

    PubMed

    Hoffmann, R F; Bonato, R A; Armitage, R; Wimmer, F L

    1996-09-01

    Previous research reported changes in steady-state brain electrical activity during sleep. However, due to the quasi-linear nature of the Direct Current (DC) changes, artifact contamination was a potential confound. The present study was performed to further explore DC potentials and to help establish its validity. Twenty-five male university students (13 control and 12 sleep-deprived; mean age 19 y (range 17-27 y) served as subjects. During wakefulness, subjects were tested every hour while standard EEG activity recordings were made, as well as DC measurement. Split plot analyses of variance (ANOVAs) revealed that changes in DC activity levels differed between the two groups. The control subjects showed the same pattern of decreasing DC observed previously with a return to baseline levels during waking hours. The sleep-deprived subjects showed a smaller decrease in DC level through the night, followed by a rise in DC level that continued until the end of the 24 h study. It was concluded that DC measurement reflects changes in brain state associated with fatigue that are not attributable to artifactual processes. PMID:8956203

  11. 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

  12. Effects of selective REM sleep deprivation on prefrontal gamma activity and executive functions.

    PubMed

    Corsi-Cabrera, M; Rosales-Lagarde, A; del Río-Portilla, Y; Sifuentes-Ortega, R; Alcántara-Quintero, B

    2015-05-01

    Given that the dorsolateral prefrontal cortex is involved in executive functions and is deactivated and decoupled from posterior associative regions during REM sleep, that Gamma temporal coupling involved in information processing is enhanced during REM sleep, and that adult humans spend about 90 min of every 24h in REM sleep, it might be expected that REM sleep deprivation would modify Gamma temporal coupling and have a deteriorating effect on executive functions. We analyzed EEG Gamma activity and temporal coupling during implementation of a rule-guided task before and after REM sleep deprivation and its effect on verbal fluency, flexible thinking and selective attention. After two nights in the laboratory for adaptation, on the third night subjects (n=18) were randomly assigned to either selective REM sleep deprivation effectuated by awakening them at each REM sleep onset or, the same number of NREM sleep awakenings as a control for unspecific effects of sleep interruptions. Implementation of abstract rules to guide behavior required greater activation and synchronization of Gamma activity in the frontopolar regions after REM sleep reduction from 20.6% at baseline to just 3.93% of total sleep time. However, contrary to our hypothesis, both groups showed an overall improvement in executive task performance and no effect on their capacity to sustain selective attention. These results suggest that after one night of selective REM sleep deprivation executive functions can be compensated by increasing frontal activation and they still require the participation of supervisory control by frontopolar regions.

  13. Effects of sleep deprivation on serum cortisol level and mental health in servicemen.

    PubMed

    Song, Hong-Tao; Sun, Xin-Yang; Yang, Ting-Shu; Zhang, Li-Yi; Yang, Jia-Lin; Bai, Jing

    2015-06-01

    This study aimed to investigate the effects of sleep deprivation on serum cortisol level and mental health and explore the correlations between them in servicemen. A total of 149 out of the 207 Chinese servicemen were randomly selected to go through 24hour sleep deprivation, leaving the rest (58) as the control group, before and after which their blood samples were drawn for cortisol measurement. Following the procedure, all the participants were administered the Military Personnel Mental Disorder Prediction Scale, taking the military norm as baseline. The results revealed that the post-deprivation serum cortisol level was positively correlated with the factor score of mania in the sleep deprivation group (rSp=0.415, p<0.001). Sleep deprivation could significantly increase serum cortisol level and may affect mental health in servicemen. The increase of serum cortisol level is significantly related to mania disorder during sleep deprivation.

  14. REM sleep deprivation in rats results in inflammation and interleukin-17 elevation.

    PubMed

    Yehuda, Shlomo; Sredni, Benjamin; Carasso, Rafi L; Kenigsbuch-Sredni, Dvora

    2009-07-01

    Sleep deprivation is a major health problem in modern society. Deprivation of rapid eye movement (REM) sleep is particularly damaging to cognition and to spatial memory; however, the mechanisms that mediate these deteriorations in function are not known. We explored the possibility that REM sleep deprivation may provoke major changes in the immune system by inducing inflammation. Rats were subjected to 72 h of REM sleep deprivation, and the plasma levels of proinflammatory cytokines (IL-1, IL-1beta, IL-6, IL-17A, and TNF-alpha), an anti-inflammatory cytokine (IL-10), the inflammatory markers homocysteine, corticosterone, and hyperthermia were measured immediately after the deprivation period, and 7 days later. The results indicate that REM sleep deprivation induced an inflammatory response. The levels of the proinflammatory cytokines and markers were significantly elevated in sleep-deprived rats as compared to control rats. After 7 days of recovery, the levels of some markers, including hyperthermia, remained higher in sleep-deprived rats versus the control animals. IL-17A appears to play a pivotal role in coordinating the inflammation. These data shed new light on the mechanism of sleep deprivation-induced inflammation.

  15. The effects of biperiden on nap sleep after sleep deprivation in depressed patients.

    PubMed

    Dressing, H; Riemann, D; Gann, H; Berger, M

    1992-08-01

    Sixteen patients with a major depressive disorder were allowed to take a nap at 5 A.M. after a period of total sleep deprivation. The patients were randomly assigned to biperiden or placebo treatment prior to the nap to test the hypothesis that anticholinergic medication is capable of preventing a nap-related worsening of mood. Total sleep deprivation positively influenced mood for the whole group. Contrary to expectations, the rate of nap-related relapses of mood did not differ between placebo- and biperiden-treated individuals, and biperiden did not significantly suppress rapid eye movement (REM) sleep. There was only a tendency for lower REM time after administration of biperiden compared to placebo. This unexpected result may be due to a high cholinergic tone in the patient group investigated and a high REM propensity in the early morning hours. Studies with more selective M1/M2 receptor antagonists are necessary to clarify whether nap-related changes of mood can be prevented by anticholinergic blockade.

  16. 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.

  17. Sleep deprivation increases A1 adenosine receptor density in the rat brain

    PubMed Central

    Elmenhorst, David; Basheer, Radhika; McCarley, Robert W.; Bauer, Andreas

    2013-01-01

    Adenosine, increasing after sleep deprivation and acting via the A1 adenosine receptor (A1AR), is likely a key factor in the homeostatic control of sleep. This study examines the impact of sleep deprivation on A1AR density in different parts of the rat brain with [3H]CPFPX autoradiography. Binding of [3H]CPFPX was significantly increased in parietal cortex (PAR) (7%), thalamus (11%) and caudate-putamen (9%) after 24 h of sleep deprivation compared to a control group with an undisturbed circadian sleep-wake rhythm. Sleep deprivation of 12 h changed receptor density regionally between −5% and +9% (motor cortex (M1), statistically significant) compared to the circadian control group. These results suggest cerebral A1ARs are involved in effects of sleep deprivation and the regulation of sleep. The increase of A1AR density could serve the purpose of not only maintaining the responsiveness to increased adenosine levels but also amplifying the effect of sleep deprivation and is in line with a sleep-induced homoeostatic reorganization at the synaptic level. PMID:19146833

  18. 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 PMID:27159583

  19. Intensive sleep deprivation and cognitive behavioral therapy for pharmacotherapy refractory insomnia in a hospitalized patient.

    PubMed

    Breitstein, Joshua; Penix, Brandon; Roth, Bernard J; Baxter, Tristin; Mysliwiec, Vincent

    2014-06-15

    The case of a 59-year-old woman psychiatrically hospitalized with comorbid insomnia, suicidal ideation, and generalized anxiety disorder is presented. Pharmacologic therapies were unsuccessful for treating insomnia prior to and during hospitalization. Intensive sleep deprivation was initiated for 40 consecutive hours followed by a recovery sleep period of 8 hours. Traditional components of cognitive behavioral therapy for insomnia (CBTi), sleep restriction, and stimulus control therapies, were initiated on the ward. After two consecutive nights with improved sleep, anxiety, and absence of suicidal ideation, the patient was discharged. She was followed in the sleep clinic for two months engaging in CBTi. Treatment resulted in substantial improvement in her insomnia, daytime sleepiness, and anxiety about sleep. Sleep deprivation regimens followed by a restricted sleep recovery period have shown antidepressant effects in depressed patients. Similar treatment protocols have not been investigated in patients with pharmacotherapy refractory insomnia and generalized anxiety disorder. PMID:24932151

  20. Effects of biperiden on sleep at baseline and after 72 h of REM sleep deprivation in the cat.

    PubMed

    Salin-Pascual, R J; Jimenez-Anguiano, A; Granados-Fuentes, D; Drucker-Colin, R

    1992-01-01

    We examined the effects of the muscarinic M1 antagonist biperiden in cats. In the first experiment a dose-response analysis was performed with intraventricular injection (IV ventricle) of biperiden. In the second experiment after REM sleep deprivation cats were injected with either biperiden (0.1 mg/kg) or saline. Biperiden produced a reduction in REM sleep percentage and an increase in REM sleep latency with these high doses. The 0.1 mg/kg biperiden dose, which did not suppress REM sleep at baseline, did reduce the REM sleep rebound. The present study suggests a modulatory role of biperiden on REM sleep regulatory processes. The fact that an effect of biperiden is noted only at the high doses suggests that at these doses the drug is influencing non-M1 receptors. Changes in the sensitivity of these receptors as a result of REM sleep deprivation might explain why a dose of biperiden will reduce REM sleep rebound, while being ineffective in suppressing REM sleep at baseline.

  1. Role of spinal 5-HT receptors in cutaneous hypersensitivity induced by REM sleep deprivation.

    PubMed

    Wei, Hong; Ma, Ainiu; Wang, Yong-Xiang; Pertovaara, Antti

    2008-06-01

    Previous studies indicate that rapid eye movement (REM) sleep deprivation facilitates pain sensitivity. Since serotoninergic raphe neurons are involved both in regulation of sleep and descending pain modulation, we studied whether spinal 5-HT receptors have a role in sleep deprivation-induced facilitation of pain-related behavior. REM sleep deprivation of 48h was induced by the flower pot method in the rat. The pain modulatory influence of various serotoninergic compounds administered intrathecally was assessed by determining limb withdrawal response to monofilaments. REM sleep deprivation produced a marked hypersensitivity. Sleep deprivation-induced hypersensitivity and normal sensitivity in controls were reduced both by a 5-HT(1A) receptor antagonist (WAY-100635) and a 5-HT(2C) receptor antagonist (RS-102221). An antagonist of the 5-HT(3) receptor (LY-278584) failed to modulate hypersensitivity in sleep-deprived or control animals. Paradoxically, sensitivity in sleep-deprived and control animals was reduced not only by a 5-HT(1A) receptor antagonist but also by a 5-HT(1A) receptor agonist (8-OHDPAT). The results indicate that serotoninergic receptors in the spinal cord have a complex role in the control of sleep-deprivation induced cutaneous hypersensitivity as well as baseline sensitivity in control conditions. While endogenous serotonin acting on 5-HT(1A) and 5-HT(2C) receptors may facilitate mechanical sensitivity in animals with a sleep deprivation-induced hypersensitivity as well as in controls, increased activation of spinal 5-HT(1A) receptors by an exogenous agonist leads to suppression of mechanical sensitivity in both conditions. Spinal 5-HT(3) receptors do not contribute to cutaneous hypersensitivity induced by sleep deprivation.

  2. 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

  3. Creatine supplementation, sleep deprivation, cortisol, melatonin and behavior.

    PubMed

    McMorris, T; Harris, R C; Howard, A N; Langridge, G; Hall, B; Corbett, J; Dicks, M; Hodgson, C

    2007-01-30

    The effect of creatine supplementation and sleep deprivation, with intermittent moderate-intensity exercise, on cognitive and psychomotor performance, mood state, effort and salivary concentrations of cortisol and melatonin were examined. Subjects were divided into a creatine supplementation group and a placebo group. They took 5 g of creatine monohydrate or a placebo, dependent on their group, four times a day for 7 days immediately prior to the experiment. They undertook tests examining central executive functioning, short-term memory, choice reaction time, balance, mood state and effort at baseline and following 18-, 24- and 36-h sleep deprivation, with moderate intermittent exercise. Saliva samples were taken prior to each set of tests. A group x time analysis of covariance, with baseline performance the covariate, showed that the creatine group performed significantly (p < 0.05) better than the placebo group on the central executive task but only at 36 h. The creatine group demonstrated a significant (p < 0.01) linear improvement in performance of the central executive task throughout the experiment, while the placebo group showed no significant effects. There were no significant differences between the groups for any of the other variables. A significant (p < 0.001) main effect of time was found for the balance test with a linear improvement being registered. Cortisol concentrations on Day 1 were significantly (p < 0.01) higher than on Day 2. Mood significantly (p < 0.001) deteriorated up to 24 h with no change from 24 to 36 h. Effort at baseline was significantly (p < 0.01) lower than in the other conditions. It was concluded that, during sleep deprivation with moderate-intensity exercise, creatine supplementation only affects performance of complex central executive tasks.

  4. Sleep deprivation, allergy symptoms, and negatively reinforced problem behavior.

    PubMed

    Kennedy, C H; Meyer, K A

    1996-01-01

    We studied the relation between the presence versus the absence of sleep deprivation or allergy symptoms and the rate and function of problem behavior. Three students whose problem behavior was negatively reinforced by escape form instruction were studied across several weeks using analogue functional analyses. Our results indicated that the extraexperimental events were associated with (a) termination of instruction functioning as a negative reinforcer, (b) increased rates of negatively reinforced problem behavior, or (c) increased rates of problem behavior across all conditions. PMID:8881356

  5. Sleep deprivation impairs recall of social transmission of food preference in rats

    PubMed Central

    Wooden, Jessica I; Pido, Jennifer; Mathews, Hunter; Kieltyka, Ryan; Montemayor, Bertha A; Ward, Christopher P

    2014-01-01

    Evidence indicates that sleep plays an important role in learning and memory, and disruption of sleep especially seems to interfere with hippocampal memory processes. Social transmission of food preference (STFP), a natural test of paired associative learning, has been shown to be dependent on the hippocampus. While social transmission of food preference is not a novel task, it has not been used to examine the role of sleep in memory consolidation. Male Sprague-Dawley rats were randomly divided into three groups: cage control; sleep-deprived; and device control. Demonstrator rats were given powdered food mixed with a target spice. Test rats then interacted with demonstrator rats before being given a two choice test of powered food with the target spice or a novel spice. Sleep-deprived rats were then placed in an automated device that prevented sleep for 24 hours. After sleep deprivation, animals were given a preference test again to determine memory for the target spice at both 24 hours and 72 hours. Polysomnography was used to validate the method of sleep deprivation. During immediate preference testing, rats demonstrated a clear preference for the food containing the target spice. Rats that experienced 24 hours of sleep deprivation following the initial testing indicated a significant reduction in the recall of the target spice at 24 and 72 hours. The cage control and device animals maintained their preference for food containing the target spice. Therefore, the loss of sleep interfered with memory consolidation for food preference learned via social transmission. PMID:25395874

  6. Combined effects of alcohol and sleep deprivation in normal young adults.

    PubMed

    Peeke, S C; Callaway, E; Jones, R T; Stone, G C; Doyle, J

    1980-01-01

    The effect of combining sleep deprivation and moderate alcohol consumption in male college students differed from the effects of each treatment alone. Following either alcohol or sleep deprivation, there was mild performance impairment, decreased alertness and reduced amplitude and increased latency of cortical evoked potential (EP) components. Heart rate increased after alcohol and anxiety increased after sleep deprivation. When alcohol and sleep deprivation were combined, antagonistic effects were found for most measures (reaction time, heart rate, alertness, anxiety, latency of early EP components), but synergistic effects also occurred (performance accuracy, latency of late EP components). These effects were found in a double-blind experiment using 24 subjects. The experimental treatments were alcohol doses of 0, 0.45 and 0.90 ml/kg of 95% ethanol and 0 and 26 h of sleep deprivation. PMID:6770408

  7. [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. PMID:24050022

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

    PubMed Central

    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

    2016-01-01

    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 eukaryotic initiation factor 4G (eIF4G) in the hippocampi of sleep-deprived mice. Increasing the abundance of 4EBP2 in hippocampal excitatory neurons prior to 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. PMID:27117251

  9. 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

    2016-01-01

    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. PMID:27117251

  10. 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.

  11. How Is Sleep Apnea Treated?

    MedlinePlus

    ... Topics CPAP High Blood Pressure Overweight and Obesity Sleep Deprivation and Deficiency Sleep Studies Send a link to ... For more information, go to the Health Topics Sleep Deprivation and Deficiency article.) If treatment and enough sleep ...

  12. Sleep Deprivation affects Extinction but Not Acquisition Memory in Honeybees

    ERIC Educational Resources Information Center

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

    2009-01-01

    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…

  13. 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

  14. Effects of sleep deprivation on sleep homeostasis and restoration during methadone-maintenance: a [31] P MRS brain imaging study

    PubMed Central

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

    2009-01-01

    SUMMARY Insomnia afflicts many individuals, but particularly those in chronic methadone treatment. Studies examining sleep deprivation (SD) have begun to identify sleep restoration processes involving brain bioenergetics. The technique [31]P magnetic resonance spectroscopy (MRS) can measure brain changes in the high-energy phosphates: alpha-, beta-, and gamma-nucleoside triphosphate (NTP). In the present study, 21 methadone-maintained (MM) and 16 control participants underwent baseline (BL), SD (40 wakeful hrs), recovery1 (RE1), and recovery2 (RE2) study nights. Polysomnographic sleep was recorded each night and [31]P MRS brain scanning conducted each morning using a 4T MR scanner (dual-tuned proton/phosphorus headcoil). Interestingly, increases in total sleep time (TST) and sleep efficiency index (SEI) commonly associated with RE sleep were not apparent in MM participants. Analysis of methadone treatment duration revealed that the lack of RE sleep increases in TST and SEI were primarily exhibited by short-term MM participants (methadone<12 months), while RE sleep in long-term MM (methadone>12 months) participants was more comparable to control participants. Slow wave sleep increased during RE1, but there was no difference between MM and control participants. Spectral power analysis revealed that compared to control participants; MM participants had greater delta, theta, and alpha spectral power during BL and RE sleep. [31]P MRS revealed that elevations in brain beta-NTP (a direct measure of ATP) following RE sleep were greater in MM compared to control participants. Results suggest that differences in sleep and brain chemistry during RE in MM participants may be reflective of a disruption in homeostatic sleep function. PMID:19775835

  15. Are You Sleep-Deprived? Learn More About Healthy Sleep | NIH MedlinePlus the Magazine

    MedlinePlus

    ... extreme daytime sleepiness), and parasomnias (abnormal sleep behaviors). Michael J. Twery, Ph.D., director of the National Center on Sleep Disorders Research Photo: Dr. Michael Twery Add to those challenges the demands of ...

  16. Differential impact of REM sleep deprivation on cytoskeletal proteins of brain regions involved in sleep regulation.

    PubMed

    Rodríguez-Vázquez, Jennifer; Camacho-Arroyo, Ignacio; Velázquez-Moctezuma, Javier

    2012-01-01

    Rapid eye movement (REM) sleep is involved in memory consolidation, which implies synaptic plasticity. This process requires protein synthesis and the reorganization of the neural cytoskeleton. REM sleep deprivation (REMSD) has an impact on some neuronal proteins involved in synaptic plasticity, such as glutamate receptors and postsynaptic density protein 95, but its effects on cytoskeletal proteins is unknown. In this study, the effects of REMSD on the content of the cytoskeletal proteins MAP2 and TAU were analyzed. Adult female rats were submitted to selective REMSD by using the multiple platform technique. After 24, 48 or 72 h of REMSD, rats were decapitated and the following brain areas were dissected: pons, preoptic area, hippocampus and frontal cortex. Protein extraction and Western blot were performed. Results showed an increase in TAU content in the pons, preoptic area and hippocampus after 24 h of REMSD, while in the frontal cortex a significant increase in TAU content was observed after 72 h of REMSD. A TAU content decrease was observed in the hippocampus after 48 h of REMSD. Interestingly, a marked increase in TAU content was observed after 72 h of REMSD. MAP2 content only increased in the preoptic area at 24 h, and in the frontal cortex after 24 and 72 h of REMSD, without significant changes in the pons and hippocampus. These results support the idea that REM sleep plays an important role in the organization of neural cytoskeleton, and that this effect is tissue-specific.

  17. Effects of Fatigue and Sleep Deprivation on Microvascular Anastomoses.

    PubMed

    Basaran, Karaca; Mercan, Ebru Sen; Aygit, Ahmet Cemal

    2015-06-01

    Previous studies have investigated the effects of various human-based factors, such as tremor, exercise, and posture, on microsurgical performance. In this study, the authors investigated the effects of sleep deprivation and fatigue on microsurgery. A total of 48 Wistar Hannover rats were divided into 3 groups (16 anastomoses in each group) to be operated on at 3 different times: in the morning at 08:00 hours (group I), at night on the same day (01:00 h, group II), and the next morning at 09:00 hours (group III) following a night with no sleep. The blindly evaluated parameters were anastomotic times, error score (ES), global rating scale (GRS), autopsy scores (ASs), and patency. There was progressive decrease in the anastomosis times between the groups (P > 0.05). The patency rates were 93% in group I, 81% in group II, and 81% in group III (P > 0.05). The ES (P < 0.01), AS (P < 0.001), and GRS (P < 0.001) revealed significant results. Comparison between the groups showed that other than the anastomosis time, the night group (group II) showed a significant drop when compared with the preceding morning group (group I) (ES P < 0.01, AS P < .001, and GRS P < 0.001). In most of the parameters, the errors occurred with fatigue after the day and reached a maximum at the end of the day (group II). This study provides valuable data that might have significant medicolegal implications for controversial issues. More studies, however, including multiple surgeons with different experience levels, might be required to fully elucidate the overall effects of fatigue and sleep deprivation on microsurgery.

  18. Sleep deprivation-induced multi-organ injury: role of oxidative stress and inflammation

    PubMed Central

    Periasamy, Srinivasan; Hsu, Dur-Zong; Fu, Yu-Hsuan; Liu, Ming-Yie

    2015-01-01

    Sleep deprivation affects all aspects of health. Adverse health effects by sleep deviation are still underestimated and undervalued in clinical practice and, to a much greater extent in monitoring human health. We hypothesized that sleep deprivation-induced mild organ injuries; oxidative stress and inflammation might play a crucial role in inducing multi-organ injury. Male C57BL/6J mice (n = 6-7) were sleep-deprived for 0-72 h using a modified multiple platform boxes method. Blood and tissue were collected. Liver, heart, kidney, lung, and pancreatic injuries were evaluated using biochemical and histological analyses. Glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), total billirubin (TBIL), creatine phosphokinase (CPK), creatine phosphokinase-myocardial band (CKMB), lactic dehydrogenase (LDH), creatinine (CRE), and blood urea nitrogen (BUN) were assayed in blood. Malondialdehyde (MDA), nitric oxide (NO), tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 levels were measured. Histology revealed mild-to-moderate liver and lung injury in sleep-deprived mice. Sleep-deprived mice had significantly higher GOT, GPT, TBIL, CPK, CKMB, LDH, BUN, and α-amylase (AMYL) levels, which indicated liver, heart, kidney, and pancreatic injuries. Serum IL-1β at 24 h and IL-6 at 72 h were significantly higher in sleep-deprived than in control mice. Hepatic TNF-α and IL-1β were significantly higher, but IL-6 significantly lower in mice that had been sleep-deprived for 72 h. Sleep deprivation-mediated inflammation may be associated with mild to moderate multi-organ damage in mice. The implication of this study indicates sleep deprivation in humans may induce multi-organ injury that negatively affects cardiovascular and gastrointestinal health. PMID:26648820

  19. Sleep deprivation-induced multi-organ injury: role of oxidative stress and inflammation.

    PubMed

    Periasamy, Srinivasan; Hsu, Dur-Zong; Fu, Yu-Hsuan; Liu, Ming-Yie

    2015-01-01

    Sleep deprivation affects all aspects of health. Adverse health effects by sleep deviation are still underestimated and undervalued in clinical practice and, to a much greater extent in monitoring human health. We hypothesized that sleep deprivation-induced mild organ injuries; oxidative stress and inflammation might play a crucial role in inducing multi-organ injury. Male C57BL/6J mice (n = 6-7) were sleep-deprived for 0-72 h using a modified multiple platform boxes method. Blood and tissue were collected. Liver, heart, kidney, lung, and pancreatic injuries were evaluated using biochemical and histological analyses. Glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), total billirubin (TBIL), creatine phosphokinase (CPK), creatine phosphokinase-myocardial band (CKMB), lactic dehydrogenase (LDH), creatinine (CRE), and blood urea nitrogen (BUN) were assayed in blood. Malondialdehyde (MDA), nitric oxide (NO), tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 levels were measured. Histology revealed mild-to-moderate liver and lung injury in sleep-deprived mice. Sleep-deprived mice had significantly higher GOT, GPT, TBIL, CPK, CKMB, LDH, BUN, and α-amylase (AMYL) levels, which indicated liver, heart, kidney, and pancreatic injuries. Serum IL-1β at 24 h and IL-6 at 72 h were significantly higher in sleep-deprived than in control mice. Hepatic TNF-α and IL-1β were significantly higher, but IL-6 significantly lower in mice that had been sleep-deprived for 72 h. Sleep deprivation-mediated inflammation may be associated with mild to moderate multi-organ damage in mice. The implication of this study indicates sleep deprivation in humans may induce multi-organ injury that negatively affects cardiovascular and gastrointestinal health. PMID:26648820

  20. 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

  1. 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

  2. Long-term sleep deprivation as a game. The wear and tear of wakefulness.

    PubMed

    Kamphuisen, H A; Kemp, B; Kramer, C G; Duijvestijn, J; Ras, L; Steens, J

    1992-01-01

    We report here the first sleep deprivation study done on a group of 5 healthy students (1 female, 4 males, 23-24 years of age) while playing a game (Triviant). In 2 persons an EEG was recorded for 6 consecutive 24 h periods with an ambulatory monitor from the baseline night until 72 h after deprivation. The baseline night showed normal hypnograms. The students were deprived of sleep for 65 h following the baseline night. Sleep deprivation was complete and resulted in bradyphrenia, loss of memory and contact with reality, ataxia, decrease in body temperature and loss of body weight. The main sign of recuperation was a strongly increased slow-wave sleep synchronization during the first recuperation period (day-time sleep) only. There were no signs of REM rebound. PMID:1320535

  3. Classifying Vulnerability to Sleep Deprivation Using Baseline Measures of Psychomotor Vigilance

    PubMed Central

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

    2015-01-01

    Objective: To identify measures derived from baseline psychomotor vigilance task (PVT) performance that can reliably predict vulnerability to sleep deprivation. Design: 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. Setting: Two academic sleep laboratories. Participants: Independent samples of 135 (69 women, age 18 to 25 y), and 45 (3 women, age 22 to 32 y) healthy adults. Measurements and Results: 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. Conclusions: 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 following sleep deprivation. Citation: Patanaik A, Kwoh CK, Chua EC, Gooley JJ, Chee MW. Classifying vulnerability to sleep deprivation using baseline measures of psychomotor vigilance. SLEEP 2015;38(5):723–734. PMID:25325482

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

    PubMed

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

    2015-10-01

    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.

  5. 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

  6. Effects of mental resilience on neuroendocrine hormones level changes induced by sleep deprivation in servicemen.

    PubMed

    Sun, Xinyang; Dai, Xuyan; Yang, Tingshu; Song, Hongtao; Yang, Jialin; Bai, Jing; Zhang, Liyi

    2014-12-01

    The aim of this study was to investigate the effects of mental resilience on the changes of serum rennin, angiotensin, and cortisol level induced by sleep deprivation in servicemen. By random cluster sampling, a total of 160 servicemen, aged from 18 to 30, were selected to undergo 24-hour total sleep deprivation and administered the military personnel mental resilience scale after the deprivation procedure. The sleep deprivation procedure started at 8 a.m. on Day 8 and ended at 8 a.m. on Day 9 after 7 days of normal sleep for baseline preparation. Blood samples were drawn from the 160 participants at 8 a.m. respectively on Day 8 and Day 9 for hormonal measurements. All blood samples were analyzed using radioimmunoassay. As hypothesized, serum rennin, angiotensin II, and cortisol level of the participants after sleep deprivation were significantly higher than those before (P < 0.05). The changes of serum rennin and cortisol in the lower mental resilience subgroup were significantly greater (P < 0.05); problem-solving skill and willpower were the leading influence factors for the increases of serum rennin and cortisol respectively induced by sleep deprivation. We conclude that mental resilience plays a significant role in alleviating the changes of neurohormones level induced by sleep deprivation in servicemen.

  7. Sleep deprivation and anxiety in humans and rodents--translational considerations and hypotheses.

    PubMed

    Pires, Gabriel Natan; Tufik, Sergio; Andersen, Monica Levy

    2015-10-01

    The effects of acute sleep deprivation on anxiety are the focus of controversy in the literature. While clinical research studies on the effects of sleep deprivation seem to show a consistent increase in acute anxiety, rodent studies have produced inconsistent results, with some experiments pointing to anxiogenesis and others to anxiolysis. Such observations impair the translational applicability of rodent models on the paradigm between sleep deprivation and anxiety. Current studies fail in the very basic principle of biomedical translational research: to provide relevant and reliable knowledge from basic experimental science that can be applied in clinical environments. Possible explanations for the disparity between human and animal studies include the accuracy of both human and rodent research, the ability of current behavioral protocols to truly reflect the anxiety response of rodents to sleep deprivation, and the nature of sleep deprivation-induced anxiety in rodents. Based on these hypotheses, we performed a brief overview of the literature on the relationship between sleep deprivation and anxiety and propose a research agenda that could lead to a better understanding of the reasons for the discrepancies found in the literature and provide more reliable data on the translational relationship between sleep deprivation and anxiety.

  8. Does sleep deprivation alter functional EEG networks in children with focal epilepsy?

    PubMed

    van Diessen, Eric; Otte, Willem M; Braun, Kees P J; Stam, Cornelis J; Jansen, Floor E

    2014-01-01

    Electroencephalography (EEG) recordings after sleep deprivation increase the diagnostic yield in patients suspected of epilepsy if the routine EEG remains inconclusive. Sleep deprivation is associated with increased interictal EEG abnormalities in patients with epilepsy, but the exact mechanism is unknown. In this feasibility study, we used a network analytical approach to provide novel insights into this clinical observation. The aim was to characterize the effect of sleep deprivation on the interictal functional network organization using a unique dataset of paired routine and sleep deprivation recordings in patients and controls. We included 21 children referred to the first seizure clinic of our center with suspected new onset focal epilepsy in whom a routine interictal and a sleep deprivation EEG (SD-EEG) were performed. Seventeen children, in whom the diagnosis of epilepsy was excluded, served as controls. For both time points weighted functional networks were constructed based on interictal artifact free time-series. Routine and sleep deprivation networks were characterized at different frequency bands using minimum spanning tree (MST) measures (leaf number and diameter) and classical measures of integration (path length) and segregation (clustering coefficient). A significant interaction was found for leaf number and diameter between patients and controls after sleep deprivation: patients showed a shift toward a more path-like MST network whereas controls showed a shift toward a more star-like MST network. This shift in network organization after sleep deprivation in patients is in accordance with previous studies showing a more regular network organization in the ictal state and might relate to the increased epileptiform abnormalities found in patients after sleep deprivation. Larger studies are needed to verify these results. Finally, MST measures were more sensitive in detecting network changes as compared to the classical measures of integration and

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

    PubMed

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

    2010-12-28

    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

  10. GABAA receptor-mediated input change on orexin neurons following sleep deprivation in mice.

    PubMed

    Matsuki, T; Takasu, M; Hirose, Y; Murakoshi, N; Sinton, C M; Motoike, T; Yanagisawa, M

    2015-01-22

    Orexins are bioactive peptides, which have been shown to play a pivotal role in vigilance state transitions: the loss of orexin-producing neurons (orexin neurons) leads to narcolepsy with cataplexy in the human. However, the effect of the need for sleep (i.e., sleep pressure) on orexin neurons remains largely unknown. Here, we found that immunostaining intensities of the α1 subunit of the GABAA receptor and neuroligin 2, which is involved in inhibitory synapse specialization, on orexin neurons of mouse brain were significantly increased by 6-h sleep deprivation. In contrast, we noted that immunostaining intensities of the α2, γ2, and β2/3 subunits of the GABAA receptor and Huntingtin-associated protein 1, which is involved in GABAAR trafficking, were not changed by 6-h sleep deprivation. Using a slice patch recording, orexin neurons demonstrated increased sensitivity to a GABAA receptor agonist together with synaptic plasticity changes after sleep deprivation when compared with an ad lib sleep condition. In summary, the GABAergic input property of orexin neurons responds rapidly to sleep deprivation. This molecular response of orexin neurons may thus play a role in the changes that accompany the need for sleep following prolonged wakefulness, in particular the decreased probability of a transition to wakefulness once recovery sleep has begun.

  11. The impact of one night of sleep deprivation on moral judgments.

    PubMed

    Tempesta, D; Couyoumdjian, A; Moroni, F; Marzano, C; De Gennaro, L; Ferrara, M

    2012-01-01

    Recent studies have shown the existence of a relationship between sleep and moral judgment. In this study, we investigated whether one night of sleep deprivation affects the ability to judge the appropriateness of moral dilemmas. Forty-eight students had to judge 30 moral dilemmas at test, after a night of home sleep, and another 30 dilemmas at retest, following one night of continuous wakefulness. The 60 dilemmas (20 moral impersonal, 20 moral personal, and 20 non-moral) were selected from Greene's dilemmas. Both groups judged the appropriateness of personal and impersonal dilemmas in the same way. A close to significant effect of sleep deprivation was observed on the reaction times for impersonal moral dilemmas, to which the deprived subjects responded faster (p = .05) than the control subjects. However, this was not the case for personal ones, for which no difference was significant. This result shows a greater ease/speed in responding to the (impersonal) dilemmas, which induce low emotional engagement after sleep deprivation, although the willingness to accept moral violations is not affected. This suggests that one night of sleep loss selectively influences the response speed only for moral impersonal dilemmas, probably due to disinhibition processes. The quality of moral judgment dilemmas does not seem to be easily influenced by a single night of sleep deprivation, but only by a longer lack of sleep. PMID:21943064

  12. 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

  13. 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. PMID:25793869

  14. 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.

  15. Sleep deprivation worsens inflammation and delays recovery in a mouse model of colitis

    PubMed Central

    Tang, Yueming; Preuss, Fabian; Turek, Fred W.; Jakate, Shriram; Keshavarzian, Ali

    2012-01-01

    Background and aim We recently showed that patients with inflammatory bowel disease (IBD) report significantly more sleep disturbances. To determine whether disrupted sleep can affect the severity of inflammation and the course of IBD, we used an animal model of colonic inflammation to determine the effects of acute and chronic intermittent sleep deprivation on the severity of colonic inflammation and tissue damage in colitis and recovery from this damage. Methods Acute sleep deprivation (ASD) consisted of 24 h of forced locomotor activity in a mechanical wheel rotating at a constant speed. Chronic intermittent sleep deprivation (CISD) consisted of an acute sleep deprivation episode, followed by additional sleep deprivation periods in the wheel for 6 h every other day throughout the 10 day study period. To induce colitis, mice were given 2% dextran sodium sulfate (DSS) in their daily drinking water for 7 days. The development and severity of colitis were monitored by measuring weight loss and tissue myeloperoxidase (MPO) activity daily and colon histology scores 10 days after initiation of colitis. Results ASD or CISD did not cause colonic inflammation in vehicle-treated mice. Changes in daily body weight, tissue MPO levels and colon histopathology score were similar between mice that were sleep deprived and controls. Daily DSS ingestion caused colitis in mice. ASD worsened colonic inflammation: tissue MPO levels in ASD/DSS-treated mice were significantly higher than in DSS-treated mice that were not sleep deprived. However, the worsening of colonic inflammation by ASD was not enough to exacerbate clinical manifestations of colitis such as weight loss. In contrast, the deleterious effects of CISD were severe enough to cause worsening of histological and clinical manifestations of colitis. The deleterious effects of sleep deprivation on severity of colitis appeared to be due to both increased colonic inflammation and a decrease in the ability of mice to recover from

  16. Neurobehavioral and Cognitive Changes Induced by Sleep Deprivation in Healthy Volunteers.

    PubMed

    Cassé-Perrot, Catherine; Lanteaume, Laura; Deguil, Julie; Bordet, Régis; Auffret, Alexandra; Otten, Lisa; Blin, Olivier; Bartrés-Faz, David; Micallef, Joëlle

    2016-01-01

    To this day, the pharmacological treatment of Alzheimer's disease remains limited to the temporary stabilisation of cognitive decline and the reduction of neuropsychiatric symptoms. It is moreover with great difficulty to predict and select promising drug candidates in the early stages of the discovery and developmental process. In this context, scientists have developed new experimental paradigms to artificially induce transient cognitive impairments in healthy volunteers akin to those observed in Alzheimer's disease, i.e. the Cognitive Challenge Models. In the last decade, a great amount of literature on Sleep Deprivation was published which mainly focused on the consequences of sleep loss for public health. However, sleep deprivation paradigm may also be regarded as a cognitive challenge model. It is commonly accepted that sleep deprivation induces cognitive impairments related to a global decrease in vigilance, while in fact, there is a controversial approach related to the selective effects on cognitive functions. The identification and validation of cognitive challenge models in healthy volunteers are suitable in early clinical development of drugs to determine the 'hint of efficacy' of drug candidates. The present review aims at exploring in detail the methods, designs and cognitive paradigms used in non pharmacological sleep deprivation studies. Sleep deprivation can be induced by different methods. Probing the four main cognitive functions will allow identifying the extent to which different sleep deprivation designs selectively compromise executive function, working memory, episodic memory and attention. Findings will be discussed in line with cognitive processing levels that are required according to the tasks. PMID:27189463

  17. A PILOT STUDY ON THE ENCODING OF A PERCEPTUAL LEARNING TASK FOLLOWING SLEEP DEPRIVATION.

    PubMed

    McWhirter, Kelly K; Morrow, Anne S; Lee, Beth A; Bishu, Shrinivas; Zametkin, Alan J; Balkin, Thomas J; Smith, Carolyn B; Picchioni, Dante

    2015-08-01

    Memory encoding sometimes must occur during a period of sleep deprivation. The question was whether one night of sleep deprivation inhibits encoding on a perceptual learning task (the texture discrimination task). The sample was 18 human participants (M age=22.1 yr., SEM=0.5; 8 men). The participants were randomized to a sleep deprivation or sleep control condition and, after the manipulation, were given two administrations of the texture discrimination task. All participants were given an opportunity for a 90 min. nap between the two administrations. Performance was measured by the interpolated stimulus-to-mask-onset asynchrony (i.e., the inter-stimulus interval), at which the percentage of correct responses for the stimuli in the participant's peripheral vision fell below 80%. Offline consolidation was defined as a decrease in this index between the two administrations. Participants who were sleep deprived prior to encoding exhibited similar offline consolidation (M=-5.3 msec., SEM=2.3) compared to participants who were not sleep deprived prior to encoding (M=-6.2 msec., SEM=3.9); the two-way interaction between time and condition was not significant. In light of reports in the literature, these results indicate encoding following sleep deprivation may be influenced by both the type of task encoded and the brain regions involved in memory processing. PMID:26226287

  18. A PILOT STUDY ON THE ENCODING OF A PERCEPTUAL LEARNING TASK FOLLOWING SLEEP DEPRIVATION.

    PubMed

    McWhirter, Kelly K; Morrow, Anne S; Lee, Beth A; Bishu, Shrinivas; Zametkin, Alan J; Balkin, Thomas J; Smith, Carolyn B; Picchioni, Dante

    2015-08-01

    Memory encoding sometimes must occur during a period of sleep deprivation. The question was whether one night of sleep deprivation inhibits encoding on a perceptual learning task (the texture discrimination task). The sample was 18 human participants (M age=22.1 yr., SEM=0.5; 8 men). The participants were randomized to a sleep deprivation or sleep control condition and, after the manipulation, were given two administrations of the texture discrimination task. All participants were given an opportunity for a 90 min. nap between the two administrations. Performance was measured by the interpolated stimulus-to-mask-onset asynchrony (i.e., the inter-stimulus interval), at which the percentage of correct responses for the stimuli in the participant's peripheral vision fell below 80%. Offline consolidation was defined as a decrease in this index between the two administrations. Participants who were sleep deprived prior to encoding exhibited similar offline consolidation (M=-5.3 msec., SEM=2.3) compared to participants who were not sleep deprived prior to encoding (M=-6.2 msec., SEM=3.9); the two-way interaction between time and condition was not significant. In light of reports in the literature, these results indicate encoding following sleep deprivation may be influenced by both the type of task encoded and the brain regions involved in memory processing.

  19. Essential Roles of GABA Transporter-1 in Controlling Rapid Eye Movement Sleep and in Increased Slow Wave Activity after Sleep Deprivation

    PubMed Central

    Xu, Xin-Hong; Qu, Wei-Min; Bian, Min-Juan; Huang, Fang; Fei, Jian; Urade, Yoshihiro; Huang, Zhi-Li

    2013-01-01

    GABA is the major inhibitory neurotransmitter in the mammalian central nervous system that has been strongly implicated in the regulation of sleep. GABA transporter subtype 1 (GAT1) constructs high affinity reuptake sites for GABA and regulates GABAergic transmission in the brain. However, the role of GAT1 in sleep-wake regulation remains elusive. In the current study, we characterized the spontaneous sleep-wake cycle and responses to sleep deprivation in GAT1 knock-out (KO) mice. GAT1 KO mice exhibited dominant theta-activity and a remarkable reduction of EEG power in low frequencies across all vigilance stages. Under baseline conditions, spontaneous rapid eye movement (REM) sleep of KO mice was elevated both during the light and dark periods, and non-REM (NREM) sleep was reduced during the light period only. KO mice also showed more state transitions from NREM to REM sleep and from REM sleep to wakefulness, as well as more number of REM and NREM sleep bouts than WT mice. During the dark period, KO mice exhibited more REM sleep bouts only. Six hours of sleep deprivation induced rebound increases in NREM and REM sleep in both genotypes. However, slow wave activity, the intensity component of NREM sleep was briefly elevated in WT mice but remained completely unchanged in KO mice, compared with their respective baselines. These results indicate that GAT1 plays a critical role in the regulation of REM sleep and homeostasis of NREM sleep. PMID:24155871

  20. Essential roles of GABA transporter-1 in controlling rapid eye movement sleep and in increased slow wave activity after sleep deprivation.

    PubMed

    Xu, Xin-Hong; Qu, Wei-Min; Bian, Min-Juan; Huang, Fang; Fei, Jian; Urade, Yoshihiro; Huang, Zhi-Li

    2013-01-01

    GABA is the major inhibitory neurotransmitter in the mammalian central nervous system that has been strongly implicated in the regulation of sleep. GABA transporter subtype 1 (GAT1) constructs high affinity reuptake sites for GABA and regulates GABAergic transmission in the brain. However, the role of GAT1 in sleep-wake regulation remains elusive. In the current study, we characterized the spontaneous sleep-wake cycle and responses to sleep deprivation in GAT1 knock-out (KO) mice. GAT1 KO mice exhibited dominant theta-activity and a remarkable reduction of EEG power in low frequencies across all vigilance stages. Under baseline conditions, spontaneous rapid eye movement (REM) sleep of KO mice was elevated both during the light and dark periods, and non-REM (NREM) sleep was reduced during the light period only. KO mice also showed more state transitions from NREM to REM sleep and from REM sleep to wakefulness, as well as more number of REM and NREM sleep bouts than WT mice. During the dark period, KO mice exhibited more REM sleep bouts only. Six hours of sleep deprivation induced rebound increases in NREM and REM sleep in both genotypes. However, slow wave activity, the intensity component of NREM sleep was briefly elevated in WT mice but remained completely unchanged in KO mice, compared with their respective baselines. These results indicate that GAT1 plays a critical role in the regulation of REM sleep and homeostasis of NREM sleep.

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

    PubMed Central

    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

    OBJECTIVE: The aim of this study was to evaluate overall genetic damage induced by total sleep deprivation in obese, female Zucker rats of differing ages. METHOD: 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. RESULTS: 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. CONCLUSION: 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. PMID:23644860

  2. 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

  3. The effect of a REM sleep deprivation procedure on different aspects of memory function in humans.

    PubMed

    Saxvig, Ingvild West; Lundervold, Astri Johansen; Grønli, Janne; Ursin, Reidun; Bjorvatn, Bjørn; Portas, Chiara Maria

    2008-03-01

    Previous studies have suggested that memory is dependent on the occurrence of REM sleep. Research has mainly focused on two distinct types of memory function, declarative and procedural, and it seems that the latter may more directly depend on REM sleep. Memory consolidation has been more investigated than acquisition, maintenance, and recall, despite the fact that sleep may affect flow of information into/from storage. Moreover, tests have often been limited to stimuli within only one modality (usually visual or verbal). This study aimed to clarify the role of REM sleep in memory by investigating aspects of memory function, processing, and modality in the same experimental setting. Tests of acquisition and consolidation of multiple aspects of memory function within the visual and verbal modalities were administrated to subjects before and after REM sleep deprivation. Results show that test performance was not affected by REM sleep deprivation.

  4. Microstructure of frontoparietal connections predicts individual resistance to sleep deprivation.

    PubMed

    Cui, Jiaolong; Tkachenko, Olga; Gogel, Hannah; Kipman, Maia; Preer, Lily A; Weber, Mareen; Divatia, Shreya C; Demers, Lauren A; Olson, Elizabeth A; Buchholz, Jennifer L; Bark, John S; Rosso, Isabelle M; Rauch, Scott L; Killgore, William D S

    2015-02-01

    Sleep deprivation (SD) can degrade cognitive functioning, but growing evidence suggests that there are large individual differences in the vulnerability to this effect. Some evidence suggests that baseline differences in the responsiveness of a fronto-parietal attention system that is activated during working memory (WM) tasks may be associated with the ability to sustain vigilance during sleep deprivation. However, the neurocircuitry underlying this network remains virtually unexplored. In this study, we employed diffusion tensor imaging (DTI) to investigate the association between the microstructure of the axonal pathway connecting the frontal and parietal regions--i.e., the superior longitudinal fasciculus (SLF)--and individual resistance to SD. Thirty healthy participants (15 males) aged 20-43 years underwent functional magnetic resonance imaging (fMRI) and diffusion tensor imaging (DTI) at rested wakefulness prior to a 28-hour period of SD. Task-related fronto-parietal fMRI activation clusters during a Sternberg WM Task were localized and used as seed regions for probabilistic fiber tractography. DTI metrics, including fractional anisotropy, mean diffusivity, axial and radial diffusivity were measured in the SLF. The psychomotor vigilance test (PVT) was used to evaluate resistance to SD. We found that activation in the left inferior parietal lobule (IPL) and dorsolateral prefrontal cortex (DLPFC) positively correlated with resistance. Higher fractional anisotropy of the left SLF comprising the primary axons connecting IPL and DLPFC was also associated with better resistance. These findings suggest that individual differences in resistance to SD are associated with the functional responsiveness of a fronto-parietal attention system and the microstructural properties of the axonal interconnections.

  5. Effect of sleep deprivation on driving safety in housestaff.

    PubMed

    Marcus, C L; Loughlin, G M

    1996-12-01

    Sleep deprivation is known to affect driving safety. Housestaff (HS) are routinely sleep-deprived when on call. We hypothesized that this would affect their driving. We therefore administered questionnaires regarding driving to 70 pediatric HS, who were on call every fourth night, and to 85 faculty members (FAC), who were rarely disturbed at night. HS were questioned about events during their residency, and FAC were questioned about events during the preceding three years. There was an 87% response rate for each group. HS slept 2.7 +/- 0.9 (SD) hours when on call vs 7.2 +/- 0.8 hours when not on call (p < 0.001). 44% of HS had fallen asleep when stopped at a light, vs 12.5% FAC (p < 0.001). 23% of HS had fallen asleep while driving vs. 8% FAC (ns). A total of 49% of HS had fallen asleep at the wheel; 90% of these events occurred post-call. In contrast, only 13% of FAC had fallen asleep at the wheel (p < 0.001). HS had received a total of 25 traffic citations for moving violations vs. 15 for FAC and were involved in 20 motor vehicle accidents vs. 11 for FAC. One traffic citation clearly resulted from HS falling asleep at the wheel vs. none for FAC. We conclude that HS frequently fall asleep when driving post-call. We speculate that current HS work schedules may place some HS at risk for injury to themselves and others. Further study, using prospectively objective measures is indicated.

  6. 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

  7. 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. PMID:26180190

  8. 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

  9. 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.

  10. [The action of ionotropic glutamate receptor channel blockers on effects of sleep deprivation in rats].

    PubMed

    Vataev, S I; Oganesian, G A; Lukomskaia, N Ia; Magazanik, L G

    2013-05-01

    The action of non-competitive glutamate receptor antagonists on the effects of sleep deprivation has been studied on Krushinskii-Molodkina rats having an inherited predisposition to audiogenic seizures and Wistar rats deprived to this respond. Two types of glutamate receptor open channels blockers were used: the selective blockers of NMDA-receptors (memantine and IEM-1921) and blockers of mixed type, impacting both on the NMDA- and presumably Ca(2+)-permeable AMPA/kainate receptors (IEM-1754 and IEM 1925). Rats were subjected to 12 hours long sleep deprivation. Immediatly after that memantine and IEM-1921 were injected, and during the first 3 hours the total or partial reduction of fast-wave (paradoxical) sleep and a significant increase of the representation of wakefulness at the cost of reducing the total time of slow-wave sleep were observed. These effects are most likely to be a consequence of the blockade of NMDA-receptors functioning in the systems of the rat brain responsible for the launch and maintenance of fast-wave sleep. Injection of IEM-1754 and IEM-1925 on background of sleep deprivation did not affect the organization of sleep during the first 3 hours of their action. During the second three-hour period the rebound effect was observed. The obtained results indicate the involvement of NMDA glutamate receptors in the functioning of various parts of the sleep system of both rat lines.

  11. [Sorption of sulfophthaleinic dyes by the brain synaptosomes of rats deprived of parodoxical sleep].

    PubMed

    Nilova, N S

    1984-12-01

    The influence of paradoxical sleep deprivation on sorption of bromphenol blue, bromcresol green and bromthymol blue by rat's brain synaptosomes was studied. Effect of sleep disturbance (increase in the number of dye bindings) was shown to augment with the increase in hydrophobicity of the sulfophtaleinic dye. PMID:6528362

  12. Cytomorphometric changes in rat brain neurons after rapid eye movement sleep deprivation.

    PubMed

    Majumdar, S; Mallick, B N

    2005-01-01

    Rapid eye movement sleep plays a vital role in the survival of animals. Its deprivation causes alterations in brain functions and behaviors including activities of important enzymes, neurotransmitter levels, impairment of neural excitability and memory consolidation. However, there was a lack of knowledge regarding the effects of rapid eye movement sleep deprivation on neuronal morphology that may get affected much earlier than any permanent damage to the neurons. In the present study, some of these issues have been addressed by studying the effects of rapid eye movement sleep deprivation on various morphological parameters viz. neuronal perimeter, area and shape of neurons located in brain areas known to regulate rapid eye movement sleep and as a control in other brain areas which do not regulate rapid eye movement sleep. The results showed that rapid eye movement sleep deprivation differentially affected neurons depending on their physiological correlates of rapid eye movement sleep and neurotransmitter content. The effects could be reversed if the animals were allowed to recover from rapid eye movement sleep loss or by applying alpha1-adrenergic antagonist, prazosin. The findings in rats support reported data and help explaining previous observations.

  13. 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.

  14. 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

  15. Caffeine and REM sleep deprivation: Effect on basal levels of signaling molecules in area CA1.

    PubMed

    Alkadhi, Karim A; Alhaider, Ibrahim A

    2016-03-01

    We have investigated the neuroprotective effect of chronic caffeine treatment on basal levels of memory-related signaling molecules in area CA1 of sleep-deprived rats. Animals in the caffeine groups were treated with caffeine in drinking water (0.3g/l) for four weeks before they were REM sleep-deprived for 24h in the Modified Multiple Platforms paradigm. Western blot analysis of basal protein levels of plasticity- and memory-related signaling molecules in hippocampal area CA1 showed significant down regulation of the basal levels of phosphorylated- and total-CaMKII, phosphorylated- and total-CREB as well as those of BDNF and CaMKIV in sleep deprived rats. All these changes were completely prevented in rats that chronically consumed caffeine. The present findings suggest an important neuroprotective property of caffeine in sleep deprivation.

  16. Caffeine and REM sleep deprivation: Effect on basal levels of signaling molecules in area CA1.

    PubMed

    Alkadhi, Karim A; Alhaider, Ibrahim A

    2016-03-01

    We have investigated the neuroprotective effect of chronic caffeine treatment on basal levels of memory-related signaling molecules in area CA1 of sleep-deprived rats. Animals in the caffeine groups were treated with caffeine in drinking water (0.3g/l) for four weeks before they were REM sleep-deprived for 24h in the Modified Multiple Platforms paradigm. Western blot analysis of basal protein levels of plasticity- and memory-related signaling molecules in hippocampal area CA1 showed significant down regulation of the basal levels of phosphorylated- and total-CaMKII, phosphorylated- and total-CREB as well as those of BDNF and CaMKIV in sleep deprived rats. All these changes were completely prevented in rats that chronically consumed caffeine. The present findings suggest an important neuroprotective property of caffeine in sleep deprivation. PMID:26767416

  17. Repeated REM sleep deprivation after chronic haloperidol administration in the rat.

    PubMed

    Salín-Pascual, R J; García-Ferreiro, R; Moro-López, M L; Blanco-Centurión, C; Drucker-Colín, R

    1997-06-01

    Repeated haloperidol administration produces up-regulation of dopamine (DA) receptors. REM sleep deprivation (REMSD) does also, but in addition, has been shown to produce REM sleep rebound. Should DA receptor up-regulation play a role in REM sleep rebound, haloperidol could conceivably have effects similar to those observed following REMSD. This is the central question investigated in this study. Male Wistar rats were prepared for sleep recordings. They were randomly assigned to the following groups: group 1, REMSD by small platforms (40 h REMSD + 8 h recording); group 2, was the large platform control group (40 h in large platforms + 8 h of recording); group 3, received 2-week daily administration of haloperidol (3 mg/kg, i.p.) plus REMSD (40 h REMSD + 8 h of recording); group 4, 2-week administration of haloperidol (3 mg/kg) without sleep manipulation and at the end 40 h were allowed to elapse, following which 8 h of sleep recordings was carried out. In each group the sleep manipulation and/or sleep recordings were repeated five consecutive times. Repeated REMSD produced increases of REM sleep time after each recovery in group 1. Large platforms did not produce increases of REM sleep during the recovery trials. The 2-week administration of haloperidol plus REMSD prevented REM sleep rebound (group 3). The 2-week administration of haloperidol without sleep manipulation (group 4) produced a REM sleep reduction. Dopamine modulation seems not to be important for REM sleep rebound. Hypersensitivity of DA receptors developed after REMSD may be an epiphenomenon associated with this sleep manipulation, but seems not to participate in REM sleep enhancement after REMSD.

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

    PubMed

    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. PMID:27549340

  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 during late pregnancy produces hyperactivity and increased risk-taking behavior in offspring.

    PubMed

    Radhakrishnan, Arathi; Aswathy, B S; Kumar, Velayudhan Mohan; Gulia, Kamalesh K

    2015-01-30

    Sleep deprivation in women resulting from their modern lifestyle, especially during pregnancy, is a serious concern as it can affect the health of the newborn. Anxiety disorders and cognitive deficits in the offspring are also on the rise. However, experimental studies on the effects of sleep loss during pregnancy, on emotional development and cognitive function of the newborn, are scanty in literature. In the current study, female rats were sleep-deprived for 5h by gentle handling, during the 6 days of the third trimester (days 14-19 of pregnancy). The effects of this sleep deprivation on anxiety-related behaviors of pups during their peri-adolescence age were studied using elevated plus maze (EPM). In addition to body weights of dams and offspring, the maternal behavior was also monitored. The weanlings of sleep-deprived dams showed heightened risk-taking behavior as they made increased explorations into the open arms of EPM. They also showed higher mobility in comparison to the control group. Though the body weights of sleep-deprived dams were comparable to those of the control group, their newborns had lower birth weight. Nevertheless, these pups gained weight and reached the control group values during the initial post-natal week. But after weaning, their rate of growth was lower than that of the control group. This is the first report providing evidences for the role of sleep during late pregnancy in shaping the neuropsychological development in offspring.

  1. 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.

  2. Evaluating the influence of sleep deprivation upon circadian rhythms of exercise metabolism.

    PubMed

    Montelpare, W J; Plyley, M J; Shephard, R J

    1992-06-01

    Cardiorespiratory and gas exchange responses to a moderate, standardized treadmill walking task showed a weak circadian rhythm, with larger superimposed peaks attributable to feeding. However, both rhythms became progressively attenuated during a period of sleep deprivation. A method of exploring this phenomenon is illustrated by an analysis of data on walking heart rate, respiratory minute volume, oxygen intake, and rating of perceived exertion, collected on 11 young men at 3-hr intervals during 60 hours of sleep deprivation.

  3. 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

  4. 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 PMID:26890247

  5. Sleep deprivation in the rat: XVIII. Regional brain levels of monoamines and their metabolites.

    PubMed

    Bergmann, B M; Seiden, L S; Landis, C A; Gilliland, M A; Rechtschaffen, A

    1994-10-01

    Several theories have linked sleep with change in monoamine activity. However, the use of sleep deprivation to show that changes in sleep generate changes in monoamines (directly or through feedback) has produced inconsistent results. To explore whether longer sleep deprivation, better documented sleep loss, more complete controls or regional brain analyses would produce clear sleep loss-induced change, eight rats were subjected to total sleep deprivation (TSD) by the disk-over-water method for 11-20 days and were guillotined along with yoked control (TSC) and home-cage control (HCC) rats. Brains were removed and dissected to obtain the caudate, frontal cortex, hippocampus, hypothalamus, midbrain and hindbrain (pons-medulla). Tissue sections were analyzed for concentrations of serotonin (5HT), its metabolite 5-hydroxyindoleacetic acid (5HIAA), dopamine (DA), its metabolite 3,4-dihydroxyphenylacetic acid (DOPAC), and either norepinephrine or, in the caudate section, the DA metabolite homovanillic acid. The ratios DOPAC/DA and 5HIAA/5HT, which under some conditions are indicators of turnover, were also calculated. Because sleep deprivation time varied across sets of TSD, TSC and HCC rats and not all eight sets were analyzed simultaneously, a repeated-measures ANOVA was performed within sets with HCC, TSC and TSD considered as successive levels of sleep deprivation treatment. In no case did TSD rats have significantly higher or lower values of amines, metabolites or ratios than both HCC and TSC rats. The most common outlying values were for TSC rats. Thus, these results failed to demonstrate sleep loss-induced regional changes in levels of major brain monoamines or their metabolites.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:7531362

  6. Cognitive deterioration and changes of P300 during total sleep deprivation.

    PubMed

    Lee, Heon-Jeong; Kim, Leen; Suh, Kwang-Yoon

    2003-10-01

    The study was conducted to evaluate the cognitive deteriorations induced by sleep deprivation with the computerized neurocognitive tests and the P300 event-related potential. Thirty healthy college students (22 men, eight women) participated in the present study. Subjects remained awake for 38 h under continuous surveillance. In the morning and the evening of the two study days, the computerized neurocognitive tests and the P300 were performed. In vigilance test and reaction unit test, there were significant cognitive impairments during sleep deprivation. However, in the cognitrone test there was significant functional improvement, which might be due to the practice effect. The P300 latency was significantly prolonged and the amplitudes decreased during sleep deprivation. The cognitive impairment during 38 h of sleep deprivation was mainly in terms of vigilance and reaction time. In contrast, higher complex cognitive function such as fine perceptual analyses, visual discrimination and working memory might be not affected by 38 h of total sleep deprivation. The changes of P300 were significantly correlated with the results of vigilance and reaction unit tests but not with the cognitrone test. Taken together, these results suggest that the P300 changes that occur during sleep deprivation are a reflection of the decrement in vigilance, which prolongs reaction time. PMID:12950703

  7. 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.

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

    PubMed Central

    Lee, Seung Hoon; Park, Hong Seok; Kim, Young Sik

    2016-01-01

    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. PMID:27550492

  9. 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. PMID:27550492

  10. Tempol protects sleep-deprivation induced behavioral deficits in aggressive male Long-Evans rats.

    PubMed

    Solanki, Naimesh; Atrooz, Fatin; Asghar, Saman; Salim, Samina

    2016-01-26

    Earlier, we reported that elevated anxiety-like behavior and high aggression in aged retired breeder Long-Evans (L-E) rats was associated with increased plasma corticosterone and elevated oxidative stress levels. In the present study, we examined how this aged aggressive and anxious rat strain responds to acute sleep deprivation (24h) and whether their behaviors can be modulated via antioxidant tempol treatment. Four groups of L-E rats were utilized: naïve control (NC), tempol treated control (T+NC), sleep deprived (SD), tempol treated and sleep deprived (T+SD). Thus, two groups were treated with tempol (1mM in drinking water for 2 weeks) while the other two were not. Two groups were subjected to acute sleep deprivation (24h) using the columns-in-water model while the other two were not. Sleep deprivation induced anxiety-like behavior, led to significant depression-like behavior and short-term memory impairment in SD rats. And, decision-making behavior also was compromised in SD rats. These behavioral and cognitive impairments were prevented with tempol treatment in T+SD rats. Tempol treatment also reduced SD-induced increase in corticosterone and oxidative stress levels in T+SD rats. These results suggest potential involvement of oxidative stress mechanisms in regulation of sleep deprivation induced behavioral and cognitive deficits in male aged-aggressive rats. PMID:26724222

  11. Tempol protects sleep-deprivation induced behavioral deficits in aggressive male Long-Evans rats.

    PubMed

    Solanki, Naimesh; Atrooz, Fatin; Asghar, Saman; Salim, Samina

    2016-01-26

    Earlier, we reported that elevated anxiety-like behavior and high aggression in aged retired breeder Long-Evans (L-E) rats was associated with increased plasma corticosterone and elevated oxidative stress levels. In the present study, we examined how this aged aggressive and anxious rat strain responds to acute sleep deprivation (24h) and whether their behaviors can be modulated via antioxidant tempol treatment. Four groups of L-E rats were utilized: naïve control (NC), tempol treated control (T+NC), sleep deprived (SD), tempol treated and sleep deprived (T+SD). Thus, two groups were treated with tempol (1mM in drinking water for 2 weeks) while the other two were not. Two groups were subjected to acute sleep deprivation (24h) using the columns-in-water model while the other two were not. Sleep deprivation induced anxiety-like behavior, led to significant depression-like behavior and short-term memory impairment in SD rats. And, decision-making behavior also was compromised in SD rats. These behavioral and cognitive impairments were prevented with tempol treatment in T+SD rats. Tempol treatment also reduced SD-induced increase in corticosterone and oxidative stress levels in T+SD rats. These results suggest potential involvement of oxidative stress mechanisms in regulation of sleep deprivation induced behavioral and cognitive deficits in male aged-aggressive rats.

  12. 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

  13. 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

  14. Enhanced brain small-worldness after sleep deprivation: a compensatory effect.

    PubMed

    Liu, Huan; Li, Hong; Wang, Yulin; Lei, Xu

    2014-10-01

    Sleep deprivation has a variable impact on extrinsic activities during multiple cognitive tasks, especially on mood and emotion processing. There is also a trait-like individual vulnerability or compensatory effect in cognition. Previous studies have elucidated the altered functional connectivity after sleep deprivation. However, it remains unclear whether the small-world properties of resting-state network are sensitive to sleep deprivation. A small-world network is a type of graph that combines a high local connectivity as well as a few long-range connections, which ensures a higher information-processing efficiency at a low cost. The complex network of the brain can be described as a small-world network, in which a node is a brain region and an edge is present when there is a functional correlation between two nodes. Here, we investigated the topological properties of the human brain networks of 22 healthy subjects under sufficient sleep and sleep-deprived conditions. Specifically, small-worldness is utilized to quantify the small-world property, by comparing the clustering coefficient and path length of a given network to an equivalent random network with same degree distribution. After sufficient sleep, the brain networks showed the property of small-worldness. Compared with the resting state under sufficient sleep, the small-world property was significantly enhanced in the sleep deprivation condition, suggesting a possible compensatory adaptation of the human brain. Specifically, the altered measurements were correlated with the neuroticism of subjects, indicating that individuals with low-levels of neuroticism are more resilient to sleep deprivation.

  15. The beneficial effects of regular exercise on cognition in REM sleep deprivation: behavioral, electrophysiological and molecular evidence.

    PubMed

    Zagaar, Munder; Alhaider, Ibrahim; Dao, An; Levine, Amber; Alkarawi, Ahmed; Alzubaidy, Mariam; Alkadhi, Karim

    2012-03-01

    Inadequate sleep is prevalent in modern societies and is known to profoundly impair cognitive function. We examined the impact of 4 weeks of regular treadmill exercise on sleep deprivation induced spatial learning and memory, synaptic plasticity and related signaling molecules in area CA1 of the rat hippocampus. Rats were exercised on a treadmill and subsequently sleep-deprived for 24h using the modified multiple platform technique. Testing of learning and short-term memory performance in the radial arm water maze showed that although sedentary sleep deprived rats were severely impaired, exercised sleep deprived rats' performance was normal. Extracellular recording from area CA1 of anesthetized rats revealed that early phase LTP (E-LTP) was markedly impaired in the sedentary sleep deprived animals, but was normal in the exercised sleep deprived group. Additionally, immunoblot analysis of CA1 area before (basal) and after expression of E-LTP indicated that the significant down-regulation of the brain derived neurotrophic factor (BDNF) and phosphorylated calcium-calmodulin dependent protein kinase II (P-CaMKII) levels in sleep deprived animals was prevented by the regular exercise regimen. The results suggest that the regular exercise protocol prevents the sleep deprivation induced impairments in short-term memory and E-LTP by preventing deleterious changes in the basal and post-stimulation levels of P-CaMKII and BDNF associated with sleep deprivation.

  16. Sleep Deprivation and Divergent Toll-like Receptor-4 Activation of Cellular Inflammation in Aging

    PubMed Central

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

    2015-01-01

    Objectives: 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. Design, Setting, and Participants: 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. Measurement and Results: 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). Conclusion: 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. Citation: Carroll JE, Carrillo C, Olmstead R, Witarama T, Breen EC, Yokomizo M, Seeman TE, Irwin MR. Sleep deprivation and divergent toll-like receptor-4 activation of cellular inflammation in aging. SLEEP

  17. 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

  18. 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

  19. REM sleep deprivation reduces auditory evoked inhibition of dorsolateral pontine neurons.

    PubMed

    Mallick, B N; Fahringer, H M; Wu, M F; Siegel, J M

    1991-06-28

    In many dorsolateral pontine neurons, auditory stimulation produces an initial excitation followed by a sustained inhibition. We now report that rapid eye movement (REM) sleep deprivation, for periods of from 22-48 h, reduced this auditory evoked inhibition of unit discharge. Inhibition returned to baseline levels after recovery REM sleep. Prior work indicates that the auditory evoked inhibition seen in noradrenergic cells in this region is partially mediated by norepinephrine. We hypothesize that the reduction in inhibition that we see is a consequence of either downregulation/desensitization of norepinephrine receptors or reduced norepinephrine release resulting from REM sleep deprivation. PMID:1913194

  20. Sleep deprivation induces changes in immunity in Trichinella spiralis-infected rats.

    PubMed

    Ibarra-Coronado, Elizabeth G; Velazquéz-Moctezuma, Javier; Diaz, Daniel; Becerril-Villanueva, Luis Enrique; Pavón, Lenin; Morales-Montor, Jorge

    2015-01-01

    Sleep is considered an important predictor of immunity. A lack of sleep may reduce immunity, which increases susceptibility to any type of infection. Moreover, sleep deprivation in humans produces changes in both, the percent of circulating immune cells (T cells and NK cells) and cytokine levels (IL-1, IFNγ, TNΦ-αα, IL-6 and IL-17). The aim of our study was to investigate whether sleep deprivation produces deregulation on immune variables during the immune response generated against the helminth parasite Trichinella spiralis. Because sleep deprivation is stressful per se, we designed another experiments to compared stress alone (consisting in movement restriction and single housing) with sleep deprivation, in both control (uninfected) and experimental (infected) rats. Our results demonstrate that the sleep deprivation and stress have a differential effect in mesenteric lymph nodes (MLN) and spleen. In uninfected rats sleep deprivation alone produces an increase in natural killer cells (NK+) and B cells (CD45+), accompanied by a decrease in cytotoxic T cells (CD3+CD8+) in spleen; while, in MLN, produces only an increase in natural killer cells (NK+). Both, SD and stress, produce an increased percentage of total T cells (CD3+) in spleen. In the MLN both are also associated to an increase in cytotoxic T cells (CD3+CD8+) and B cells (CD45+). In the spleens of parasitized rats, cell populations did not change. In spleens of both, sleep-deprived and stressed infected rats, we observed an increase in B cells (CD45+). In infected rats, sleep deprivation alone produced an increase in NK cells (NK+). In mesenteric node cell populations of parasitized rats, we observed a decrease in NK cells and an increase in T helper (CD4+) cells in both SD and stressed rats. Rats that were only subjected to stress showed a decrease in B cells (CD45+). These findings suggest that the immune response generated against infection caused by T. spiralis is affected when the sleep pattern is

  1. Sleep Deprivation Induces Changes in Immunity in Trichinella spiralis-Infected Rats

    PubMed Central

    Ibarra-Coronado, Elizabeth G.; Velazquéz-Moctezuma, Javier; Diaz, Daniel; Becerril-Villanueva, Luis Enrique; Pavón, Lenin; Morales-Montor, Jorge

    2015-01-01

    Sleep is considered an important predictor of immunity. A lack of sleep may reduce immunity, which increases susceptibility to any type of infection. Moreover, sleep deprivation in humans produces changes in both, the percent of circulating immune cells (T cells and NK cells) and cytokine levels (IL-1, IFNγ, TNΦ-αα, IL-6 and IL-17). The aim of our study was to investigate whether sleep deprivation produces deregulation on immune variables during the immune response generated against the helminth parasite Trichinella spiralis. Because sleep deprivation is stressful per se, we designed another experiments to compared stress alone (consisting in movement restriction and single housing) with sleep deprivation, in both control (uninfected) and experimental (infected) rats. Our results demonstrate that the sleep deprivation and stress have a differential effect in mesenteric lymph nodes (MLN) and spleen. In uninfected rats sleep deprivation alone produces an increase in natural killer cells (NK+) and B cells (CD45+), accompanied by a decrease in cytotoxic T cells (CD3+CD8+) in spleen; while, in MLN, produces only an increase in natural killer cells (NK+). Both, SD and stress, produce an increased percentage of total T cells (CD3+) in spleen. In the MLN both are also associated to an increase in cytotoxic T cells (CD3+CD8+) and B cells (CD45+). In the spleens of parasitized rats, cell populations did not change. In spleens of both, sleep-deprived and stressed infected rats, we observed an increase in B cells (CD45+). In infected rats, sleep deprivation alone produced an increase in NK cells (NK+). In mesenteric node cell populations of parasitized rats, we observed a decrease in NK cells and an increase in T helper (CD4+) cells in both SD and stressed rats. Rats that were only subjected to stress showed a decrease in B cells (CD45+). These findings suggest that the immune response generated against infection caused by T. spiralis is affected when the sleep pattern is

  2. 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.

  3. Sleep and Metabolism: An Overview

    PubMed Central

    Sharma, Sunil; Kavuru, Mani

    2010-01-01

    Sleep and its disorders are increasingly becoming important in our sleep deprived society. Sleep is intricately connected to various hormonal and metabolic processes in the body and is important in maintaining metabolic homeostasis. Research shows that sleep deprivation and sleep disorders may have profound metabolic and cardiovascular implications. Sleep deprivation, sleep disordered breathing, and circadian misalignment are believed to cause metabolic dysregulation through myriad pathways involving sympathetic overstimulation, hormonal imbalance, and subclinical inflammation. This paper reviews sleep and metabolism, and how sleep deprivation and sleep disorders may be altering human metabolism. PMID:20811596

  4. REM sleep deprivation of rats induces acute phase response in liver.

    PubMed

    Pandey, Atul Kumar; Kar, Santosh Kumar

    2011-07-01

    REM sleep is essential for maintenance of body physiology and its deprivation is fatal. We observed that the levels of ALT and AST enzymes and pro-inflammatory cytokines like IL-1 β, IL-6 and IL-12 circulating in the blood of REM sleep deprived rats increased in proportion to the extent of sleep loss. But in contrast the levels of IFN-γ and a ∼200 kDa protein, identified by N-terminal sequencing to be alpha-1-inhibitor-3(A1I3), decreased significantly. Quantitative PCR analysis confirmed that REM sleep deprivation down regulates AII3 gene and up regulates IL1 β, IL6 and their respective receptors gene expression in the liver initiating its inflammation.

  5. Sleep Deprivation Is Associated with Bicycle Accidents and Slip and Fall Injuries in Korean Adolescents

    PubMed Central

    Kim, So Young; Sim, Songyong; Kim, Sung-Gyun; Choi, Hyo Geun

    2015-01-01

    Objective This study sought to evaluate associations between sleep time and bicycle accidents, falls under various circumstances, and dental injuries in adolescents. Methods A total of 61,696 participants ranging from 12 to 18 years of age who completed the Korea Youth Risk Behavior Web-based Survey (KYRBWS) in 2013 were enrolled in this study. Bicycle riding accidents were analyzed for 17,232 bicycle-riding participants. Data were collected regarding the weekday sleep duration for the most recent 7 days, which was categorized as < 5.5 h, 5.5–6.5 h, 6.5–7.5 h, or ≥ 7.5 h per day, and the incidence of bicycle accidents, slips and falls under various circumstances, and dental injuries in the most recent 12 months. Adjusted odds ratios (aORs) were calculated among sleep groups for bicycle accidents, slips and falls, and dental injuries using simple and multiple logistic regression analyses with complex sampling. Results Bicycle riding accidents and slips and falls in classrooms, corridors, the ground, toilets, stairs, and other unspecified situations showed positive correlations with sleep deprivation. Comparisons of groups with ≥ 7.5 h sleep, < 5.5 h, 5.5–6.5 h sleep, and 6.5–7.5 h sleep revealed increased associations with slips and falls under various circumstances. In particular, the aORs were higher in the groups with less sleep (aOR of the 5.5 h group > the 5.5–6.5 h group > the 6.5–7.5 h group). There was no significant relationship between sleep deprivation and dental injury. Conclusions This study demonstrated that sleep deprivation among Korean adolescents was associated with bicycle accidents and falls at home and school. Thus, adequate sleep may be needed to prevent accidents and falls. PMID:26280345

  6. The Association of Sleep Deprivation on the Occurrence of Errors by Nurses Who Work the Night Shift

    PubMed Central

    RAMADAN, MOHAMED ZAKI; AL-SALEH, KHALID SAAD

    2014-01-01

    Purpose: To determine the influence of sleep deprivation on the occurrence of errors by registered nurses working in night shift in intensive care departments. Methods: The study utilized a multi-part questionnaire which included items about demographic characteristics, reported medical errors, and Pittsburgh Sleep Quality Index (PSQI) 300 questionnaires were distributed to registered nurses working in intensive care departments. 138 of the 153 (51% response rate) collected questionnaires were analyzed using correlation and stepwise logistic multiple regression. Results: Registered nurses who were sleep deprived had worse sleep quality in terms of high PSQI than those who were not. None of the demographic variables was statistically significant, not providing evidence that these variables may explain odds for being sleep deprived in the population. Conclusions: Work schedule changes, offering shorter periods of time on night shift and less working hours in the week may lead to better sleep quality and less sleep deprivation. PMID:25729589

  7. Dopaminergic augmentation of sleep deprivation effects in bipolar depression.

    PubMed

    Benedetti, F; Campori, E; Barbini, B; Fulgosi, M C; Colombo, C

    2001-11-30

    Total sleep deprivation (TSD) has been used in association with lithium salts and with serotonergic and noradrenergic antidepressants, leading to sustained improvements in patients affected by major depression. Current theories on the neurobiological mechanism of action of TSD propose a major role for enhanced dopamine activity. To test the clinical relevance of dopaminergic enhancement in TSD, we treated a homogeneous sample of 28 bipolar depressed patients with three cycles of TSD combined with placebo or with the dopaminergic antidepressant amineptine. Changes in mood over time were rated with self-administered visual analogue scales and with the Montgomery-Asberg Depression Rating Scale. Patients showed improved mean daily-mood scores after TSD, an effect that was highest at the first cycle and decreased with treatment repetition. Amineptine enhanced the effects of TSD on perceived mood during the first two TSD cycles, but patients in the placebo and amineptine groups showed comparable results at the end of the treatment. Despite its theoretical importance, the clinical usefulness of combining TSD with a dopaminergic agent must be questioned.

  8. 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

  9. Performance monitoring following total sleep deprivation: effects of task type and error rate.

    PubMed

    Renn, Ryan P; Cote, Kimberly A

    2013-04-01

    There is a need to understand the neural basis of performance deficits that result from sleep deprivation. Performance monitoring tasks generate response-locked event-related potentials (ERPs), generated from the anterior cingulate cortex (ACC) located in the medial surface of the frontal lobe that reflect error processing. The outcome of previous research on performance monitoring during sleepiness has been mixed. The purpose of this study was to evaluate performance monitoring in a controlled study of experimental sleep deprivation using a traditional Flanker task, and to broaden this examination using a response inhibition task. Forty-nine young adults (24 male) were randomly assigned to a total sleep deprivation or rested control group. The sleep deprivation group was slower on the Flanker task and less accurate on a Go/NoGo task compared to controls. General attentional impairments were evident in stimulus-locked ERPs for the sleep deprived group: P300 was delayed on Flanker trials and smaller to Go-stimuli. Further, N2 was smaller to NoGo stimuli, and the response-locked ERN was smaller on both tasks, reflecting neurocognitive impairment during performance monitoring. In the Flanker task, higher error rate was associated with smaller ERN amplitudes for both groups. Examination of ERN amplitude over time showed that it attenuated in the rested control group as error rate increased, but such habituation was not apparent in the sleep deprived group. Poor performing sleep deprived individuals had a larger Pe response than controls, possibly indicating perseveration of errors. These data provide insight into the neural underpinnings of performance failure during sleepiness and have implications for workplace and driving safety.

  10. Failure to find executive function deficits following one night's total sleep deprivation in university students under naturalistic conditions.

    PubMed

    Pace-Schott, Edward F; Hutcherson, Cendri A; Bemporad, Brenda; Morgan, Alexandra; Kumar, Arjun; Hobson, J Allan; Stickgold, Robert

    2009-01-01

    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, multitask 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, participants sleep deprived 35 to 39 hr showed few performance deficits among tests in this battery when compared with non-sleep-deprived controls. Sleep-deprived participants 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

  11. REM sleep deprivation attenuates actin-binding protein cortactin: a link between sleep and hippocampal plasticity.

    PubMed

    Davis, Christopher J; Meighan, Peter C; Taishi, Ping; Krueger, James M; Harding, Joseph W; Wright, John W

    2006-06-12

    Rapid eye-movement sleep (REMS) is thought to affect synaptic plasticity. Cortactin is a cytoskeletal protein critically involved in the regulation of actin branching and stabilization including the actin backbone of dendritic spines. Hippocampal cortactin levels, phosphorylation, and processing appear to be altered during learning and long-term potentiation (LTP); consistent with a role for cortactin in the dendritic restructuring that accompanies synaptic plasticity. In this study juvenile male Sprague-Dawley rats were selectively REMS-deprived (RD) for 48 h by the flowerpot method. Cage control (CC) and large pedestal control (PC) animals were used for comparison. Animals were euthanized immediately, or 12 h, after removal from the pedestal. The hippocampus was dissected, flash-frozen, and stored for subsequent Western blot or quantitative RT-PCR analysis of cortactin. Cortactin mRNA/cDNA levels initially rose in PC and RD rats but returned to CC levels by 12 h after removal from the pedestal. Predictably cortactin protein levels were initially unchanged but were up-regulated after 12 h. The PC group had more total and tyrosine-phosphorylated cortactin protein expression than the RD and CC groups. This increase in cortactin was likely due to the exposure of the rats to the novel environment of the deprivation chambers thus triggering plasticity events. The lack of REMS, however, severely hampered cortactin protein up-regulation and phosphorylation observed in the PC group suggesting an attenuation of plasticity-related events. Thus, these data support a functional link between REMS and cytoskeletal reorganization in the hippocampus, a process that is essential for synaptic plasticity.

  12. 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

  13. Effects of rapid eye movement sleep deprivation on fear extinction recall and prediction error signaling.

    PubMed

    Spoormaker, Victor I; Schröter, Manuel S; Andrade, Kátia C; Dresler, Martin; Kiem, Sara A; Goya-Maldonado, Roberto; Wetter, Thomas C; Holsboer, Florian; Sämann, Philipp G; Czisch, Michael

    2012-10-01

    In a temporal difference learning approach of classical conditioning, a theoretical error signal shifts from outcome deliverance to the onset of the conditioned stimulus. Omission of an expected outcome results in a negative prediction error signal, which is the initial step towards successful extinction and may therefore be relevant for fear extinction recall. As studies in rodents have observed a bidirectional relationship between fear extinction and rapid eye movement (REM) sleep, we aimed to test the hypothesis that REM sleep deprivation impairs recall of fear extinction through prediction error signaling in humans. In a three-day design with polysomnographically controlled REM sleep deprivation, 18 young, healthy subjects performed a fear conditioning, extinction and recall of extinction task with visual stimuli, and mild electrical shocks during combined functional magnetic resonance imaging (fMRI) and skin conductance response (SCR) measurements. Compared to the control group, the REM sleep deprivation group had increased SCR scores to a previously extinguished stimulus at early recall of extinction trials, which was associated with an altered fMRI time-course in the left middle temporal gyrus. Post-hoc contrasts corrected for measures of NREM sleep variability also revealed between-group differences primarily in the temporal lobe. Our results demonstrate altered prediction error signaling during recall of fear extinction after REM sleep deprivation, which may further our understanding of anxiety disorders in which disturbed sleep and impaired fear extinction learning coincide. Moreover, our findings are indicative of REM sleep related plasticity in regions that also show an increase in activity during REM sleep.

  14. Sleep deprivation does not affect neuronal susceptibility to mild traumatic brain injury in the rat

    PubMed Central

    Caron, Aimee M; Stephenson, Richard

    2015-01-01

    Mild and moderate traumatic brain injuries (TBIs) (and concussion) occur frequently as a result of falls, automobile accidents, and sporting activities, and are a major cause of acute and chronic disability. Fatigue and excessive sleepiness are associated with increased risk of accidents, but it is unknown whether prior sleep debt also affects the pathophysiological outcome of concussive injury. Using the “dark neuron” (DN) as a marker of reversible neuronal damage, we tested the hypothesis that acute (48 hours) total sleep deprivation (TSD) and chronic sleep restriction (CSR; 10 days, 6-hour sleep/day) affect DN formation following mild TBI in the rat. TSD and CSR were administered using a walking wheel apparatus. Mild TBI was administered under anesthesia using a weight-drop impact model, and the acute neuronal response was observed without recovery. DNs were detected using standard bright-field microscopy with toluidine blue stain following appropriate tissue fixation. DN density was low under home cage and sleep deprivation control conditions (respective median DN densities, 0.14% and 0.22% of neurons), and this was unaffected by TSD alone (0.1%). Mild TBI caused significantly higher DN densities (0.76%), and this was unchanged by preexisting acute or chronic sleep debt (TSD, 0.23%; CSR, 0.7%). Thus, although sleep debt may be predicted to increase the incidence of concussive injury, the present data suggest that sleep debt does not exacerbate the resulting neuronal damage. PMID:26124685

  15. Sleep deprivation does not affect neuronal susceptibility to mild traumatic brain injury in the rat.

    PubMed

    Caron, Aimee M; Stephenson, Richard

    2015-01-01

    Mild and moderate traumatic brain injuries (TBIs) (and concussion) occur frequently as a result of falls, automobile accidents, and sporting activities, and are a major cause of acute and chronic disability. Fatigue and excessive sleepiness are associated with increased risk of accidents, but it is unknown whether prior sleep debt also affects the pathophysiological outcome of concussive injury. Using the "dark neuron" (DN) as a marker of reversible neuronal damage, we tested the hypothesis that acute (48 hours) total sleep deprivation (TSD) and chronic sleep restriction (CSR; 10 days, 6-hour sleep/day) affect DN formation following mild TBI in the rat. TSD and CSR were administered using a walking wheel apparatus. Mild TBI was administered under anesthesia using a weight-drop impact model, and the acute neuronal response was observed without recovery. DNs were detected using standard bright-field microscopy with toluidine blue stain following appropriate tissue fixation. DN density was low under home cage and sleep deprivation control conditions (respective median DN densities, 0.14% and 0.22% of neurons), and this was unaffected by TSD alone (0.1%). Mild TBI caused significantly higher DN densities (0.76%), and this was unchanged by preexisting acute or chronic sleep debt (TSD, 0.23%; CSR, 0.7%). Thus, although sleep debt may be predicted to increase the incidence of concussive injury, the present data suggest that sleep debt does not exacerbate the resulting neuronal damage. PMID:26124685

  16. Exploring association between sleep deprivation and chronic periodontitis: A pilot study

    PubMed Central

    Grover, Vishakha; Malhotra, Ranjan; Kaur, Harleen

    2015-01-01

    Background: Sleep deprivation has become a global phenomenon, and epidemiologic data indicate that short sleep duration adversely impacts human physical health. Underlying mechanisms involve modulation of immune-inflammatory mechanisms. These changes might contribute to potentiation of destructive periodontal disease. Therefore, the present study aimed to assess if there is an association of sleep deprivation with chronic periodontal diseases. Materials and Methods: Sixty subjects were categorized into 3 groups (n = 20 each) viz. clinically healthy, gingivitis and periodontitis. Periodontal status of subjects was assessed by gingival index and pocket probing depth. All the study subjects were administered Pittsburgh Sleep Quality Index (PSQI) questionnaire for the assessment of sleep deprivation. Results: Present investigation revealed that mean PSQI was highest in the periodontitis group as compared to other two groups and the difference among three groups was statistically significant. Conclusion: The present study with preliminary results suggestive of the association of sleep deprivation with severity of periodontal disease, definitely calls on for future studies with larger samples. PMID:26229272

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

    PubMed Central

    Dixit, Abhinav; Mittal, Tushar

    2015-01-01

    Background: 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. Materials and Methods: 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. Results: 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. Conclusion: 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

  18. 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

  19. Impact of total sleep deprivation on behavioural neural processing of emotionally expressive faces.

    PubMed

    Cote, K A; Mondloch, C J; Sergeeva, V; Taylor, M; Semplonius, T

    2014-05-01

    Sleep deprivation impacts subjective mood states, but very little research has examined the impact on processing emotional information. In the current study, we investigated the impact of total sleep deprivation on neural responses to emotional facial expressions as well as the accuracy and speed with which these faces were categorized. Forty-nine participants completed two tasks in which they were asked to categorize emotional facial expressions as Happy, Sad, Angry, or Fearful. They were shown the 'full' expression of the emotions in one task and more subtle expressions in a second task in which expressions were 'morphed' with neutral faces so that the intensity of emotion varied. It was expected that sleep deprivation would lead to greater reactivity (indexed by larger amplitude N170 event-related potentials), particularly for negative and more subtle facial expressions. In the full face task, sleep-deprived (SD) participants were significantly less accurate than controls (C) at identifying Sad faces and slower to identify all emotional expressions. P1 was smaller and N170 was larger for the SD compared to C group, but for all emotions, indicating generalized impairment in low-level visual processing. In the more difficult morphed face task, SD participants were less accurate than C participants for Sad faces; as well, the group difference in reaction time was greatest for Sad faces. For the SD group, N170 increased in amplitude with increasing perceptual difficulty for the Fearful and Angry faces, but decreased in amplitude with increasing difficulty for Sad faces. These data illustrate that sleep deprivation led to greater neural reactivity for the threat-related negative emotions as they became more subtle; however, there was a failure to engage these perceptual resources for the processing of Sad faces. Sleep loss preferentially impacted the processing of Sad faces; this has widespread implications for sleep-deprived groups.

  20. Exercise improves learning and memory impairments in sleep deprived female rats.

    PubMed

    Saadati, Hakimeh; Esmaeili-Mahani, Saeed; Esmaeilpour, Khadije; Nazeri, Masoud; Mazhari, Shahrzad; Sheibani, Vahid

    2015-01-01

    Inadequate sleep is a common problem in modern societies. It has been previously shown that female rats are more vulnerable to the deleterious effects of sleep deprivation on cognitive functions. Physical exercise has been suggested to attenuate the cognitive impairments induced by sleep deprivation in male rats. The objective of the current study was to investigate the effects of physical exercise on cognitive functions of female rats following paradoxical sleep deprivation. Intact and ovariectomized (OVX) female Wistar rats were used in the present study. The exercise protocol was 4 weeks of treadmill running. The multiple platform method was applied for the induction of 72h paradoxical sleep deprivation and the cognitive function was evaluated using Morris water maze (MWM). Plasma corticosterone level was evaluated in separate groups of study. ANOVA and repeated measures were used to analyze the data and P<0.05 was considered statistically significant. Throughout the investigation, significant learning impairment was observed in sleep-deprived OVX rats compared to the intact and the other OVX groups. Short term memory impairment was observed in both sleep-deprived OVX and intact groups. Physical exercise alleviated the PSD-induced learning and memory impairments in both intact and OVX groups. Corticosterone levels were not statistically significant among the different groups. The results of our study confirmed the negative effects of PSD on cognitive functions in female rats and regular physical exercise seems to protect rats from these effects. Further studies are suggested to be carried out in order to evaluate the possible underlying mechanisms, and also to evaluate the possible interactions between sex hormones and PSD-induced cognitive impairments.

  1. Exploring the effect of vitamin C on sleep deprivation induced memory impairment.

    PubMed

    Mhaidat, Nizar M; Alzoubi, Karem H; Khabour, Omar F; Tashtoush, Noor H; Banihani, Saleem A; Abdul-razzak, Khalid K

    2015-04-01

    In the current study, the possible beneficial effect of vitamin C (VitC) against sleep deprivation induced memory impairment was examined. Chronic sleep deprivation was induced via placing rats in a modified multiple platform apparatus for 8h/day for a period of 6 weeks. Concomitantly, VitC was administered to animals at doses of 150 and 500 mg/kg/day. After 6 weeks of treatment, the radial arm water maze (RAWM) was used to test for spatial learning and memory performance. Moreover, the hippocampus was dissected; and levels/activities of antioxidant defense biomarkers glutathione reduced (GSH), glutathione oxidized (GSSG), GSH/GSSG ratio, catalase, superoxide dismutase (SOD), and thiobarbituric acid reactive substances (TBARS), were evaluated. Results revealed that chronic sleep deprivation impaired short- and long-term memories (P<0.05). This impairment was prevented by chronic VitC treatments. In addition, VitC normalized sleep deprivation induced decreases in hippocamppal GSH/GSSG ratio (P<0.05), and activities of catalase, and SOD, and increase in GSSG levels (P<0.05). Collectively, spatial memory impairment was induced by chronic sleep deprivation, and VitC treatment prevented such impairment. This was possibly achieved via normalizing antioxidant defense mechanisms of the hippocampus.

  2. Predictive visual tracking: specificity in mild traumatic brain injury and sleep deprivation.

    PubMed

    Maruta, Jun; Heaton, Kristin J; Maule, Alexis L; Ghajar, Jamshid

    2014-06-01

    We tested whether reduced cognitive function associated with mild traumatic brain injury (mTBI) and sleep deprivation can be detected and distinguished using indices of predictive visual tracking. A circular visual tracking test was given to 13 patients with acute mTBI (recruited within 2 weeks of injury), 127 normal control subjects, and 43 healthy subjects who were fatigued by 26-hour sleep deprivation. Eye movement was monitored with video-oculography. In the mTBI-related portion of the study, visual tracking performance of acute mTBI patients was significantly worse than normal subjects (p < 0.001). In the sleep-deprivation-related portion of the study, no change was detected between the two baseline measures separated by 2 to 3 weeks, but the 26-hour sleep deprivation significantly degraded the visual tracking performance (p < 0.001). The mTBI subjects had substantially worse visual tracking than sleep-deprived subjects that could also be identified with different visual tracking indices, indicating possible different neurophysiological mechanisms. Results suggest that cognitive impairment associated with mTBI and fatigue may be triaged with the aid of visual tracking measures.

  3. Prior regular exercise prevents synaptic plasticity impairment in sleep deprived female rats.

    PubMed

    Saadati, Hakimeh; Sheibani, Vahid; Esmaeili-Mahani, Saeed; Hajali, Vahid; Mazhari, Shahrzad

    2014-09-01

    Previous studies have indicated that physical exercise plays a preventive role in synaptic plasticity deficits in the hippocampus of sleep-deprived male rats. The objective of the present study was to evaluate the effects of treadmill running on early long term potentiation (E-LTP) at the Cornu Ammonis (CA1) area of the hippocampus in sleep-deprived female rats. Intact and ovariectomiezed (OVX) female Wistar rats were used in the present study. The exercise protocol was four weeks treadmill running and the multiple platform method was applied to induce 72 h sleep deprivation (SD). We examine the effect of exercise and/or SD on synaptic plasticity using in vivo extracellular recording in the CA1 area of the hippocampus. The field excitatory post-synaptic potential (fEPSP) slope was measured before and 2h after high frequency stimulation (HFS) in the experimental groups. Field potential recording indicated that the induction and maintenance phase of E-LTP impaired in the sleep deprived animals compared to the other groups. After 72 h SD, E-LTP impairments were prevented by 4 weeks of regular treadmill exercise. In conclusion, the synaptic plasticity deficit in sleep-deprived female rats was improved by regular physical exercise. Further studies are suggested to evaluate the possible underlying mechanisms.

  4. 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.

  5. Sleep deprivation and oxidative stress in animal models: a systematic review.

    PubMed

    Villafuerte, Gabriel; Miguel-Puga, Adán; Rodríguez, Eric Murillo; 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

  6. Sleep deprivation and oxidative stress in animal models: a systematic review.

    PubMed

    Villafuerte, Gabriel; Miguel-Puga, Adán; Rodríguez, Eric Murillo; 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.

  7. 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

  8. Rhythms of ghrelin, leptin, and sleep in rats: effects of the normal diurnal cycle, restricted feeding, and sleep deprivation.

    PubMed

    Bodosi, B; Gardi, J; Hajdu, I; Szentirmai, E; Obal, F; Krueger, J M

    2004-11-01

    To determine the relationships among plasma ghrelin and leptin concentrations and hypothalamic ghrelin contents, and sleep, cortical brain temperature (Tcrt), and feeding, we determined these parameters in rats in three experimental conditions: in free-feeding rats with normal diurnal rhythms, in rats with feeding restricted to the 12-h light period (RF), and in rats subjected to 5-h of sleep deprivation (SD) at the beginning of the light cycle. Plasma ghrelin and leptin displayed diurnal rhythms with the ghrelin peak preceding and the leptin peak following the major daily feeding peak in hour 1 after dark onset. RF reversed the diurnal rhythm of these hormones and the rhythm of rapid-eye-movement sleep (REMS) and significantly altered the rhythm of Tcrt. In contrast, the duration and intensity of non-REMS (NREMS) were hardly responsive to RF. SD failed to change leptin concentrations, but it promptly stimulated plasma ghrelin and induced eating. SD elicited biphasic variations in the hypothalamic ghrelin contents. SD increased plasma corticosterone, but corticosterone did not seem to influence either leptin or ghrelin. The results suggest a strong relationship between feeding and the diurnal rhythm of leptin and that feeding also fundamentally modulates the diurnal rhythm of ghrelin. The variations in hypothalamic ghrelin contents might be associated with sleep-wake activity in rats, but, unlike the previous observations in humans, obvious links could not be detected between sleep and the diurnal rhythms of plasma concentrations of either ghrelin or leptin in the rat. PMID:15475503

  9. Acute sleep deprivation: the effects of the AMPAKINE compound CX717 on human cognitive performance, alertness and recovery sleep.

    PubMed

    Boyle, Julia; Stanley, Neil; James, Lynette M; Wright, Nicola; Johnsen, Sigurd; Arbon, Emma L; Dijk, Derk-Jan

    2012-08-01

    AMPA receptor modulation is a potential novel approach to enhance cognitive performance. CX717 is a positive allosteric modulator of the AMPA receptor that has shown efficacy in rodent and primate cognition models. CX717 (100 mg, 300 mg and 1000 mg) and placebo were studied in 16 healthy male volunteers (18-45 years) in a randomized, crossover study. Cognitive function, arousal and recovery sleep (by polysomnography) were assessed during the extended wakefulness protocol. Placebo condition was associated with significant decrements in cognition, particularly at the circadian nadir (between 03:00 and 05:00). Pre-specified primary and secondary analyses (general linear mixed modelling, GLMM) at each separate time point did not reveal consistent improvements in performance or objective alertness with any dose of CX717. Exploratory repeated measures analysis, a method used to take into account the influence of individual differences, demonstrated an improvement in attention-based task performance following the 1000 mg dose. Analysis of the recovery sleep showed that CX717 1000 mg significantly reduced stage 4 and slow-wave sleep (p ≤ 0.05) with evidence of reduced electroencephalogram (EEG) slow-wave and spindle activity. The study suggests that CX717 only at the 1000 mg dose may counteract effects of sleep deprivation on attention-based tasks and that it may interfere with subsequent recovery sleep.

  10. Effects of sleep deprivation on autonomic and endocrine functions throughout the day and on exercise tolerance in the evening.

    PubMed

    Konishi, Masayuki; Takahashi, Masaki; Endo, Naoya; Numao, Shigeharu; Takagi, Shun; Miyashita, Masashi; Midorikawa, Taishi; Suzuki, Katsuhiko; Sakamoto, Shizuo

    2013-01-01

    The aim of this study was to investigate the effects of sleep deprivation on autonomic and endocrine functions during the day and on exercise tolerance in the evening. Ten healthy young males completed two, 2-day control and sleep deprivation trials. For the control trial, participants were allowed normal sleep from 23:00 to 07:00 h. For the sleep deprivation trial, participants did not sleep for 34 h. Autonomic activity was measured from 19:00 h on day 1 to 16:00 h on day 2 by frequency-domain measures of heart rate variability. Endocrine function was examined by measuring adrenocorticotropic hormone and cortisol from venous blood samples collected on day 2 at 09:00, 13:00, and 17:00 h and immediately after an exercise tolerance testing. Autonomic regulation, particularly parasympathetic regulation estimated from the high-frequency component of heart rate variability analysis, was significantly higher in the sleep deprivation trial than in the control trial in the morning and afternoon of day 2. Plasma adrenocorticotropic hormone concentrations were significantly higher at 09:00 and 13:00 h of day 2 under sleep deprivation. Heart rate during exercise was significantly lower following sleep deprivation. Therefore, the effects of sleep deprivation on autonomic regulation depend on the time of the day.

  11. 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.

  12. Stress hormones, sleep deprivation and cognition in older adults.

    PubMed

    Maggio, Marcello; Colizzi, Elena; Fisichella, Alberto; Valenti, Giorgio; Ceresini, Graziano; Dall'Aglio, Elisabetta; Ruffini, Livia; Lauretani, Fulvio; Parrino, Liborio; Ceda, Gian Paolo

    2013-09-01

    Cognition can be deteriorated in older persons because of several potential mechanisms including the hormonal changes occurring with age. Stress events cause modification in hormonal balance with acute and chronic changes such as increase in cortisol and thyroid hormones, and simultaneous alterations in dehydroepiandrosterone sulphate, testosterone and insulin like growth factor-1 levels. The ability to cope with stress and regain previous healthy status, also called resiliency, is particularly impaired in older persons Thus, stressful conditions and hormonal dysregulation might concur to the onset of cognitive impairment in this population. In this review we address the relationship between stress hormones and cognitive function in older persons focusing on the role of one of the main stress factors, such as sleep deprivation (SD). We extracted and cross-checked data from 2000 to 2013 March and selected 112 full-text articles assessed for eligibility. In particular we considered 68 studies regarding the contribution of hormonal pathway to cognition in older adults, and 44 regarding hormones and SD both in rats and humans. We investigated how the activation of a stress-pattern response, like the one evoked from SD, can influence cognitive development and worsen cognitive status in the elderly. We will show the limited number of studies targeting the effects of SD and the consequent changes in stress hormones on cognitive function in this age group. We conclude that the current literature is not strong enough to give definitive answers on the role of stress hormonal pathway to the development of cognitive impairment in older individuals.

  13. Sleep Deprivation Accelerates Delay-Related Loss of Visual Short-Term Memories Without Affecting Precision

    PubMed Central

    Wee, Natalie; Asplund, Christopher L.; Chee, Michael W. L.

    2013-01-01

    Study Objectives: 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. Design: 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. Setting: Sleep laboratory. Participants: Nineteen healthy college age volunteers (seven females) with regular sleep patterns. Interventions: Approximately 24 hours of total SD. Measurements and Results: 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. Conclusions: Visual short-term memory is compromised during sleep deprivation, an effect compounded by delay. However, when memories are retrieved, they tend to be intact. Citation: Wee N; Asplund CL; Chee MWL. Sleep deprivation accelerates delay-related loss of visual short-term memories without affecting precision. SLEEP 2013;36(6):849-856. PMID:23729928

  14. Sleep deprivation amplifies reactivity of brain reward networks, biasing the appraisal of positive emotional experiences.

    PubMed

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

    2011-03-23

    Appropriate interpretation of pleasurable, rewarding experiences favors decisions that enhance survival. Conversely, dysfunctional affective brain processing can lead to life-threatening risk behaviors (e.g., addiction) and emotion imbalance (e.g., mood disorders). The state of sleep deprivation continues to be associated with maladaptive emotional regulation, leading to exaggerated neural and behavioral reactivity to negative, aversive experiences. However, such detrimental consequences are paradoxically aligned with the perplexing antidepressant benefit of sleep deprivation, elevating mood in a proportion of patients with major depression. Nevertheless, it remains unknown how sleep loss alters the dynamics of brain and behavioral reactivity to rewarding, positive emotional experiences. Using functional magnetic resonance imaging (fMRI), here we demonstrate that sleep deprivation amplifies reactivity throughout human mesolimbic reward brain networks in response to pleasure-evoking stimuli. In addition, this amplified reactivity was associated with enhanced connectivity in early primary visual processing pathways and extended limbic regions, yet with a reduction in coupling with medial frontal and orbitofrontal regions. These neural changes were accompanied by a biased increase in the number of emotional stimuli judged as pleasant in the sleep-deprived group, the extent of which exclusively correlated with activity in mesolimbic regions. Together, these data support a view that sleep deprivation not only is associated with enhanced reactivity toward negative stimuli, but imposes a bidirectional nature of affective imbalance, associated with amplified reward-relevant reactivity toward pleasure-evoking stimuli also. Such findings may offer a neural foundation on which to consider interactions between sleep loss and emotional reactivity in a variety of clinical mood disorders.

  15. 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

  16. The effects of sleep deprivation on divergent thinking and attention processes.

    PubMed

    Wimmer; Hoffmann; Bonato; Moffitt

    1992-12-01

    Twelve male undergraduate students were deprived of sleep for one night and were tested with a series of cognitive tasks. Their performance was compared to the performance of thirteen control subjects. Two hourly tasks and three occasional tasks were administered in order to examine cognitive performance following sleep loss. In an attempt to replicate the findings of Horne (1988a), the figural form of the Torrance Tests of Creative Thinking was administered. To explore the effects of short-term sleep deprivation on attention, the following tasks were also administered: a working memory task, a trail-making task, a vowel/consonant discrimination task, and a letter recognition task. Results of the Torrance test, trail-making task and letter recognition task revealed decreases in cognitive abilities following sleep loss, although all tasks required less than 10 minutes to administer. The results of this study suggest that cognitive measures following sleep deprivation have not been adequately explored. Results support the hypothesis that sleep serves a function of cognitive restitution, particularly in the maintenance of attentional mechanisms. PMID:10607055

  17. Self-awakening improves alertness in the morning and during the day after partial sleep deprivation.

    PubMed

    Ikeda, Hiroki; Kubo, Tomohide; Kuriyama, Kenichi; Takahashi, Masaya

    2014-12-01

    The ability to awaken at a predetermined time without an alarm is known as self-awakening. Self-awakening improves morning alertness by eliminating sleep inertia; however, the effects of self-awakening on daytime alertness and alertness that has deteriorated as a result of sleep loss are unknown. The aim of this study was to determine the effects of self-awakening on both morning and daytime alertness after partial sleep deprivation. Fifteen healthy males without the habit of self-awakening participated in a cross-over trial including forced awakening and self-awakening conditions. In each condition, participants' sleep was restricted to 5 h per night in their homes for 4 consecutive days. They completed a psychomotor vigilance task and subjective ratings of sleepiness immediately upon awakening each morning. On the fourth day, participants completed subjective ratings of sleepiness, a psychomotor vigilance task and sleep latency tests in the laboratory seven times at 1-h intervals during the day. The response speed on the psychomotor vigilance task, in the morning and during the day, was higher in the self-awakening than the forced awakening condition. Our results showed that self-awakening improved alertness (assessed by response speeds) by reducing sleep inertia and alleviated daytime sleepiness heightened by partial sleep deprivation.

  18. 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

  19. 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.…

  20. 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. PMID:27345144

  1. 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.

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

    SciTech Connect

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

    2006-05-01

    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 fields 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.

  3. 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

  4. REM sleep deprivation induces changes of down regulatory antagonist modulator (DREAM) expression in the ventrobasal thalamic nuclei of sprague-dawley rats.

    PubMed

    Siran, Rosfaiizah; Ahmad, Asma Hayati; Abdul Aziz, Che Badariah; Ismail, Zalina

    2014-12-01

    REM sleep is a crucial component of sleep. Animal studies indicate that rapid eye movement (REM) sleep deprivation elicits changes in gene expression. Down regulatory antagonist modulator (DREAM) is a protein which downregulates other gene transcriptions by binding to the downstream response element site. The aim of this study is to examine the effect of REM sleep deprivation on DREAM expression in ventrobasal thalamic nuclei (VB) of rats. Seventy-two male Sprague-Dawley rats were divided into four major groups consisting of free-moving control rats (FMC) (n = 18), 72-h REM sleep-deprived rats (REMsd) (n = 18), 72-h REM sleep-deprived rats with 72-h sleep recovery (RG) (n = 18), and tank control rats (TC) (n = 18). REM sleep deprivation was elicited using the inverted flower pot technique. DREAM expression was examined in VB by immunohistochemical, Western blot, and quantitative real-time polymerase chain reaction (qRT-PCR) studies. The DREAM-positive neuronal cells (DPN) were decreased bilaterally in the VB of rats deprived of REM sleep as well as after sleep recovery. The nuclear DREAM extractions were increased bilaterally in animals deprived of REM sleep. The DREAM messenger RNA (mRNA) levels were decreased after sleep recovery. The results demonstrated a link between DREAM expression and REM sleep deprivation as well as sleep recovery which may indicate potential involvement of DREAM in REM sleep-induced changes in gene expression, specifically in nociceptive processing.

  5. 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. PMID:25708092

  6. 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.

  7. Tinospora cordifolia ameliorates anxiety-like behavior and improves cognitive functions in acute sleep deprived rats.

    PubMed

    Mishra, Rachana; Manchanda, Shaffi; Gupta, Muskan; Kaur, Taranjeet; Saini, Vedangana; Sharma, Anuradha; Kaur, Gurcharan

    2016-01-01

    Sleep deprivation (SD) leads to the spectrum of mood disorders like anxiety, cognitive dysfunctions and motor coordination impairment in many individuals. However, there is no effective pharmacological remedy to negate the effects of SD. The current study examined whether 50% ethanolic extract of Tinospora cordifolia (TCE) can attenuate these negative effects of SD. Three groups of adult Wistar female rats - (1) vehicle treated-sleep undisturbed (VUD), (2) vehicle treated-sleep deprived (VSD) and (3) TCE treated-sleep deprived (TSD) animals were tested behaviorally for cognitive functions, anxiety and motor coordination. TSD animals showed improved behavioral response in EPM and NOR tests for anxiety and cognitive functions, respectively as compared to VSD animals. TCE pretreatment modulated the stress induced-expression of plasticity markers PSA-NCAM, NCAM and GAP-43 along with proteins involved in the maintenance of LTP i.e., CamKII-α and calcineurin (CaN) in hippocampus and PC regions of the brain. Interestingly, contrary to VSD animals, TSD animals showed downregulated expression of inflammatory markers such as CD11b/c, MHC-1 and cytokines along with inhibition of apoptotic markers. This data suggests that TCE alone or in combination with other memory enhancing agents may help in managing sleep deprivation associated stress and improving cognitive functions. PMID:27146164

  8. Tinospora cordifolia ameliorates anxiety-like behavior and improves cognitive functions in acute sleep deprived rats

    PubMed Central

    Mishra, Rachana; Manchanda, Shaffi; Gupta, Muskan; Kaur, Taranjeet; Saini, Vedangana; Sharma, Anuradha; Kaur, Gurcharan

    2016-01-01

    Sleep deprivation (SD) leads to the spectrum of mood disorders like anxiety, cognitive dysfunctions and motor coordination impairment in many individuals. However, there is no effective pharmacological remedy to negate the effects of SD. The current study examined whether 50% ethanolic extract of Tinospora cordifolia (TCE) can attenuate these negative effects of SD. Three groups of adult Wistar female rats - (1) vehicle treated-sleep undisturbed (VUD), (2) vehicle treated-sleep deprived (VSD) and (3) TCE treated-sleep deprived (TSD) animals were tested behaviorally for cognitive functions, anxiety and motor coordination. TSD animals showed improved behavioral response in EPM and NOR tests for anxiety and cognitive functions, respectively as compared to VSD animals. TCE pretreatment modulated the stress induced-expression of plasticity markers PSA-NCAM, NCAM and GAP-43 along with proteins involved in the maintenance of LTP i.e., CamKII-α and calcineurin (CaN) in hippocampus and PC regions of the brain. Interestingly, contrary to VSD animals, TSD animals showed downregulated expression of inflammatory markers such as CD11b/c, MHC-1 and cytokines along with inhibition of apoptotic markers. This data suggests that TCE alone or in combination with other memory enhancing agents may help in managing sleep deprivation associated stress and improving cognitive functions. PMID:27146164

  9. Effects of sleep deprivation and aging on long-term and remote memory in mice

    PubMed Central

    Vecsey, Christopher G.; Park, Alan J.; Khatib, Nora

    2015-01-01

    Sleep deprivation (SD) following hippocampus-dependent learning in young mice impairs memory when tested the following day. Here, we examined the effects of SD on remote memory in both young and aged mice. In young mice, we found that memory is still impaired 1 mo after training. SD also impaired memory in aged mice 1 d after training, but, by a month after training, sleep-deprived and control aged animals performed similarly, primarily due to remote memory decay in the control aged animals. Gene expression analysis supported the finding that SD has similar effects on the hippocampus in young and aged mice. PMID:25776037

  10. Individual differences in physiologic measures are stable across repeated exposures to total sleep deprivation

    PubMed Central

    Chua, Eric Chern‐Pin; Yeo, Sing‐Chen; Lee, Ivan Tian‐Guang; Tan, Luuan‐Chin; Lau, Pauline; Tan, Sara S.; Ho Mien, Ivan; Gooley, Joshua J.

    2014-01-01

    Abstract Some individuals show severe cognitive impairment when sleep deprived, whereas others are able to maintain a high level of performance. Such differences are stable and trait‐like, but it is not clear whether these findings generalize to physiologic responses to sleep loss. Here, we analyzed individual differences in behavioral and physiologic measures in healthy ethnic‐Chinese male volunteers (n = 12; aged 22–30 years) who were kept awake for at least 26 h in a controlled laboratory environment on two separate occasions. Every 2 h, sustained attention performance was assessed using a 10‐min psychomotor vigilance task (PVT), and sleepiness was estimated objectively by determining percentage eyelid closure over the pupil over time (PERCLOS) and blink rate. Between‐subject differences in heart rate and its variability, and electroencephalogram (EEG) spectral power were also analyzed during each PVT. To assess stability of individual differences, intraclass correlation coefficients (ICC) were determined using variance components analysis. Consistent with previous work, individual differences in PVT performance were reproducible across study visits, as were baseline sleep measures prior to sleep deprivation. In addition, stable individual differences were observed during sleep deprivation for PERCLOS, blink rate, heart rate and its variability, and EEG spectral power in the alpha frequency band, even after adjusting for baseline differences in these measures (range, ICC = 0.67–0.91). These findings establish that changes in ocular, ECG, and EEG signals are highly reproducible across a night of sleep deprivation, hence raising the possibility that, similar to behavioral measures, physiologic responses to sleep loss are trait‐like. PMID:25263200

  11. Anxiety-like effects of meta-chlorophenylpiperazine in paradoxically sleep-deprived mice.

    PubMed

    Polesel, Daniel Ninello; Fukushiro, Daniela Fukue; Andersen, Monica Levy; Nozoe, Karen Tieme; Mári-Kawamoto, Elisa; Saito, Luís Paulo; Carvalho, Fábio Ramos Souza; Alvarenga, Tathiana Aparecida; Freitas, Denise; Tufik, Sergio; Frussa-Filho, Roberto; Lanaro, Rafael; Costa, José Luiz; Tavares, Marina Franco Maggi

    2014-03-01

    Chlorophenylpiperazines (CPP) are psychotropic drugs used in nightclub parties and are frequently used in a state of sleep deprivation, a condition which can potentiate the effects of psychoactive drugs. This study aimed to investigate the effects of sleep deprivation and sleep rebound (RB) on anxiety-like measures in mCPP-treated mice using the open field test. We first optimized our procedure by performing dose-effect curves and examining different pretreatment times in naïve male Swiss mice. Subsequently, a separate cohort of mice underwent paradoxical sleep deprivation (PSD) for 24 or 48h. In the last experiment, immediately after the 24h-PSD period, mice received an injection of saline or mCPP, but their general activity was quantified in the open field only after the RB period (24 or 48h). The dose of 5mgmL(-1) of mCPP was the most effective at decreasing rearing behavior, with peak effects 15min after injection. PSD decreased locomotion and rearing behaviors, thereby inhibiting a further impairment induced by mCPP. Plasma concentrations of mCPP were significantly higher in PSD 48h animals compared to the non-PSD control group. Twenty-four hours of RB combined with mCPP administration produced a slight reduction in locomotion. Our results show that mCPP was able to significantly change the behavior of naïve, PSD, and RB mice. When combined with sleep deprivation, there was a higher availability of drug in plasma levels. Taken together, our results suggest that sleep loss can enhance the behavioral effects of the potent psychoactive drug, mCPP, even after a period of rebound sleep.

  12. Widespread Changes in White Matter Microstructure after a Day of Waking and Sleep Deprivation

    PubMed Central

    Elvsåshagen, Torbjørn; Norbom, Linn B.; Pedersen, Per Ø.; Quraishi, Sophia H.; Bjørnerud, Atle; Malt, Ulrik F.; Groote, Inge R.; Westlye, Lars T.

    2015-01-01

    Background Elucidating the neurobiological effects of sleep and waking remains an important goal of the neurosciences. Recently, animal studies indicated that sleep is important for cell membrane and myelin maintenance in the brain and that these structures are particularly susceptible to insufficient sleep. Here, we tested the hypothesis that a day of waking and sleep deprivation would be associated with changes in diffusion tensor imaging (DTI) indices of white matter microstructure sensitive to axonal membrane and myelin alterations. Methods Twenty-one healthy adult males underwent DTI in the morning [7:30AM; time point (TP)1], after 14 hours of waking (TP2), and then after another 9 hours of waking (TP3). Whole brain voxel-wise analysis was performed with tract based spatial statistics. Results A day of waking was associated with widespread increases in white matter fractional anisotropy, which were mainly driven by radial diffusivity reductions, and sleep deprivation was associated with widespread fractional anisotropy decreases, which were mainly explained by reductions in axial diffusivity. In addition, larger decreases in axial diffusivity after sleep deprivation were associated with greater sleepiness. All DTI changes remained significant after adjusting for hydration measures. Conclusions This is the first DTI study of sleep deprivation in humans. Although previous studies have observed localized changes in DTI indices of cerebral microstructure over the course of a few hours, further studies are needed to confirm widespread DTI changes within hours of waking and to clarify whether such changes in white matter microstructure serve as neurobiological substrates of sleepiness. PMID:26020651

  13. 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. PMID:27310475

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

    PubMed Central

    Boström, Adrian E.; Mwinyi, Jessica; Schiöth, Helgi B.

    2016-01-01

    Abstract 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. PMID:27310475

  15. Opposite effects of sleep deprivation on the continuous reaction times in patients with liver cirrhosis and normal persons.

    PubMed

    Lauridsen, Mette Munk; Frøjk, Jesper; de Muckadell, Ove B Schaffalitzky; Vilstrup, Hendrik

    2014-09-01

    The continuous reaction times (CRT) method describes arousal functions. Reaction time instability in a patient with liver disease indicates covert hepatic encephalopathy (cHE). The effects of sleep deprivation are unknown although cirrhosis patients frequently suffer from sleep disorders. The aim of this study was to determine if sleep deprivation influences the CRT test. Eighteen cirrhosis patients and 27 healthy persons were tested when rested and after one night's sleep deprivation. The patients filled out validated sleep quality questionnaires. Seven patients (38%) had unstable reaction times (a CRTindex < 1.9) compatible with cHE. In these patients, the wakefulness improved or normalized their reaction speed and CRTindex (p = 0.01). There was no change in the other patients' reaction speed or stability. Seven patients (38%) reported poor sleep that was not related to their CRT tests before or after the sleep deprivation. In the healthy participants, the sleep deprivation slowed their reaction times by 11% (p < 0.0001) and in 7 persons (25%) destabilized them. The acute sleep deprivation normalized or improved the reaction time stability of the patients with a CRTindex below 1.9 and had no effect in the patients with a CRTindex above 1.9. There was no relation between reported sleep quality and reaction time results. Thus, in cirrhosis patients, sleep disturbances do not lead to 'falsely' slowed and unstable reaction times. In contrast, the acute sleep deprivation slowed and destabilized the reaction times of the healthy participants. This may have negative consequences for decision-making.

  16. Does one night of partial sleep deprivation affect the evening performance during intermittent exercise in Taekwondo players?

    PubMed

    Mejri, Mohamed Arbi; Yousfi, Narimen; Mhenni, Thouraya; Tayech, Amel; Hammouda, Omar; Driss, Tarak; Chaouachi, Anis; Souissi, Nizar

    2016-02-01

    Athletes and coaches believe that adequate sleep is essential for peak performance. There is ample scientific evidence which support the conclusion that sleep loss seems to stress many physiological functions in humans. The aim of this study was to determine the effect of one night's sleep deprivation on intermittent exercise performance in the evening of the following day. Ten male Taekwondo players performed the Yo-Yo intermittent recovery test (YYIRT) in three sleep conditions (reference sleep night [RN], partial sleep deprivation at the beginning of night [PSDBN], partial sleep deprivation at the end of night [PSDEN]) in a counterbalanced order, allowing a recovery period ≥36 hr in between them. Heart rate peak (HRpeak), plasma lactate concentrations (Lac) and rating of perceived exertion (RPE) were measured during the test. A significant effect of sleep restriction was observed on the total distance covered in YYIRT (P<0.0005) and Lac (P<0.01) in comparison with the RN. In addition, performance more decreased after PSDEN (P<0.0005) than PSDBN (P<0.05). Also, Lac decreased significantly only after PS-DEN (P<0.05) compared with RN. However, there were no significant changes in HRpeak and RPE after the two types of partial sleep deprivation compared to RN. The present study indicates that short-term sleep restriction affect the intermittent performance, as well as the Lac levels of the Taekwondo players in the evening of the following day, without alteration of HRpeak and RPE.

  17. Does one night of partial sleep deprivation affect the evening performance during intermittent exercise in Taekwondo players?

    PubMed Central

    Mejri, Mohamed Arbi; Yousfi, Narimen; Mhenni, Thouraya; Tayech, Amel; Hammouda, Omar; Driss, Tarak; Chaouachi, Anis; Souissi, Nizar

    2016-01-01

    Athletes and coaches believe that adequate sleep is essential for peak performance. There is ample scientific evidence which support the conclusion that sleep loss seems to stress many physiological functions in humans. The aim of this study was to determine the effect of one night’s sleep deprivation on intermittent exercise performance in the evening of the following day. Ten male Taekwondo players performed the Yo-Yo intermittent recovery test (YYIRT) in three sleep conditions (reference sleep night [RN], partial sleep deprivation at the beginning of night [PSDBN], partial sleep deprivation at the end of night [PSDEN]) in a counterbalanced order, allowing a recovery period ≥36 hr in between them. Heart rate peak (HRpeak), plasma lactate concentrations (Lac) and rating of perceived exertion (RPE) were measured during the test. A significant effect of sleep restriction was observed on the total distance covered in YYIRT (P<0.0005) and Lac (P<0.01) in comparison with the RN. In addition, performance more decreased after PSDEN (P<0.0005) than PSDBN (P<0.05). Also, Lac decreased significantly only after PS-DEN (P<0.05) compared with RN. However, there were no significant changes in HRpeak and RPE after the two types of partial sleep deprivation compared to RN. The present study indicates that short-term sleep restriction affect the intermittent performance, as well as the Lac levels of the Taekwondo players in the evening of the following day, without alteration of HRpeak and RPE. PMID:26933660

  18. Does one night of partial sleep deprivation affect the evening performance during intermittent exercise in Taekwondo players?

    PubMed

    Mejri, Mohamed Arbi; Yousfi, Narimen; Mhenni, Thouraya; Tayech, Amel; Hammouda, Omar; Driss, Tarak; Chaouachi, Anis; Souissi, Nizar

    2016-02-01

    Athletes and coaches believe that adequate sleep is essential for peak performance. There is ample scientific evidence which support the conclusion that sleep loss seems to stress many physiological functions in humans. The aim of this study was to determine the effect of one night's sleep deprivation on intermittent exercise performance in the evening of the following day. Ten male Taekwondo players performed the Yo-Yo intermittent recovery test (YYIRT) in three sleep conditions (reference sleep night [RN], partial sleep deprivation at the beginning of night [PSDBN], partial sleep deprivation at the end of night [PSDEN]) in a counterbalanced order, allowing a recovery period ≥36 hr in between them. Heart rate peak (HRpeak), plasma lactate concentrations (Lac) and rating of perceived exertion (RPE) were measured during the test. A significant effect of sleep restriction was observed on the total distance covered in YYIRT (P<0.0005) and Lac (P<0.01) in comparison with the RN. In addition, performance more decreased after PSDEN (P<0.0005) than PSDBN (P<0.05). Also, Lac decreased significantly only after PS-DEN (P<0.05) compared with RN. However, there were no significant changes in HRpeak and RPE after the two types of partial sleep deprivation compared to RN. The present study indicates that short-term sleep restriction affect the intermittent performance, as well as the Lac levels of the Taekwondo players in the evening of the following day, without alteration of HRpeak and RPE. PMID:26933660

  19. A prospective analysis of sleep deprivation and disturbance in surgical patients

    PubMed Central

    Dolan, Ross; Huh, Jae; Tiwari, Neil; Sproat, Tom; Camilleri-Brennan, John

    2016-01-01

    Introduction Sleep deprivation has a potentially deleterious effect on postoperative recovery. The aim of our prospective study was to identify the factors contributing to postoperative sleep deprivation and disturbance in order to recommend improvements in postoperative care. Methods 102 consecutive patients attending for elective general and orthopaedic surgery were interviewed preoperatively (baseline) and postoperatively on their duration of sleep, number of wakenings during the night, factors contributing to sleep loss and the use of analgesia and night sedation. Results Patients woke up a median of 5 times in the first postoperative night compared to a median of 3 times preoperatively (p = 0.01). Pain was the predominant factor preventing sleep, affecting 39% of patients preoperatively and 48% of patients on the first postoperative day. Other factors included noise from other patients and nursing staff, and using the toilet. Analgesia was taken by more than 90% of patients in the first two days, this number gradually reducing over the postoperative period. On the other hand, in the first two postoperative days, only about 5% of patients had night sedation. Discussion and conclusions Apart from highlighting the need for effective pain management postoperatively, we believe that our study supports the drive towards single bed bays, where steps can be taken to minimize the impact of environmental factors on sleep. PMID:26909151

  20. Sleep deprivation induces differential morphological changes in the hippocampus and prefrontal cortex in young and old rats.

    PubMed

    Acosta-Peña, Eva; Camacho-Abrego, Israel; Melgarejo-Gutiérrez, Montserrat; Flores, Gonzalo; Drucker-Colín, René; García-García, Fabio

    2015-01-01

    Sleep is a fundamental state necessary for maintenance of physical and neurological homeostasis throughout life. Several studies regarding the functions of sleep have been focused on effects of sleep deprivation on synaptic plasticity at a molecular and electrophysiological level, and only a few studies have studied sleep function from a structural perspective. Moreover, during normal aging, sleep architecture displays some changes that could affect normal development in the elderly. In this study, using a Golgi-Cox staining followed by Sholl analysis, we evaluate the effects of 24 h of total sleep deprivation on neuronal morphology of pyramidal neurons from Layer III of the prefrontal cortex (PFC) and the dorsal hippocampal CA1 region from male Wistar rats at two different ages (3 and 22 months). We found no differences in total dendritic length and branching length in both analyzed regions after sleep deprivation. Spine density was reduced in the CA1 of young-adults, and interestingly, sleep deprivation increased spine density in PFC of aged animals. Taken together, our results show that 24 h of total sleep deprivation have different effects on synaptic plasticity and could play a beneficial role in cognition during aging.

  1. 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. PMID:19831107

  2. Effect of sleep deprivation on overnight bronchoconstriction in nocturnal asthma.

    PubMed

    Catterall, J R; Rhind, G B; Stewart, I C; Whyte, K F; Shapiro, C M; Douglas, N J

    1986-09-01

    Nocturnal cough and wheeze are common in asthma. The cause of nocturnal asthma is unknown and there is conflicting evidence on whether sleep is a factor. Twelve adult asthmatic subjects with nocturnal wheeze were studied on two occasions: on one night subjects were allowed to sleep and on the other they were kept awake all night, wakefulness being confirmed by electroencephalogram. Every patient developed bronchoconstriction overnight both on the asleep night, when peak expiratory flow (PEF) fell from a mean (SE) of 418 (40) 1 min-1 at 10 pm to 270 (46) 1 min-1 in the morning, and on the awake night (PEF 10 pm 465 (43), morning 371 (43) 1 min-1). The morning values of PEF were, however, higher (p less than 0.1) after the awake night and both the absolute and the percentage overnight falls in PEF were greater when the patients slept (asleep night 38% (6%), awake night 20% (4%); p less than 0.01). This study suggests that sleep is an important factor in determining overnight bronchoconstriction in patients with nocturnal asthma.

  3. [Impact of sleep deprivation on coronary heart disease and progress in prevention and treatment with traditional Chinese medicines].

    PubMed

    Yuan, Rong; Wang, Jie; Guo, Li-li

    2015-05-01

    Sleep deprivation (SD) has been taken as an independent predictor for cardiovascular risks, which was closely related to the increased morbidity and mortality in coronary heart disease (CHD). In this article, after reviewing the impact of modern medical method sleep deprivation on CHD and studies on principle method recipe medicines for preventing and treating CHD, the authors observed the autonomic nerve dysfunction, hormonal metabolism dysfunction, endothelial dysfunction and inflammatory responses after sleep deprivation, which can cause or aggravate CHD. On the basis of the traditional Chinese medicine theories of "heart dominating the blood and vessels and the mind", the authors considered that traditional Chinese medicines can tonify heart and soothe the nerves, reducing all of the risk factors through multi-target and multi-pathway, and improve sleep and decrease the risk factors caused by sleep deprivation, which provides a new idea for the prevention and treatment of CHD. PMID:26323126

  4. Sleep deprivation and hippocampal vulnerability: changes in neuronal plasticity, neurogenesis and cognitive function.

    PubMed

    Kreutzmann, J C; Havekes, R; Abel, T; Meerlo, P

    2015-11-19

    Despite the ongoing fundamental controversy about the physiological function of sleep, there is general consensus that sleep benefits neuronal plasticity, which ultimately supports brain function and cognition. In agreement with this are numerous studies showing that sleep deprivation (SD) results in learning and memory impairments. Interestingly, such impairments appear to occur particularly when these learning and memory processes require the hippocampus, suggesting that this brain region may be particularly sensitive to the consequences of sleep loss. Although the molecular mechanisms underlying sleep and memory formation remain to be investigated, available evidence suggests that SD may impair hippocampal neuronal plasticity and memory processes by attenuating intracellular cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) signaling which may lead to alterations in cAMP response element binding protein (CREB)-mediated gene transcription, neurotrophic signaling, and glutamate receptor expression. When restricted sleep becomes a chronic condition, it causes a reduction of hippocampal cell proliferation and neurogenesis, which may eventually lead to a reduction in hippocampal volume. Ultimately, by impairing hippocampal plasticity and function, chronically restricted and disrupted sleep contributes to cognitive disorders and psychiatric diseases.

  5. Sleep deprivation and hippocampal vulnerability: changes in neuronal plasticity, neurogenesis and cognitive function.

    PubMed

    Kreutzmann, J C; Havekes, R; Abel, T; Meerlo, P

    2015-11-19

    Despite the ongoing fundamental controversy about the physiological function of sleep, there is general consensus that sleep benefits neuronal plasticity, which ultimately supports brain function and cognition. In agreement with this are numerous studies showing that sleep deprivation (SD) results in learning and memory impairments. Interestingly, such impairments appear to occur particularly when these learning and memory processes require the hippocampus, suggesting that this brain region may be particularly sensitive to the consequences of sleep loss. Although the molecular mechanisms underlying sleep and memory formation remain to be investigated, available evidence suggests that SD may impair hippocampal neuronal plasticity and memory processes by attenuating intracellular cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) signaling which may lead to alterations in cAMP response element binding protein (CREB)-mediated gene transcription, neurotrophic signaling, and glutamate receptor expression. When restricted sleep becomes a chronic condition, it causes a reduction of hippocampal cell proliferation and neurogenesis, which may eventually lead to a reduction in hippocampal volume. Ultimately, by impairing hippocampal plasticity and function, chronically restricted and disrupted sleep contributes to cognitive disorders and psychiatric diseases. PMID:25937398

  6. 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.

  7. 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.

  8. Changes in cerebral hemodynamics during a sleep-deprived video-electroencephalogram in healthy children.

    PubMed

    Peng, Bingwei; Li, Jialing; Wang, Jing; Liang, Xiuqiong; Zheng, Zhiying; Mai, Jianning

    2016-07-01

    This study investigates the cerebral hemodynamic changes during a routine sleep-deprived video-electroencephalogram (SD-VEEG) in healthy children. Forty-two children with normal intelligence were examined. The children were 5-14 years of age, and their electroencephalograms (EEGs) were within the normal range. Each subject was deprived of a routine night's sleep and then examined during non-drug-induced sleep in the daytime. The awake and sleep stages were evaluated using EEGs, according to the American Academy of Sleep Medicine. Stable transcranial Doppler ultrasound (TCD) tracings through real-time TCD-VEEG monitoring were recorded. The mean systolic cerebral blood flow velocity (CBFV), diastolic CBFV, pulsatility index and resistance index of each artery were analyzed for 30 s per stage. A multivariate analysis of variance was conducted to compare the hemodynamic parameters for the awake stage versus light sleep and deep sleep stages. Non-rapid eye movement sleep was associated with an increased CBFV in the middle (164.38  ±  27.28) and anterior cerebral artery (131.81  ±  21.55) during light sleep (stages N1 and N2) (P  =  0.0001), a reduced systolic CBFV in all vascular arteries (LMCA, 138.73  ±  20.64; LACA, 108.33  ±  22.33; LPCA, 83.9  ±  18.6) during deep sleep (stage N3) compared with light sleep (P  =  0.0001), and a sustained increased PI (LMCA, 0.92  ±  0.13; LACA, 0.964  ±  0.18) during deep sleep (P  <  0.05). These findings indicate distinct cerebral hemodynamic alterations during SD-VEEG in children. This study utilized real-time TCD-VEEG monitoring during SD-EEG to further investigate neurovascular coupling in interictal epileptic discharges and understand its potential influence on cognition in the developing brain. PMID:27244460

  9. 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.

  10. 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

  11. Enhanced emotional reactivity after selective REM sleep deprivation in humans: an fMRI study.

    PubMed

    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.

  12. A Meta-Analysis of the Impact of Short-Term Sleep Deprivation on Cognitive Variables

    ERIC Educational Resources Information Center

    Lim, Julian; Dinges, David F.

    2010-01-01

    A substantial amount of research has been conducted in an effort to understand the impact of short-term (less than 48 hr) total sleep deprivation (SD) on outcomes in various cognitive domains. Despite this wealth of information, there has been disagreement on how these data should be interpreted, arising in part because the relative magnitude of…

  13. 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…

  14. Effects of Sleep Deprivation and Aging on Long-Term and Remote Memory in Mice

    ERIC Educational Resources Information Center

    Vecsey, Christopher G.; Park, Alan J.; Khatib, Nora; Abel, Ted

    2015-01-01

    Sleep deprivation (SD) following hippocampus-dependent learning in young mice impairs memory when tested the following day. Here, we examined the effects of SD on remote memory in both young and aged mice. In young mice, we found that memory is still impaired 1 mo after training. SD also impaired memory in aged mice 1 d after training, but, by a…

  15. [Phototherapy and sleep deprivation as additional methods of treating bronchial asthma patients].

    PubMed

    Maevskiĭ, A A

    1991-05-01

    Correction of internal desynchronosis in bronchial asthma by means of phototherapy and partial sleep deprivation was instituted in 4 hormone-dependent patients with bronchial asthma for 13 months. The results were positive: the frequency and severity of night attacks reduced, the condition of the patients improved.

  16. 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…

  17. Preserved calibration of persistence based on delay-timing distribution during sleep deprivation.

    PubMed

    Massar, Stijn A A; Chee, Michael W L

    2015-12-01

    We frequently encounter decisions where we have to determine whether to wait for a certain reward delayed for an uncertain duration or to move on. The appropriate decision depends upon the underlying temporal distribution of the delay. With some distributions it is best to be completely persistent, whereas in others it is more appropriate to abandon waiting after a certain period of time. The current study examined whether the ability to form temporal expectations and adjust persistence accordingly is compromised by sleep deprivation. Participants performed a willingness-to-wait task either in a well-rested state or after a night of total sleep deprivation. Participants had to decide either to wait for a larger reward or to abandon waiting in favour of a smaller immediate reward. Delays were drawn from either a uniform distribution, where being persistent yields maximal returns, or from a heavy-tailed distribution, where occasional long delays render full persistence suboptimal. In spite of increased sleepiness and decreased vigilance, sleep-deprived participants were able to adjust waiting time appropriate to the experienced timing distribution. Additionally, sleep deprivation did not affect the foreperiod effect, indicating intact perception of conditional probability of temporal events and ability to adjust preparation accordingly. PMID:26179859

  18. Preserved calibration of persistence based on delay-timing distribution during sleep deprivation.

    PubMed

    Massar, Stijn A A; Chee, Michael W L

    2015-12-01

    We frequently encounter decisions where we have to determine whether to wait for a certain reward delayed for an uncertain duration or to move on. The appropriate decision depends upon the underlying temporal distribution of the delay. With some distributions it is best to be completely persistent, whereas in others it is more appropriate to abandon waiting after a certain period of time. The current study examined whether the ability to form temporal expectations and adjust persistence accordingly is compromised by sleep deprivation. Participants performed a willingness-to-wait task either in a well-rested state or after a night of total sleep deprivation. Participants had to decide either to wait for a larger reward or to abandon waiting in favour of a smaller immediate reward. Delays were drawn from either a uniform distribution, where being persistent yields maximal returns, or from a heavy-tailed distribution, where occasional long delays render full persistence suboptimal. In spite of increased sleepiness and decreased vigilance, sleep-deprived participants were able to adjust waiting time appropriate to the experienced timing distribution. Additionally, sleep deprivation did not affect the foreperiod effect, indicating intact perception of conditional probability of temporal events and ability to adjust preparation accordingly.

  19. Prevalence of Sleep Deprivation and Relation with Depressive Symptoms among Medical Residents in King Fahd University Hospital, Saudi Arabia

    PubMed Central

    Al-Maddah, Esraa M.; Al-Dabal, Badria K.; Khalil, Mohammad S.

    2015-01-01

    Objectives: Sleep deprivation is common among medical residents of all specialties. This study aimed to determine the prevalence of sleep deprivation and depressive symptoms among medical residents in King Fahd University Hospital (KFUH) in Al Khobar, Saudi Arabia. Furthermore, the association between sleep deprivation, sleepiness and depressive symptoms was examined. Methods: This cross-sectional study took place between February and April 2012 and involved 171 KFUH medical residents of different specialties. Data were collected using a specifically designed questionnaire eliciting demographic information, working hours and number of hours of sleep. In addition, validated Arabic versions of the Epworth Sleepiness Scale and the Beck Depression Inventory-2 (BDI-2) were used. Results: The prevalence of acute sleep deprivation and chronic sleep deprivation among residents in KFUH was 85.9% and 63.2%, respectively. The prevalence of overall sleepiness was 52%; 43.3% reported being excessively sleepy in certain situations while 8.8% reported being excessively sleepy regardless of the situation. Based on the BDI-2, the prevalence of mild, moderate and severe depressive symptoms was 43.3%, 15.2% and 4.7%, respectively. Significant associations were found between sleep deprivation and depressive symptoms; depressive symptoms and sleepiness, and depressive symptoms and being a female resident. Conclusion: The vast majority of medical residents had acute sleep deprivation, with more than half suffering from chronic sleep deprivation. The number of hours and quality of sleep among the residents were strongly associated with depressive symptoms. New regulations are recommended regarding the number of working hours and night duties for medical residents. Further studies should assess these new regulations on a regular basis. PMID:25685390

  20. 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

  1. 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

  2. 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

  3. Sleep Disorders

    MedlinePlus

    ... the day, even if you have had enough sleep? You might have a sleep disorder. The most common kinds are Insomnia - a hard time falling or staying asleep Sleep apnea - breathing interruptions during sleep Restless legs syndrome - ...

  4. Sleep Problems

    MedlinePlus

    ... For Consumers Consumer Information by Audience For Women Sleep Problems Share Tweet Linkedin Pin it More sharing ... PDF 474KB) En Español Medicines to Help You Sleep Tips for Better Sleep Basic Facts about Sleep ...

  5. Effects of Sleep Deprivation on Mice Bone Marrow and Spleen B Lymphopoiesis.

    PubMed

    Lungato, Lisandro; Nogueira-Pedro, Amanda; Carvalho Dias, Carolina; Paredes-Gamero, Edgar Julian; Tufik, Sergio; D'Almeida, Vânia

    2016-06-01

    B lymphocytes are immune cells crucial for the maintenance and viability of the humoral response. Sleep is an essential event for the maintenance and integrity of all systems, including the immune system (IS). Thus, sleep deprivation (SD) causes problems in metabolism and homeostasis in many cell systems, including the IS. In this study, our goal was to determine changes in B lymphocytes from the bone marrow (BM) and spleen after SD. Three-month-old male Swiss mice were used. These mice were sleep deprived through the modified multiple platform method for different periods (24, 48, and 72 h), whereas another group was allowed to sleep for 24 h after 72 h of SD (rebound group) and a third group was allowed to sleep normally during the entire experiment. After this, the spleen and BM were collected, and cell analyses were performed. The numbers of B lymphocytes in the BM and spleen were reduced by SD. Additionally, reductions in the percentage of lymphocyte progenitors and their ability to form colonies were observed. Moreover, an increase in the death of B lymphocytes from the BM and spleen was associated with an increase in oxidative stress indicators, such as DCFH-DA, CAT, and mitochondrial SOD. Rebound was not able to reverse most of the alterations elicited by SD. The reduction in B lymphocytes and their progenitors by cell death, with a concomitant increase in oxidative stress, showed that SD promoted a failure in B lymphopoiesis.

  6. 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

    2014-10-01

    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.

  7. 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

  8. 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

  9. 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

    2014-10-01

    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. PMID:24859426

  10. Effects of Sleep Deprivation on Mice Bone Marrow and Spleen B Lymphopoiesis.

    PubMed

    Lungato, Lisandro; Nogueira-Pedro, Amanda; Carvalho Dias, Carolina; Paredes-Gamero, Edgar Julian; Tufik, Sergio; D'Almeida, Vânia

    2016-06-01

    B lymphocytes are immune cells crucial for the maintenance and viability of the humoral response. Sleep is an essential event for the maintenance and integrity of all systems, including the immune system (IS). Thus, sleep deprivation (SD) causes problems in metabolism and homeostasis in many cell systems, including the IS. In this study, our goal was to determine changes in B lymphocytes from the bone marrow (BM) and spleen after SD. Three-month-old male Swiss mice were used. These mice were sleep deprived through the modified multiple platform method for different periods (24, 48, and 72 h), whereas another group was allowed to sleep for 24 h after 72 h of SD (rebound group) and a third group was allowed to sleep normally during the entire experiment. After this, the spleen and BM were collected, and cell analyses were performed. The numbers of B lymphocytes in the BM and spleen were reduced by SD. Additionally, reductions in the percentage of lymphocyte progenitors and their ability to form colonies were observed. Moreover, an increase in the death of B lymphocytes from the BM and spleen was associated with an increase in oxidative stress indicators, such as DCFH-DA, CAT, and mitochondrial SOD. Rebound was not able to reverse most of the alterations elicited by SD. The reduction in B lymphocytes and their progenitors by cell death, with a concomitant increase in oxidative stress, showed that SD promoted a failure in B lymphopoiesis. PMID:26517012

  11. Excess diuresis and natriuresis during acute sleep deprivation in healthy adults.

    PubMed

    Kamperis, Konstantinos; Hagstroem, Soren; Radvanska, Eva; Rittig, Soren; Djurhuus, Jens Christian

    2010-08-01

    The transition from wakefulness to sleep is associated with a pronounced decline in diuresis, a necessary physiological process that allows uninterrupted sleep. The aim of this study was to assess the effect of acute sleep deprivation (SD) on urine output and renal water, sodium, and solute handling in healthy young volunteers. Twenty young adults (10 male) were recruited for two 24-h studies under standardized dietary conditions. During one of the two admissions, subjects were deprived of sleep. Urine output, electrolyte excretions, and osmolar excretions were calculated. Activated renin, angiotensin II, aldosterone, arginine vasopressin, and atrial natriuretic peptide were measured in plasma, whereas prostaglandin E(2) and melatonin were measured in urine. SD markedly increased the diuresis and led to excess renal sodium excretion. The effect was more pronounced in men who shared significantly higher diuresis levels during SD compared with women. Renal water handling and arginine vasopressin levels remained unaltered during SD, but the circadian rhythm of the hormones of the renin-angiotensin-aldosterone system was significantly affected. Urinary melatonin and prostaglandin E(2) excretion levels were comparable between SD and baseline night. Hemodynamic changes were characterized by the attenuation of nocturnal blood pressure dipping and an increase in creatinine clearance. Acute deprivation of sleep induces natriuresis and osmotic diuresis, leading to excess nocturnal urine production, especially in men. Hemodynamic changes during SD may, through renal and hormonal processes, be responsible for these observations. Sleep architecture disturbances should be considered in clinical settings with nocturnal polyuria such as enuresis in children and nocturia in adults.

  12. 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…

  13. Sleep deprivation as a method of chronotherapy in the treatment of depression.

    PubMed

    Dopierała, Ewa; Rybakowski, Janusz

    2015-01-01

    Disturbances of circadian rhythms play an important role in the pathogenesis of affective illnesses, and their normalisation with methods of chronotherapy might become an important element of therapeutic treatment. Chronotherapy is based on a controlled exposure to environmental stimuli which affect biorhythms. One of the chronotherapeutic methods is sleep deprivation (SD). The article discusses the present status of SD in psychiatry, its methods and application in depression treatment. Presently the most recommended pattern is combining total sleep deprivation (TSD), sleep phase advance (SPA), pharmacotherapy, and sometimes also phototherapy. Such proceedings have proven short-term and long-term effectiveness, and they may also have beneficial effect in drug resistant depression. Among the therapeutic mechanisms of the sleep deprivation treatment, the following are influenced: catecholaminergic, serotonergic and glutamatergic neurotransmission, neurotrophic factors (mainly the brain-derived neurotrophic factor - BDNF), the immune system, the endocrine system, metabolism of some brain structures (mostly the prefrontal cortex) and gene expression related to biological clock. On the grounds of the efficiency, simplicity and safety of this method, authors think that SD in its modern version with SPA should be used more often as an element of depression treatment. PMID:26276912

  14. Adaptation of visual tracking synchronization after one night of sleep deprivation.

    PubMed

    Tong, Jianliang; Maruta, Jun; Heaton, Kristin J; Maule, Alexis L; Ghajar, Jamshid

    2014-01-01

    The temporal delay between sensory input and motor execution is a fundamental constraint in interactions with the environment. Predicting the temporal course of a stimulus and dynamically synchronizing the required action with the stimulus are critical for offsetting this constraint, and this prediction-synchronization capacity can be tested using visual tracking of a target with predictable motion. Although the role of temporal prediction in visual tracking is assumed, little is known of how internal predictions interact with the behavioral outcome or how changes in the cognitive state influence such interaction. We quantified and compared the predictive visual tracking performance of military volunteers before and after one night of sleep deprivation. The moment-to-moment synchronization of visual tracking during sleep deprivation deteriorated with sensitivity changes greater than 40 %. However, increased anticipatory saccades maintained the overall temporal accuracy with near zero phase error. Results suggest that acute sleep deprivation induces instability in visuomotor prediction, but there is compensatory visuomotor adaptation. Detection of these visual tracking features may aid in the identification of insufficient sleep.

  15. Effect of flumazenil-augmentation on microsleep and mood in depressed patients during partial sleep deprivation.

    PubMed

    Hemmeter, Ulrich; Hatzinger, Martin; Brand, Serge; Holsboer-Trachsler, Edith

    2007-11-01

    The antidepressive effect of sleep deprivation (SD) in depressed patients disappears after sleep of the recovery night and after early morning naps. Both can provoke a rapid relapse into depression in SD-responders. In addition, the occurrence of short episodes of sleep (termed microsleep, MS) during partial SD (PSD) is associated with SD-nonresponse, suggesting that MS during the time awake may be related to relapse or PSD-nonresponse. The GABA-benzodiazepine receptor antagonist flumazenil augments vigilance and reduces NonREM-sleep pressure in early morning recovery sleep in volunteers after SD. Therefore, in this study 27 patients with major depression were subjected to a PSD. In a double blind randomized design either flumazenil or placebo was orally applied during PSD in order to examine whether the application of flumazenil reduces sleep propensity and thus, increases antidepressant efficacy of PSD. EEG was registered continuously for 60h by a portable device for the assessment of microsleep episodes at baseline and during PSD. Flumazenil application significantly suppressed frequency and total amount of MS. While the antidepressant efficacy of PSD was not different between flumazenil and placebo during PSD, the subjective mood improved after the recovery night in patients treated with flumazenil. It is concluded that GABAergic mechanisms are involved in the regulation of MS during PSD, which may be related to a mood stabilizing effect after the recovery night. However, the mechanisms underlying the association between the occurrence of MS during PSD and mood variation have to be further clarified. PMID:16978648

  16. 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

  17. Noradrenaline acting on alpha1-adrenoceptor mediates REM sleep deprivation-induced increased membrane potential in rat brain synaptosomes.

    PubMed

    Das, Gitanjali; Mallick, Birendra Nath

    2008-01-01

    We hypothesized that one of the functions of REM sleep is to maintain brain excitability and therefore, REM sleep deprivation is likely to modulate neuronal transmembrane potential; however, so far there was no direct evidence to support the claim. In this study a cationic dye, 3,3'-diethylthiacarbocyanine iodide was used to estimate the potential in synaptosomal samples prepared from control and REM sleep deprived rat brains. The activity of Na-K-ATPase that maintains the transmembrane potential was also estimated in the same sample. Further, the roles of noradrenaline and alpha1-adrenoceptor in mediating the responses were studied both in vivo as well as in vitro. Rats were REM sleep deprived for 4 days by the classical flower-pot method; large platform and recovery controls were carried out in addition to free-moving control. The fluorescence intensity increased in samples prepared from REM sleep deprived rat brain as compared to control, which reflected synaptosomal depolarization after deprivation. The Na-K-ATPase activity also increased in the same deprived sample. Furthermore, both the effects were mediated by noradrenaline acting on alpha1-adrenoceptors in the brain. This is the first direct evidence showing that REM sleep deprivation indeed increased neuronal depolarization, which is the likely cause for increased brain excitability, thus supporting our hypothesis and the effect was mediated by noradrenaline acting through the alpha1-adrenoceptor.

  18. Occupational Sleep Medicine.

    PubMed

    Cheng, Philip; Drake, Christopher

    2016-03-01

    Sleep and circadian rhythms significantly impact almost all aspects of human behavior and are therefore relevant to occupational sleep medicine, which is focused predominantly around workplace productivity, safety, and health. In this article, 5 main factors that influence occupational functioning are reviewed: (1) sleep deprivation, (2) disordered sleep, (3) circadian rhythms, (4) common medical illnesses that affect sleep and sleepiness, and (5) medications that affect sleep and sleepiness. Consequences of disturbed sleep and sleepiness are also reviewed, including cognitive, emotional, and psychomotor functioning and drowsy driving. PMID:26972034

  19. Metabolic complications of obstructive sleep apnea syndrome.

    PubMed

    Ahmed, Qanta A

    2008-01-01

    Obstructive sleep apnea syndrome is a widely prevalent disorder, hallmarked by partial or total upper airway obstruction during sleep. These events fracture sleep integrity resulting in chronic partial sleep deprivation with destructive metabolic sequelae, the focus of this review.

  20. Reducing trial length in force platform posturographic sleep deprivation measurements

    NASA Astrophysics Data System (ADS)

    Forsman, P.; Hæggström, E.; Wallin, A.

    2007-09-01

    Sleepiness correlates with sleep-related accidents, but convenient tests for sleepiness monitoring are scarce. The posturographic test is a method to assess balance, and this paper describes one phase of the development of a posturographic sleepiness monitoring method. We investigated the relationship between trial length and accuracy of the posturographic time-awake (TA) estimate. Twenty-one healthy adults were kept awake for 32 h and their balance was recorded, 16 times with 30 s trials, as a function of TA. The balance was analysed with regards to fractal dimension, most common sway amplitude and time interval for open-loop stance control. While a 30 s trial allows estimating the TA of individual subjects with better than 5 h accuracy, repeating the analysis using shorter trial lengths showed that 18 s sufficed to achieve the targeted 5 h accuracy. Moreover, it was found that with increasing TA, the posturographic parameters estimated the subjects' TA more accurately.

  1. Serotonin turnover in different duration of sleep recovery in discrete regions of young rat brain after 24 h REM sleep deprivation.

    PubMed

    Senthilvelan, M; Ravindran, R; Samson, J; Devi, R Sheela

    2006-09-01

    Sleep plays an important role in restorative function and serotonin (5-hydroxytryptamine: 5HT) equally plays important roles in sleep. Though various studies have revealed the roles of 5HT in sleep/wake cycle, the mechanism involved is yet unclear. In the present study we investigated alteration of the 5HT turnover in various regions of the young rat brains after 24 hours (h) REM sleep (sREM) deprivation to elucidate the roles of 5HT in sleep restoration function in the these regions. The 5HT turnover was evaluated by the ratio of 5-hydroxyindole acetic acid against 5HT. The sREM deprivation was performed by the inverted flowerpot technique. The 5HT turnover showed significant alteration in the all regions of the brain examined after 24h sREM deprivation, particular depending on the brain region. These results revealed that sREM modulates the 5HT turnover in the brain with region specificity and this may be one of the restorative functions of sleep indicating that sREM is regionally generated.

  2. The effects of total sleep deprivation on semantic priming: event-related potential evidence for automatic and controlled processing strategies.

    PubMed

    López Zunini, Rocío; Muller-Gass, Alexandra; Campbell, Kenneth

    2014-02-01

    There is general consensus that performance on a number of cognitive tasks deteriorates following total sleep deprivation. At times, however, subjects manage to maintain performance. This may be because of an ability to switch cognitive strategies including the exertion of compensatory effort. The present study examines the effects of total sleep deprivation on a semantic word priming task. Word priming is unique because it can be carried out using different strategies involving either automatic, effortless or controlled, effortful processing. Twelve subjects were presented with word pairs, a prime and a target, that were either highly semantically associated (cat…dog), weakly associated (cow…barn) or unassociated (apple…road). In order to increase the probability of the use of controlled processing following normal sleep, the subject's task was to determine if the target word was semantically related to the prime. Furthermore, the time between the offset of the prime and the onset of the target was relatively long, permitting the use of an effortful, expectancy-predictive strategy. Event-related potentials (ERPs) were recorded from 64 electrode sites. After normal sleep, RTs were faster and accuracy higher to highly associated targets; this performance advantage was also maintained following sleep deprivation. A large negative deflection, the N400, was larger to weakly associated and unassociated targets in both sleep-deprived and normal conditions. The overall N400 was however larger in the normal sleep condition. Moreover, a long-lasting negative slow wave developed between the offset of the prime and the onset of the target. These physiological measures are consistent with the use of an effortful, predictive strategy following normal sleep but an automatic, effortless strategy following total sleep deprivation. A picture priming task was also run. This task benefits less from the use of a predictive strategy. Accordingly, in this task, ERPs following the

  3. Overexpression of circadian clock protein cryptochrome (CRY) 1 alleviates sleep deprivation-induced vascular inflammation in a mouse model.

    PubMed

    Qin, Bing; Deng, Yunlong

    2015-01-01

    Disturbance of the circadian clock by sleep deprivation has been proposed to be involved in the regulation of inflammation. However, the underlying mechanism of circadian oscillator components in regulating the pro-inflammatory process during sleep deprivation remains poorly understood. Using a sleep deprivation mouse model, we showed here that sleep deprivation increased the expression of pro-inflammatory cytokines expression and decreased the expression of cryptochrome 1 (CRY1) in vascular endothelial cells. Furthermore, the adhesion molecules including intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and E-selectin were elevated in vascular endothelial cells and the monocytes binding to vascular endothelial cells were also increased by sleep deprivation. Interestingly, overexpression of CRY1 in a mouse model by adenovirus vector significantly inhibited the expression of inflammatory cytokines and adhesion molecules, and NF-κB signal pathway activation, as well as the binding of monocytes to vascular endothelial cells. Using a luciferase reporter assay, we found that CRY1 could repress the transcriptional activity of nuclear factor (NF)-κB in vitro. Subsequently, we demonstrated that overexpression of CRY1 inhibited the basal concentration of cyclic adenosine monophosphate (cAMP), leading to decreased protein kinase A activity, which resulted in decreased phosphorylation of p65. Taken together, these results suggested that the overexpression of CRY1 inhibited sleep deprivation-induced vascular inflammation that might be associated with NF-κB and cAMP/PKA pathways.

  4. 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

    2012-05-01

    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.

  5. Total Sleep Deprivation Alters Endothelial Function in Rats: A Nonsympathetic Mechanism

    PubMed Central

    Sauvet, Fabien; Florence, Geneviève; Van Beers, Pascal; Drogou, Catherine; Lagrume, Christophe; Chaumes, Cyrielle; Ciret, Sylvain; Leftheriotis, Georges; Chennaoui, Mounir

    2014-01-01

    Study Objectives: Sleep loss is suspected to induce endothelial dysfunction, a key factor in cardiovascular risk. We examined whether sympathetic activity is involved in the endothelial dysfunction caused by total sleep deprivation (TSD). Design: Two groups: TSD (24-h wakefulness), using slowly rotating wheels, and wheel control (WC). Participants: Seven-month-old male Wistar rats. Interventions: Pharmacological sympathectomy (reserpine, 5 mg/kg, intraperitoneal), nitric oxide synthase (NOS) inhibition (NG-nitro-L-arginine, 20 mg/kg, intraperitoneally 30 min before experiment) and cyclooxygenase (COX) inhibition (indomethacin, 5 mg/kg, intraperitoneally 30 min before experiment). Measurements and Results: In protocol 1, changes in heart rate (HR) and blood pressure were continuously recorded in the sympathectomized and non-sympathectomized rats. Blood pressure and HR increased during TSD in non-sympathectomized rats. In protocol 2, changes in skin blood flow (vasodilation) were assessed in the sympathectomized and non-sympathectomized rats using laser-Doppler flowmetry coupled with iontophoretic delivery of acetylcholine (ACh), sodium nitroprusside (SNP), and anodal and cathodal currents. ACh- and cathodal current-induced vasodilations were significantly attenuated after TSD in non-sympathectomized and sympathectomized rats (51% and 60%, respectively). In protocol 3, ACh-induced vasodilation was attenuated after NOS and COX inhibition (66% and 49%, respectively). Cathodal current-induced vasodilation decreased by 40% after COX inhibition. In TSD compared to WC a decrease in ACh-induced vasodilation was still observed after COX inhibition. No changes in SNP- and anodal current-induced vasodilation were detected. Conclusion: These results demonstrate that total sleep deprivation induces a reduction in endothelial-dependent vasodilation. This endothelial dysfunction is independent of blood pressure and sympathetic activity but associated with nitric oxide synthase and

  6. 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. PMID:10327892

  7. The effect of sleep deprivation on the encoding of contextual and non-contextual aspects of emotional memory.

    PubMed

    Tempesta, Daniela; Socci, Valentina; Coppo, Martina; Dello Ioio, Giada; Nepa, Valeria; De Gennaro, Luigi; Ferrara, Michele

    2016-05-01

    Sleep loss affects emotional memory, but the specific effects on its contextual and non-contextual aspects are unknown. In this study we investigated the possible differential influence of one night of sleep deprivation on the encoding and subsequent recall of these two aspects of emotional information. Forty-eight healthy subjects, divided in a sleep deprivation (SD) and a well-rested group (WR), completed two testing sessions: the encoding session took place after one night of sleep for the WR and after one night of sleep deprivation for the SD group; the recall session after two nights of recovery sleep for both groups. During the encoding session, 6 clips of films of different valence (2 positive, 2 neutral and 2 negative) were presented to the participants. During the recall session, the non-contextual emotional memory was assessed by a recognition task, while the contextual emotional memory was evaluated by a temporal order task. The SD group showed a worst non-contextual recognition of positive and neutral events compared to WR subjects, while recognition of negative items was similar in the two groups. Instead, the encoding of the temporal order resulted deteriorated in the SD participants, independent of the emotional valence of the items. These results indicate that sleep deprivation severely impairs the encoding of both contextual and non-contextual aspects of memory, resulting in significantly worse retention two days later. However, the preserved recognition of negative non-contextual events in sleep deprived subjects suggests that the encoding of negative stimuli is more "resistant" to the disruptive effects of sleep deprivation. PMID:26976090

  8. The effect of acute sleep deprivation and fatigue in cardiovascular perfusion students: a mixed methods study.

    PubMed

    Hodge, Ashley B; Snyder, Alexandra C; Fernandez, Adam L; Boan, Andrea D; Malek, Angela M; Sistino, Joseph J

    2012-09-01

    Sleep deprivation as a result of long working hours has been associated with an increased risk of adverse events in healthcare professions but not in cardiovascular perfusion. The purpose of this study is to investigate the impact of sleep deprivation on cardiovascular perfusion students. Testing with high-fidelity simulation after 24 hours of sleep deprivation allowed investigators to assess user competency and the effect of fatigue on performance. After informed consent, seven senior perfusion students were enrolled in the study (three declined to participate). The qualitative portion of the study included a focus group session, whereas the quantitative portion included administration of questionnaires, including the Epworth Sleepiness Scale (ESS) and the Stanford Sleepiness Scale (SSS), as well as clinical skills assessment using high-fidelity simulation. Subjects were assessed at three different intervals of sleep deprivation over a 24-hour period: baseline (6:00 AM), 12 hours (6:00 PM), 16 hours (10:00 PM), and 24 hours (6:00 AM) of wakefulness. During each scenario, normally monitored bypass parameters, including mean arterial pressure, activated clotting times, partial pressures of oxygen, partial pressures of carbon dioxide, and venous flow, were manipulated, and the subjects were required to return the parameters to normal levels. In addition, the scenario required calculation of the final protamine dose (using a dose-response curve) and detection of electrocardiography changes. Each task was varied at the different simulation sessions to decrease the effect of learning. Despite any lack of sleep, we hypothesized that, because of repetition, the times to complete the task would decrease at each session. We also hypothesized that the ESS and SSS scores would increase over time. We expected that the students would anticipate which tasks were being evaluated and would react more quickly. The average ESS scores progressively increased at each time period

  9. The Effect of Acute Sleep Deprivation and Fatigue in Cardiovascular Perfusion Students: A Mixed Methods Study

    PubMed Central

    Hodge, Ashley B.; Snyder, Alexandra C.; Fernandez, Adam L.; Boan, Andrea D.; Malek, Angela M.; Sistino, Joseph J.

    2012-01-01

    Abstract: Sleep deprivation as a result of long working hours has been associated with an increased risk of adverse events in healthcare professions but not in cardiovascular perfusion. The purpose of this study is to investigate the impact of sleep deprivation on cardiovascular perfusion students. Testing with highfidelity simulation after 24 hours of sleep deprivation allowed investigators to assess user competency and the effect of fatigue on performance. After informed consent, seven senior perfusion students were enrolled in the study (three declined to participate). The qualitative portion of the study included a focus group session, whereas the quantitative portion included administration of questionnaires, including the Epworth Sleepiness Scale (ESS) and the Stanford Sleepiness Scale (SSS), as well as clinical skills assessment using high-fidelity simulation. Subjects were assessed at three different intervals of sleep deprivation over a 24-hour period: baseline (6:00 am), 12 hours (6:00 pm), 16 hours (10:00 pm), and 24 hours (6:00 am) of wakefulness. During each scenario, normally monitored bypass parameters, including mean arterial pressure, activated clotting times, partial pressures of oxygen, partial pressures of carbon dioxide, and venous flow, were manipulated, and the subjects were required to return the parameters to normal levels. In addition, the scenario required calculation of the final protamine dose (using a dose–response curve) and detection of electrocardiography changes. Each task was varied at the different simulation sessions to decrease the effect of learning. Despite any lack of sleep, we hypothesized that, because of repetition, the times to complete the task would decrease at each session. We also hypothesized that the ESS and SSS scores would increase over time. We expected that the students would anticipate which tasks were being evaluated and would react more quickly. The average ESS scores progressively increased at each time

  10. The effect of acute sleep deprivation and fatigue in cardiovascular perfusion students: a mixed methods study.

    PubMed

    Hodge, Ashley B; Snyder, Alexandra C; Fernandez, Adam L; Boan, Andrea D; Malek, Angela M; Sistino, Joseph J

    2012-09-01

    Sleep deprivation as a result of long working hours has been associated with an increased risk of adverse events in healthcare professions but not in cardiovascular perfusion. The purpose of this study is to investigate the impact of sleep deprivation on cardiovascular perfusion students. Testing with high-fidelity simulation after 24 hours of sleep deprivation allowed investigators to assess user competency and the effect of fatigue on performance. After informed consent, seven senior perfusion students were enrolled in the study (three declined to participate). The qualitative portion of the study included a focus group session, whereas the quantitative portion included administration of questionnaires, including the Epworth Sleepiness Scale (ESS) and the Stanford Sleepiness Scale (SSS), as well as clinical skills assessment using high-fidelity simulation. Subjects were assessed at three different intervals of sleep deprivation over a 24-hour period: baseline (6:00 AM), 12 hours (6:00 PM), 16 hours (10:00 PM), and 24 hours (6:00 AM) of wakefulness. During each scenario, normally monitored bypass parameters, including mean arterial pressure, activated clotting times, partial pressures of oxygen, partial pressures of carbon dioxide, and venous flow, were manipulated, and the subjects were required to return the parameters to normal levels. In addition, the scenario required calculation of the final protamine dose (using a dose-response curve) and detection of electrocardiography changes. Each task was varied at the different simulation sessions to decrease the effect of learning. Despite any lack of sleep, we hypothesized that, because of repetition, the times to complete the task would decrease at each session. We also hypothesized that the ESS and SSS scores would increase over time. We expected that the students would anticipate which tasks were being evaluated and would react more quickly. The average ESS scores progressively increased at each time period

  11. Replication and Pedagogy in the History of Psychology IV: Patrick and Gilbert (1896) on Sleep Deprivation

    NASA Astrophysics Data System (ADS)

    Fuchs, Thomas; Burgdorf, Jeffrey

    2008-05-01

    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 first formally trained psychologists. We attempted to recreate the original experience in two subjects, using similar apparatus and methodology, and drawing direct comparisons to the original study whenever possible. We argue for a strong influence of an ‘Americanized’ Wundtian psychology on Patrick and Gilbert, a claim supported biographically by their education and by their experimental methods. The replication thus opens interesting new perspectives, which are unlikely to be generated by any other historical approach.

  12. 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.

  13. 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. PMID:17937364

  14. Blockage of dopaminergic D(2) receptors produces decrease of REM but not of slow wave sleep in rats after REM sleep deprivation.

    PubMed

    Lima, Marcelo M S; Andersen, Monica L; Reksidler, Angela B; Silva, Andressa; Zager, Adriano; Zanata, Sílvio M; Vital, Maria A B F; Tufik, Sergio

    2008-04-01

    Dopamine (DA) has, as of late, become singled out from the profusion of other neurotransmitters as what could be called a key substance, in the regulation of the sleep-wake states. We have hypothesized that dopaminergic D(2) receptor blockage induced by haloperidol could generate a reduction or even an ablation of rapid eye movement (REM) sleep. Otherwise, the use of the selective D(2) agonist, piribedil, could potentiate REM sleep. Electrophysiological findings demonstrate that D(2) blockage produced a dramatic reduction of REM sleep during the rebound (REB) period after 96 h of REM sleep deprivation (RSD). This reduction of REM sleep was accompanied by an increment in SWS, which is possibly accounted for the observed increase in the sleep efficiency. Conversely, our findings also demonstrate that the administration of piribedil did not generate additional increase of REM sleep. Additionally, D(2) receptors were found down-regulated, in the haloperidol group, after RSD, and subsequently up-regulated after REB group, contrasting to the D(1) down-regulation at the same period. In this sense, the current data indicate a participation of the D(2) receptor for REM sleep regulation and consequently in the REM sleep/SWS balance. Herein, we propose that the mechanism underlying the striatal D(2) up-regulation is due to an effect as consequence of RSD which originally produces selective D(2) supersensitivity, and after its period probably generates a surge in D(2) expression. In conclusion we report a particular action of the dopaminergic neurotransmission in REM sleep relying on D(2) activation.

  15. One night of partial sleep deprivation affects habituation of hypothalamus and skin conductance responses.

    PubMed

    Peters, Anja C; Blechert, Jens; Sämann, Philipp G; Eidner, Ines; Czisch, Michael; Spoormaker, Victor I

    2014-09-15

    Sleep disturbances are prevalent in clinical anxiety, but it remains unclear whether they are cause and/or consequence of this condition. Fear conditioning constitutes a valid laboratory model for the acquisition of normal and pathological anxiety. To explore the relationship between disturbed sleep and anxiety in more detail, the present study evaluated the effect of partial sleep deprivation (SD) on fear conditioning in healthy individuals. The neural correlates of 1) nonassociative learning and physiological processing and 2) associative learning (differential fear conditioning) were addressed. Measurements entailed simultaneous functional MRI, EEG, skin conductance response (SCR), and pulse recordings. Regarding nonassociative learning, partial SD resulted in a generalized failure to habituate during fear conditioning, as evidenced by reduced habituation of SCR and hypothalamus responses to all stimuli. Furthermore, SCR and hypothalamus activity were correlated, supporting their functional relationship. Regarding associative learning, effects of partial SD on the acquisition of conditioned fear were weaker and did not reach statistical significance. The hypothalamus plays an integral role in the regulation of sleep and autonomic arousal. Thus sleep disturbances may play a causal role in the development of normal and possibly pathological fear by increasing the susceptibility of the sympathetic nervous system to stressful experiences.

  16. Role of the ovarian cycle on neural cardiovascular control in sleep-deprived women

    PubMed Central

    Yang, Huan; Durocher, John J.; Larson, Robert A.

    2014-01-01

    The midluteal (ML) phase of the ovarian cycle is often sympathoexcitatory compared with the early follicular (EF) phase. We recently reported that 24-h total sleep deprivation (TSD) augmented cardiovascular reactivity in both men and women, but that sex differences existed in resting muscle sympathetic nerve activity (MSNA) responses to TSD. In the present study, we hypothesized increased resting MSNA and augmented cardiovascular reactivity to acute laboratory stressors during the ML phase in sleep-deprived women. Heart rate (HR), mean arterial pressure (MAP), forearm vascular conductance (FVC), and MSNA were measured in 14 eumenorrheic women (age, 20 ± 1 yr) during 10 min supine rest, 5 min mental stress (MS) trial, and 2 min cold pressor test (CPT) trial. Subjects were tested twice after TSD: once during EF phase and once during ML phase (randomized, crossover design). Estradiol (29 ± 2 vs. 63 ± 8 pg/ml, P = 0.001) and progesterone (1.6 ± 0.2 vs. 4.4 ± 0.7 ng/ml, P = 0.002) were elevated during the ML phase. Resting supine MAP (75 ± 2 vs. 72 ± 1 mmHg, P = 0.042) was lower during the ML phase. In contrast, resting supine HR, MSNA, and FVC were not significantly different between EF and ML phases. MAP, HR and FVC reactivity to MS were not statistically different between the EF and ML phases. Similarly, MAP and HR reactivity to CPT were not different between the ovarian phases. Contrary to our original hypothesis, the ML phase was not associated with sympathoexcitation or exaggerated cardiovascular reactivity in sleep-deprived premenopausal women. However, our data reveal elevated resting blood pressure during the EF phase in sleep-deprived women. PMID:25539931

  17. Role of the ovarian cycle on neural cardiovascular control in sleep-deprived women.

    PubMed

    Yang, Huan; Durocher, John J; Larson, Robert A; Carter, Jason R

    2015-02-15

    The midluteal (ML) phase of the ovarian cycle is often sympathoexcitatory compared with the early follicular (EF) phase. We recently reported that 24-h total sleep deprivation (TSD) augmented cardiovascular reactivity in both men and women, but that sex differences existed in resting muscle sympathetic nerve activity (MSNA) responses to TSD. In the present study, we hypothesized increased resting MSNA and augmented cardiovascular reactivity to acute laboratory stressors during the ML phase in sleep-deprived women. Heart rate (HR), mean arterial pressure (MAP), forearm vascular conductance (FVC), and MSNA were measured in 14 eumenorrheic women (age, 20 ± 1 yr) during 10 min supine rest, 5 min mental stress (MS) trial, and 2 min cold pressor test (CPT) trial. Subjects were tested twice after TSD: once during EF phase and once during ML phase (randomized, crossover design). Estradiol (29 ± 2 vs. 63 ± 8 pg/ml, P = 0.001) and progesterone (1.6 ± 0.2 vs. 4.4 ± 0.7 ng/ml, P = 0.002) were elevated during the ML phase. Resting supine MAP (75 ± 2 vs. 72 ± 1 mmHg, P = 0.042) was lower during the ML phase. In contrast, resting supine HR, MSNA, and FVC were not significantly different between EF and ML phases. MAP, HR and FVC reactivity to MS were not statistically different between the EF and ML phases. Similarly, MAP and HR reactivity to CPT were not different between the ovarian phases. Contrary to our original hypothesis, the ML phase was not associated with sympathoexcitation or exaggerated cardiovascular reactivity in sleep-deprived premenopausal women. However, our data reveal elevated resting blood pressure during the EF phase in sleep-deprived women. PMID:25539931

  18. Sleep deprivation alters choice strategy without altering uncertainty or loss aversion preferences.

    PubMed

    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.

  19. Adaptation of Sensorimotor Coupling in Postural Control Is Impaired by Sleep Deprivation

    PubMed Central

    2015-01-01

    The purpose of the study was to investigate the effects of sleep deprivation (SD) in adaptation of the coupling between visual information and body sway in young adults’ postural control due to changes in optic flow characteristics. Fifteen young adults were kept awake for approximately 25 hours and formed the SD group, while fifteen adults who slept normally the night before the experiment participated as part of the control group. All participants stood as still as possible in a moving room before and after being exposed to one trial with higher amplitude and velocity of room movement. Postural performance and the coupling between visual information, provided by a moving room, and body sway were examined. Results showed that after an abrupt change in visual cues, larger amplitude, and higher velocity of the room, the influence of room motion on body sway was decreased in both groups. However, such a decrease was less pronounced in sleep deprived as compared to control subjects. Sleep deprived adults were able to adapt motor responses to the environmental change provided by the increase in room motion amplitude. Nevertheless, they were not as efficient as control subjects in doing so, which demonstrates that SD impairs the ability to adapt sensorimotor coupling while controlling posture when a perturbation occurs. PMID:25799560

  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. Aerobic exercise attenuates inhibitory avoidance memory deficit induced by paradoxical sleep deprivation in rats.

    PubMed

    Fernandes, Jansen; Baliego, Luiz Guilherme Zaccaro; Peixinho-Pena, Luiz Fernando; de Almeida, Alexandre Aparecido; Venancio, Daniel Paulino; Scorza, Fulvio Alexandre; de Mello, Marco Tulio; Arida, Ricardo Mario

    2013-09-01

    The deleterious effects of paradoxical sleep deprivation (SD) on memory processes are well documented. Physical exercise improves many aspects of brain functions and induces neuroprotection. In the present study, we investigated the influence of 4 weeks of treadmill aerobic exercise on both long-term memory and the expression of synaptic proteins (GAP-43, synapsin I, synaptophysin, and PSD-95) in normal and sleep-deprived rats. Adult Wistar rats were subjected to 4 weeks of treadmill exercise training for 35 min, five times per week. Twenty-four hours after the last exercise session, the rats were sleep-deprived for 96 h using the modified multiple platform method. To assess memory after SD, all animals underwent training for the inhibitory avoidance task and were tested 24h later. The aerobic exercise attenuated the long-term memory deficit induced by 96 h of paradoxical SD. Western blot analysis of the hippocampus revealed increased levels of GAP-43 in exercised rats. However, the expression of synapsin I, synaptophysin, and PSD-95 was not modified by either exercise or SD. Our results suggest that an aerobic exercise program can attenuate the deleterious effects of SD on long-term memory and that this effect is not directly related to changes in the expression of the pre- and post-synaptic proteins analyzed in the study.

  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. Alcohol disrupts sleep homeostasis.

    PubMed

    Thakkar, Mahesh M; Sharma, Rishi; Sahota, Pradeep

    2015-06-01

    Alcohol is a potent somnogen and one of the most commonly used "over the counter" sleep aids. In healthy non-alcoholics, acute alcohol decreases sleep latency, consolidates and increases the quality (delta power) and quantity of NREM sleep during the first half of the night. However, sleep is disrupted during the second half. Alcoholics, both during drinking periods and during abstinences, suffer from a multitude of sleep disruptions manifested by profound insomnia, excessive daytime sleepiness, and altered sleep architecture. Furthermore, subjective and objective indicators of sleep disturbances are predictors of relapse. Finally, within the USA, it is estimated that societal costs of alcohol-related sleep disorders exceeds $18 billion. Thus, although alcohol-associated sleep problems have significant economic and clinical consequences, very little is known about how and where alcohol acts to affect sleep. In this review, we have described our attempts to unravel the mechanism of alcohol-induced sleep disruptions. We have conducted a series of experiments using two different species, rats and mice, as animal models. We performed microdialysis, immunohistochemical, pharmacological, sleep deprivation and lesion studies which suggest that the sleep-promoting effects of alcohol may be mediated via alcohol's action on the mediators of sleep homeostasis: adenosine (AD) and the wake-promoting cholinergic neurons of the basal forebrain (BF). Alcohol, via its action on AD uptake, increases extracellular AD resulting in the inhibition of BF wake-promoting neurons. Since binge alcohol consumption is a highly prevalent pattern of alcohol consumption and disrupts sleep, we examined the effects of binge drinking on sleep-wakefulness. Our results suggest that disrupted sleep homeostasis may be the primary cause of sleep disruption observed following binge drinking. Finally, we have also shown that sleep disruptions observed during acute withdrawal, are caused due to impaired

  4. Diagnosing Sleep Disorders | NIH MedlinePlus the Magazine

    MedlinePlus

    ... page please turn Javascript on. Feature: Are You Sleep-Deprived? Diagnosing Sleep Disorders Past Issues / Summer 2012 Table of Contents ... reach REM sleep during their naps. What are Sleep Studies? Sleep studies are tests that measure how ...

  5. Sleep-wake behavior and responses to sleep deprivation of mice lacking both interleukin-1 beta receptor 1 and tumor necrosis factor-alpha receptor 1.

    PubMed

    Baracchi, Francesca; Opp, Mark R

    2008-08-01

    Data indicate that interleukin (IL)-1 beta and tumor necrosis factor-alpha (TNFalpha) are involved in the regulation of non-rapid eye movement sleep (NREMS). Previous studies demonstrate that mice lacking the IL-1 beta type 1 receptor spend less time in NREMS during the light period, whereas mice lacking the p55 (type 1) receptor for TNFalpha spend less time in NREMS during the dark period. To further investigate roles for IL-1 beta and TNFalpha in sleep regulation we phenotyped sleep and responses to sleep deprivation of mice lacking both the IL-1 beta receptor 1 and TNFalpha receptor 1 (IL-1R1/TNFR1 KO). Male adult mice (IL-1R1/TNFR1 KO, n=14; B6129SF2/J, n=14) were surgically instrumented with EEG electrodes and with a thermistor to measure brain temperature. After recovery and adaptation to the recording apparatus, 48 h of undisturbed baseline recordings were obtained. Mice were then subjected to 6h sleep deprivation at light onset by gentle handling. IL-1R1/TNFR1 KO mice spent less time in NREMS during the last 6h of the dark period and less time in rapid eye movement sleep (REMS) during the light period. There were no differences between strains in the diurnal timing of delta power during NREMS. However, there were strain differences in the relative power spectra of the NREMS EEG during both the light period and the dark period. In addition, during the light period relative power in the theta frequency band of the REMS EEG differed between strains. After sleep deprivation, control mice exhibited prolonged increases in NREMS and REMS, whereas the duration of the NREMS increase was shorter and there was no increase in REMS of IL-1R1/TNFR1 KO mice. Delta power during NREMS increased in both strains after sleep deprivation, but the increase in delta power during NREMS of IL-1R1/TNFR1 KO mice was of greater magnitude and of longer duration than that observed in control mice. These results provide additional evidence that the IL-1 beta and TNFalpha cytokine systems

  6. Sleep-wake behavior and responses to sleep deprivation of mice lacking both interleukin-1 beta receptor 1 and tumor necrosis factor-alpha receptor 1.

    PubMed

    Baracchi, Francesca; Opp, Mark R

    2008-08-01

    Data indicate that interleukin (IL)-1 beta and tumor necrosis factor-alpha (TNFalpha) are involved in the regulation of non-rapid eye movement sleep (NREMS). Previous studies demonstrate that mice lacking the IL-1 beta type 1 receptor spend less time in NREMS during the light period, whereas mice lacking the p55 (type 1) receptor for TNFalpha spend less time in NREMS during the dark period. To further investigate roles for IL-1 beta and TNFalpha in sleep regulation we phenotyped sleep and responses to sleep deprivation of mice lacking both the IL-1 beta receptor 1 and TNFalpha receptor 1 (IL-1R1/TNFR1 KO). Male adult mice (IL-1R1/TNFR1 KO, n=14; B6129SF2/J, n=14) were surgically instrumented with EEG electrodes and with a thermistor to measure brain temperature. After recovery and adaptation to the recording apparatus, 48 h of undisturbed baseline recordings were obtained. Mice were then subjected to 6h sleep deprivation at light onset by gentle handling. IL-1R1/TNFR1 KO mice spent less time in NREMS during the last 6h of the dark period and less time in rapid eye movement sleep (REMS) during the light period. There were no differences between strains in the diurnal timing of delta power during NREMS. However, there were strain differences in the relative power spectra of the NREMS EEG during both the light period and the dark period. In addition, during the light period relative power in the theta frequency band of the REMS EEG differed between strains. After sleep deprivation, control mice exhibited prolonged increases in NREMS and REMS, whereas the duration of the NREMS increase was shorter and there was no increase in REMS of IL-1R1/TNFR1 KO mice. Delta power during NREMS increased in both strains after sleep deprivation, but the increase in delta power during NREMS of IL-1R1/TNFR1 KO mice was of greater magnitude and of longer duration than that observed in control mice. These results provide additional evidence that the IL-1 beta and TNFalpha cytokine systems

  7. Childhood epilepsy and sleep

    PubMed Central

    Al-Biltagi, Mohammed A

    2014-01-01

    Sleep and epilepsy are two well recognized conditions that interact with each other in a complex bi-directional way. Some types of epilepsies have increased activity during sleep disturbing it; while sleep deprivation aggravates epilepsy due to decreased seizure threshold. Epilepsy can deteriorate the sleep-related disorders and at the same time; the parasomnias can worsen the epilepsy. The secretion of sleep-related hormones can also be affected by the occurrence of seizures and supplementation of epileptic patients with some of these sleep-related hormones may have a beneficial role in controlling epilepsy. PMID:25254184

  8. Adenosine and sleep

    SciTech Connect

    Yanik, G.M. Jr.

    1987-01-01

    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% and 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.

  9. Differential effects of paradoxical sleep deprivation on memory and oxidative stress.

    PubMed

    Lima, Alisson Menezes Araujo; de Bruin, Veralice Meireles Sales; Rios, Emiliano Ricardo Vasconcelos; de Bruin, Pedro Felipe Carvalhedo

    2014-05-01

    Sleep has important functions for every organ in the body and sleep deprivation (SD) leads to disorders that cause irreparable damage. The aim of this study was to investigate behavioral and brain structural alterations in mice deprived of paradoxical sleep for 48 and 72 h. Working memory, aversive memory as well as levels of nitric oxide (NO) and thiobarbituric acid reactive substances (TBARS) in the hippocampus, body striatum, and prefrontal cortex were evaluated. Working memory was affected in the 48- and 72-h SD groups while aversive memory was altered only in the 48-h SD group (p ≤ 0.05). Our findings showed that SD reduces NO levels in most brain areas (p < 0.05): NO levels were unaltered in the striatum of animals sleep-deprived for 48 h. Higher levels of TBARS were observed in all areas of the SD groups (p ≤ 0.05). Thus, we confirmed that SD has duration-dependent effects on behavior as well as on NO and TBARS levels in the brain. Preserved striatum NO levels suggest that this structure is less vulnerable to oxidative stress and is only affected by SD of longer duration. Increased TBARS and reduced NO levels in the hippocampus and prefrontal cortex confirm a central role for both these structures in working memory and aversive memory. Contextual fear conditioning was not affected by longer periods of SD. Thus, our findings suggest that shorter SD time may be more beneficial to avoid aversive memory where this may have implications for the management of posttraumatic stress.

  10. Sleep Deprivation Impairs Object-Selective Attention: A View from the Ventral Visual Cortex

    PubMed Central

    Lim, Julian; Tan, Jiat Chow; Parimal, Sarayu; Dinges, David F.; Chee, Michael W. L.

    2010-01-01

    Background 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. Methodology/Principal Findings 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. Conclusions/Significance 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. PMID:20140099

  11. 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

  12. Sleep Quiz

    MedlinePlus

    Skip Navigation Bar Home Current Issue Past Issues Sleep Quiz Past Issues / Summer 2007 Table of Contents ... on. Photo: iStock Take the National Center on Sleep Disorders Research Sleep Quiz TRUE OR FALSE ? _____1. ...

  13. Sleep Quiz

    MedlinePlus

    ... Home » About the NHLBI » Organization » National Center on Sleep Disorders Research (NCSDR) » Patient & Public Information » Sleep Quiz National Center on Sleep Disorders Research Research Professional Education Patient & Public Information Communications ...

  14. Slow wave activity and slow oscillations in sleepwalkers and controls: effects of 38 h of sleep deprivation.

    PubMed

    Perrault, Rosemarie; Carrier, Julie; Desautels, Alex; Montplaisir, Jacques; Zadra, Antonio

    2013-08-01

    Sleepwalkers have been shown to have an unusually high number of arousals from slow wave sleep and lower slow wave activity (SWA) power during the night than controls. Because sleep deprivation increases the frequency of slow wave sleep (SWS) arousals in sleepwalkers, it may also affect the expression of the homeostatic process to a greater extent than shown previously. We thus investigated SWA power as well as slow wave oscillation (SWO) density in 10 sleepwalkers and nine controls at baseline and following 38 h of sleep deprivation. There was a significant increase in SWA during participants' recovery sleep, especially during their second non-rapid eye movement (NREM) period. SWO density was similarly increased during recovery sleep's first two NREM periods. A fronto-central gradient in SWA and SWO was also present on both nights. However, no group differences were noted on any of the 2 nights on SWA or SWO. This unexpected result may be related to the heterogeneity of sleepwalkers as a population, as well as our small sample size. SWA pressure after extended sleep deprivation may also result in a ceiling effect in both sleepwalkers and controls. PMID:23398262

  15. Slow wave activity and slow oscillations in sleepwalkers and controls: effects of 38 h of sleep deprivation.

    PubMed

    Perrault, Rosemarie; Carrier, Julie; Desautels, Alex; Montplaisir, Jacques; Zadra, Antonio

    2013-08-01

    Sleepwalkers have been shown to have an unusually high number of arousals from slow wave sleep and lower slow wave activity (SWA) power during the night than controls. Because sleep deprivation increases the frequency of slow wave sleep (SWS) arousals in sleepwalkers, it may also affect the expression of the homeostatic process to a greater extent than shown previously. We thus investigated SWA power as well as slow wave oscillation (SWO) density in 10 sleepwalkers and nine controls at baseline and following 38 h of sleep deprivation. There was a significant increase in SWA during participants' recovery sleep, especially during their second non-rapid eye movement (NREM) period. SWO density was similarly increased during recovery sleep's first two NREM periods. A fronto-central gradient in SWA and SWO was also present on both nights. However, no group differences were noted on any of the 2 nights on SWA or SWO. This unexpected result may be related to the heterogeneity of sleepwalkers as a population, as well as our small sample size. SWA pressure after extended sleep deprivation may also result in a ceiling effect in both sleepwalkers and controls.

  16. Sleep locally, act globally.

    PubMed

    Rattenborg, Niels C; Lima, Steven L; Lesku, John A

    2012-10-01

    In most animals, sleep is considered a global brain and behavioral state. However, recent intracortical recordings have shown that aspects of non-rapid eye movement (NREM) sleep and wakefulness can occur simultaneously in different parts of the cortex in mammals, including humans. Paradoxically, however, NREM sleep still manifests as a global behavioral shutdown. In this review, the authors examine this paradox from an evolutionary perspective. On the basis of strategic modeling, they suggest that in animals with brains composed of heavily interconnected and functionally interdependent units, a global regulator of sleep maintains the behavioral shutdown that defines sleep and thereby ensures that local use-dependent functions are performed in a safe and efficient manner. This novel perspective has implications for understanding deficits in human cognitive performance resulting from sleep deprivation, sleep disorders such as sleepwalking, changes in consciousness that occur during sleep, and the function of sleep itself. PMID:22572533

  17. The effects of leptin on REM sleep and slow wave delta in rats are reversed by food deprivation.

    PubMed

    Sinton, C M; Fitch, T E; Gershenfeld, H K

    1999-09-01

    Leptin (ob protein) is an adipose tissue derived circulating hormone that acts at specific receptors in the hypothalamus to reduce food intake. The protein is also critically involved in energy balance and metabolic status. Here the effect of leptin on sleep architecture in rats was evaluated because food consumption and metabolic status are known to influence sleep. Sprague-Dawley rats were chronically implanted with electrodes for EEG and EMG recording and diurnal sleep parameters were quantified over 9-h periods following leptin administration. Murine recombinant leptin (rMuLep) was administered systemically to rats that either had undergone 18 h of prior food deprivation or had received food ad libitum. In the normally fed rats, leptin significantly decreased the duration of rapid eye movement sleep (REMS) by about 30% and increased the duration of slow wave sleep (SWS) by about 13%, the latter effect reflecting enhanced power in the delta frequency band. These results are consistent with studies that have linked changes in metabolic rate with effects on sleep. Leptin administration has previously been shown to alter neuroendocrine parameters that could have mediated these changes in sleep architecture. Unexpectedly, prior food deprivation negated the effect of leptin on both REMS and SWS, a result that emphasizes the significance of the apparent coupling between sleep parameters and energy status.

  18. A Local, Bottom-Up Perspective on Sleep Deprivation and Neurobehavioral Performance

    PubMed Central

    Van Dongen, Hans P.A.; Belenky, Gregory; Krueger, James M.

    2011-01-01

    Waking neurobehavioral performance is temporally regulated by a sleep/wake homeostatic process and a circadian process in interaction with a time-on-task effect. Neurobehavioral impairment resulting from these factors is task-specific, and characterized by performance variability. Several aspects of these phenomena are not well understood, and cannot be explained solely by a top-down (subcortically driven) view of sleep/wake and performance regulation. We present a bottom-up theory, where we postulate that task performance is degraded by local, use-dependent sleep in neuronal groups subserving cognitive processes associated with the task at hand. The theory offers explanations for the temporal dependence of neurobehavioral performance on time awake, time on task, and their interaction; for the effectiveness of task switching and rest breaks to overcome the time-on-task effect (but not the effects of sleep deprivation); for the task-specific nature of neurobehavioral impairment; and for the stochastic property of performance variability. PMID:21906023

  19. REM sleep deprivation generates cognitive and neurochemical disruptions in the intranigral rotenone model of Parkinson's disease.

    PubMed

    Dos Santos, Ana Carolina D; Castro, Marcela Alexandra V; Jose, Elis Angela K; Delattre, Ana Márcia; Dombrowski, Patrícia A; Da Cunha, Claudio; Ferraz, Anete C; Lima, Marcelo M S

    2013-11-01

    The recently described intranigral rotenone model of Parkinson's disease (PD) in rodents provides an interesting model for studying mechanisms of toxin-induced dopaminergic neuronal injury. The relevance of this model remains unexplored with regard to sleep disorders that occur in PD. On this basis, the construction of a PD model depicting several behavioral and neurochemical alterations related to sleep would be helpful in understanding the association between PD and sleep regulation. We performed bilateral intranigral injections of rotenone (12 μg) on day 0 and the open-field test initially on day 20 after rotenone. Acquisition phase of the object-recognition test, executed also during day 20, was followed by an exact period of 24 hr of rapid eye movement (REM) sleep deprivation (REMSD; day 21). In the subsequent day (22), the rats were re-exposed to the open-field test and to the object-recognition test (choice phase). After the last session of behavioral tests, the rat brains were immediately dissected, and their striata were collected for neurochemical purposes. We observed that a brief exposure to REMSD was able to impair drastically the object-recognition test, similarly to a nigrostriatal lesion promoted by intranigral rotenone. However, the combination of REMSD and rotenone surprisingly did not inflict memory impairment, concomitant with a moderate compensatory mechanism mediated by striatal dopamine release. In addition, we demonstrated the existence of changes in serotonin and noradrenaline neurotransmissions within the striatum mostly as a function of REMSD and REMSD plus rotenone, respectively.

  20. REM sleep deprivation increases the expression of interleukin genes in mice hypothalamus.

    PubMed

    Kang, Won Sub; Park, Hae Jeong; Chung, Joo-Ho; Kim, Jong Woo

    2013-11-27

    Recently, evidence has suggested the possible involvement of inflammatory cytokines in sleep deprivation (SD). In this study, we assessed the patterns of inflammatory gene regulation in the hypothalamus of REM SD mice. C57BL/6 mice were randomly assigned to two groups, SD (n=15) and control groups (n=15). Mice in the SD group were sleep-deprived for 72h using modified multiple platforms. Microarray analysis on inflammatory genes was performed in mice hypothalamus. In addition, interleukin 1 beta (IL1β) protein expression was analyzed by the immunochemistry method. Through microarray analysis, we found that expressions of IL subfamily genes, such as IL1β (2.55-fold), IL18 (1.92-fold), IL11 receptor alpha chain 1 (1.48-fold), IL5 (1.41-fold), and IL17E genes (1.31-fold), were up-regulated in the hypothalamus of SD mice compared to the control. The increase in the expression of these genes was also confirmed by RT-PCR. Among these genes, the expression of IL1β was particularly increased in the hypothalamus of SD mice. Interestingly, we found that the protein expression of endogenous IL1β was also elevated in the hypothalamus of SD mice compared to the control mice. These results implicate that IL subfamily genes, and in particular, IL1β, may play a role in sleep regulation in the hypothalamus of REM SD mice.

  1. Dual conception of risk in the Iowa Gambling Task: effects of sleep deprivation and test-retest gap

    PubMed Central

    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

  2. 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

  3. 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

  4. Effects of chronic sleep deprivation on autonomic activity by examining heart rate variability, plasma catecholamine, and intracellular magnesium levels.

    PubMed

    Takase, Bonpei; Akima, Takashi; Satomura, Kimio; Ohsuzu, Fumitaka; Mastui, Takemi; Ishihara, Masayuki; Kurita, Akira

    2004-10-01

    Chronic sleep deprivation is associated with cardiovascular events. In addition, autonomic activity determined from the levels of the heart rate variability (HRV), plasma catecholamine, and intracellular magnesium (Mg) are important in the pathophysiology of cardiovascular events. This study therefore aimed to determine the effects of chronic sleep deprivation on autonomic activity by examining the HRV, plasma catecholamine, and intracellular magnesium levels. Thirty (30) healthy male college students ranging in age from 20 to 24 years of age (average 22 +/- 1 years; mean +/- SD) with no coronary risk factors such as hypertension, diabetes mellitus, hyperlipidemia or a family history of premature coronary artery disease (CAD) were included in the study. Over a 4-week period, the volunteers' plasma levels of epinephrine, norepinephrine, and erythrocyte-Mg were measured. The study was made during the 4 weeks before and immediately after college finals exams. HRV, obtained from 24-hour ambulatory ECG monitoring, included time and frequency domain indices. The HRV indices and erythrocyte-Mg decreased while norepinephrine increased during chronic sleep deprivation. It is concluded that chronic sleep deprivation causes an autonomic imbalance and decreases intracellular Mg, which could be associated with chronic sleep deprivation-induced cardiovascular events. PMID:15754837

  5. Diffusion model for one-choice reaction-time tasks and the cognitive effects of sleep deprivation.

    PubMed

    Ratcliff, Roger; Van Dongen, Hans P A

    2011-07-01

    One-choice reaction-time (RT) tasks are used in many domains, including assessments of motor vehicle driving and assessments of the cognitive/behavioral consequences of sleep deprivation. In such tasks, subjects are asked to respond when they detect the onset of a stimulus; the dependent variable is RT. We present a cognitive model for one-choice RT tasks that uses a one-boundary diffusion process to represent the accumulation of stimulus information. When the accumulated evidence reaches a decision criterion, a response is initiated. This model is distinct in accounting for the RT distributions observed for one-choice RT tasks, which can have long tails that have not been accurately captured by earlier cognitive modeling approaches. We show that the model explains performance on a brightness-detection task (a "simple RT task") and on a psychomotor vigilance test. The latter is used extensively to examine the clinical and behavioral effects of sleep deprivation. For the brightness-detection task, the model explains the behavior of RT distributions as a function of brightness. For the psychomotor vigilance test, it accounts for lapses in performance under conditions of sleep deprivation and for changes in the shapes of RT distributions over the course of sleep deprivation. The model also successfully maps the rate of accumulation of stimulus information onto independently derived predictions of alertness. The model is a unified, mechanistic account of one-choice RT under conditions of sleep deprivation. PMID:21690336

  6. Exercise and sleep deprivation do not change cytokine expression levels in patients with chronic fatigue syndrome.

    PubMed

    Nakamura, Toru; Schwander, Stephan; Donnelly, Robert; Cook, Dane B; Ortega, Felix; Togo, Fumiharu; Yamamoto, Yoshiharu; Cherniack, Neil S; Klapholz, Marc; Rapoport, David; Natelson, Benjamin H

    2013-11-01

    A major hypothesis regarding the cause of chronic fatigue syndrome (CFS) is immune dysregulation, thought to be reflected in upregulated proinflammatory cytokines leading to the symptoms that are characteristic of this illness. Because the symptoms worsen with physical exertion or sleep loss, we hypothesized that we could use these stressors to magnify the underlying potential pathogenic abnormalities in the cytokine systems of people with CFS. We conducted repeat blood sampling for cytokine levels from healthy subjects and CFS patients during both postexercise and total sleep deprivation nights and assayed for protein levels in the blood samples, mRNA activity in peripheral blood lymphocytes (PBLs), and function in resting and stimulated PBLs. We found that these environmental manipulations did not produce clinically significant upregulation of proinflammatory cytokines. These data do not support an important role of immune dysregulation in the genesis of stress-induced worsening of CFS.

  7. Sleep and Chronic Disease

    MedlinePlus

    ... CDC Cancel Submit Search The CDC Sleep and Sleep Disorders Note: Javascript is disabled or is not supported ... CDC.gov . Sleep About Us About Sleep Key Sleep Disorders Sleep and Chronic Disease How Much Sleep Do ...

  8. 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…

  9. 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

  10. 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.

  11. Sex-related effects of sleep deprivation on depressive- and anxiety-like behaviors in mice

    PubMed Central

    Gonzalez-Castañeda, Rocio E.; Galvez-Contreras, Alma Y.; Martínez-QUEZADA, Carlos J.; Jauregui-Huerta, Fernando; Grcia-Estrada, Joaquin; Ramos-Zuñiga; Luquin; Gonzalez-Perez

    2015-01-01

    Anxiety and depressive symptoms are generated after paradoxical sleep deprivation (PSD). However, it is not clear whether PSD produces differential effects between females and males. The aim of this study was to assess the effect of PSD on anxiety- and depressive-like behaviors between sexes. Male and female BALB/c mice were divided in three groups: the control group, the 48-h PSD group and the 96-h PSD group. Immediately after PSD protocols, the forced swimming and open field test were applied. Sucrose consumption test was used to evaluate the middle-term effect of PSD. We found that corticosterone serum levels showed significant differences in the 96-h PSD females as compared to 96-h PSD males. In the open-field test, the 48-h and 96-h PSD females spent more time at the periphery of the field, and showed high locomotion as compared to males. In the elevated plus maze, the 48-h PSD females spent more time in closed arms than males, which is compatible with anxiety-like behavior. The forced swim test indicated that the 96-h PSD males spent more time swimming as compared to the 96-h PSD females. Remarkably, the 96-h PSD males had lower sucrose intake than the 96-h PSD females, which suggest that male mice have proclivity to develop a persistent depressive-like behavior late after PSD. In conclusion, male mice showed a significant trend to depressive-like behaviors late after sleep deprivation. Conversely, female have a strong tendency to display anxiety- and depressive-like behaviors immediately after sleep deprivation. PMID:26548630

  12. Sex-related effects of sleep deprivation on depressive- and anxiety-like behaviors in mice.

    PubMed

    Gonzalez-Castañeda, Rocio E; Galvez-Contreras, Alma Y; Martínez-Quezada, Carlos J; Jauregui-Huerta, Fernando; Grcia-Estrada, Joaquin; Ramos-Zuñiga, Rodrigo; Luquin, Sonia; Gonzalez-Perez, Oscar

    2016-01-01

    Anxiety and depressive symptoms are generated after paradoxical sleep deprivation (PSD). However, it is not clear whether PSD produces differential effects between females and males. The aim of this study was to assess the effect of PSD on anxiety- and depressive-like behaviors between sexes. Male and female BALB/c mice were divided in three groups: the control group, the 48-h PSD group and the 96-h PSD group. Immediately after PSD protocols, the forced swimming and open field test were applied. Sucrose consumption test was used to evaluate the middle-term effect of PSD. We found that corticosterone serum levels showed significant differences in the 96-h PSD females as compared to 96-h PSD males. In the open-field test, the 48-h and 96-h PSD females spent more time at the periphery of the field, and showed high locomotion as compared to males. In the elevated plus maze, the 48-h PSD females spent more time in closed arms than males, which is compatible with anxiety-like behavior. The forced swim test indicated that the 96-h PSD males spent more time swimming as compared to the 96-h PSD females. Remarkably, the 96-h PSD males had lower sucrose intake than the 96-h PSD females, which suggest that male mice have proclivity to develop a persistent depressive-like behavior late after PSD. In conclusion, male mice showed a significant trend to depressive-like behaviors late after sleep deprivation. Conversely, female have a strong tendency to display anxiety- and depressive-like behaviors immediately after sleep deprivation. PMID:26548630

  13. Effects of sleep deprivation and time-of-day on selected physical abilities in off-road motorcycle riders.

    PubMed

    Bougard, Clément; Davenne, Damien

    2012-01-01

    The aim of this study was to observe how the combined effects of time-of-day and sleep deprivation impact motocross riders' physical abilities. Balance, flexibility and maximal anaerobic alactic power were tested across laboratory tests that required only one ability (stork stand test, sit-and-reach test, Abalakov test) or across field tests that concentrated on a particular ability (narrow board riding test, riding under a rod test, long jump riding test) to maximise the sensitivity of the assessments and the interpretability of findings. Eight motocross riders of confirmed level took part in test sessions set up at 0600 and 1800 hours following a normal night's sleep and a night of sleep deprivation, i.e. after 1, 13, 23 and 35 waking hours. On the one hand, the results confirmed the influence of time-of-day on riders' physical abilities, performances being better at 1800 hours than at 0600 hours after the normal night's sleep. On the other hand, as far as sleep deprivation effects are concerned, the results seemed to differ on the basis of the ability under consideration and the type of test that had been set up. Performance in the field tests still presented a diurnal fluctuation, whereas this improvement over the day did not occur for the performance in the laboratory tests. It seems that compensation mechanisms between the various abilities brought into play are set up in order to moderate the effects of the lack of sleep when riding.

  14. The effects of long-term sleep deprivation on the long-term potentiation in the dentate gyrus and brain oxidation status in rats.

    PubMed

    Süer, Cem; Dolu, Nazan; Artis, A Seda; Sahin, Leyla; Yilmaz, Alpaslan; Cetin, Aysun

    2011-05-01

    Some evidence suggests that sleep deprivation might impair synaptic plasticity and produce oxidative stress in the hippocampus. However it is not clear whether impairment of long-term potentiation depends on the oxidative stress evoked by sleep deprivation protocol. In this study we aimed to investigate the effects of a 21-day sleep deprivation period on long-term plasticity taking into account the stressful effect of sleep deprivation. Sleep deprivation was carried out using the multiple platforms method on adult male Wistar rats. Long-term potentiation was studied in the medial perforant pathway-dentate gyrus synapses. Elevated T test was applied, and blood corticosterone levels were measured. Lipid peroxidation products in whole brain and hippocampus were determined. No significant difference was found between the sleep deprived, pedestal and cage control groups at the end of the 21-day period when corticosterone levels were compared. The results of the elevated T test indicated that sleep deprivation did not change the anxiety-like behavior of the animals. When compared with cage or pedestal control groups, sleep deprived rats displayed elevated malondialdehyde levels, and decreased superoxide dismutase and glutathione peroxidase activities together with impaired long-term potentiation maintenance. It can be argued that 21-day SD may impair the maintenance of long-term potentiation evoked in the dentate gyrus, and the balance between oxidant and antioxidant defenses of the hippocampus. PMID:21256900

  15. Increased turnover of Na-K ATPase molecules in rat brain after rapid eye movement sleep deprivation.

    PubMed

    Majumdar, Sudipta; Faisal, Mohd; Madan, Vibha; Mallick, Birendra N

    2003-09-15

    It has been shown that rapid eye movement (REM) sleep deprivation increases Na-K ATPase activity. Based on kinetic study, it was proposed that increased activity was due to enhanced turnover of enzyme molecules. To test this, anti-alpha1 Na-K ATPase monoclonal antibody (mAb 9A7) was used to label Na-K ATPase molecules. These labeled enzymes were quantified on neuronal membrane by two methods: histochemically on neurons in tissue sections from different brain areas, and by Western blot analysis in control and REM sleep-deprived rat brains. The specific enzyme activity was also estimated and found to be increased, as in previous studies. The results confirmed our hypothesis that after REM sleep deprivation, increased Na-K ATPase activity was at least partly due to increased turnover of Na-K ATPase molecules in the rat brain.

  16. 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

    2016-01-01

    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. PMID:27089346

  17. Acute Sleep Deprivation Induces a Local Brain Transfer Information Increase in the Frontal Cortex in a Widespread Decrease Context

    PubMed Central

    Alonso, Joan F.; Romero, Sergio; Mañanas, Miguel A.; Alcalá, Marta; Antonijoan, Rosa M.; Giménez, Sandra

    2016-01-01

    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. PMID:27089346

  18. Effects of Sleep Deprivation on Action Potential and Transient Outward Potassium Current in Ventricular Myocytes in Rats

    PubMed Central

    Fang, Zhou; Ren, Yi-Peng; Lu, Cai-Yi; Li, Yang; Xu, Qiang; Peng, Li; Fan, Yong-Yan

    2015-01-01

    Background Sleep deprivation contributes to the development and recurrence of ventricular arrhythmias. However, the electrophysiological changes in ventricular myocytes in sleep deprivation are still unknown. Material/Methods Sleep deprivation was induced by modified multiple platform technique. Fifty rats were assigned to control and sleep deprivation 1, 3, 5, and 7 days groups, and single ventricular myocytes were enzymatically dissociated from rat hearts. Action potential duration (APD) and transient outward current (Ito) were recorded using whole-cell patch clamp technique. Results Compared with the control group, the phases of APD of ventricular myocytes in 3, 5, and 7 days groups were prolonged and APD at 20% and 50% level of repolarization (APD20 and APD50) was significantly elongated (The APD20 values of control, 1, 3, 5, and 7 days groups: 5.66±0.16 ms, 5.77±0.20 ms, 8.28±0.30 ms, 11.56±0.32 ms, 13.24±0.56 ms. The APD50 values: 50.66±2.16 ms, 52.77±3.20 ms, 65.28±5.30 ms, 83.56±7.32 ms, 89.24±5.56 ms. P<0.01, n=18). The current densities of Ito significantly decreased. The current density-voltage (I–V) curve of Ito was vitally suppressed downward. The steady-state inactivation curve and steady-state activation curve of Ito were shifted to left and right, respectively, in sleep deprivation rats. The inactivation recovery time of Ito was markedly retarded and the time of closed-state inactivation was markedly accelerated in 3, 5, and 7 days groups. Conclusions APD of ventricular myocytes in sleep deprivation rats was significantly prolonged, which could be attributed to decreased activation and accelerated inactivation of Ito. PMID:25694200

  19. Rapid eye movement (REM) sleep deprivation in 6-OHDA nigro-striatal lesioned rats with and without transplants of dissociated chromaffin cells.

    PubMed

    Drucker-Colín, R; Durán-Vázquez, A; Salín-Pascual, R J; Verdugo-Díaz, L; Mendoza-Ramírez, J L; Jiménez-Anguiano, A

    1996-08-12

    Since both REM sleep deprivation and unilateral 6-OHDA lesions induce supersensitivity of DA receptors, the purpose of this study was to determine whether the response of rats with such lesions would be modified by REM sleep deprivation. In addition, the effect of grafts of dissociated chromaffin cells was also tested. Rats with 6-OHDA lesions were subjected to 24 or 72 h of REM sleep deprivation and tested with various doses of apomorphine to determine turning behavior frequencies. At end of those experiments, the animals were transplanted with dissociated chromaffin cells and turning behavior was tested again. The results showed that REM sleep deprivation nearly doubled the turning behavior frequency, that chromaffin cell grafts decreased it, but that REM deprivation in grafted animals still seemed to produce an increase of post-synaptic supersensitivity independent of denervation. The results were discussed in terms of the possible relationship of sleep with Parkinson's disease through the DA system.

  20. Sleep Deprivation in Critical Illness: Its Role in Physical and Psychological Recovery

    PubMed Central

    Kamdar, Biren B.; Needham, Dale M.; Collop, Nancy A.

    2012-01-01

    Critically ill patients frequently experience poor sleep, characterized by frequent disruptions, loss of circadian rhythms, and a paucity of time spent in restorative sleep stages. Factors that are associated with sleep disruption in the intensive care unit (ICU) include patient-ventilator dysynchrony, medications, patient care interactions, and environmental noise and light. As the field of critical care increasingly focuses on patients' physical and psychological outcomes following critical illness, understanding the potential contribution of ICU-related sleep disruption on patient recovery is an important area of investigation. This review article summarizes the literature regarding sleep architecture and measurement in the critically ill, causes of ICU sleep fragmentation, and potential implications of ICU-related sleep disruption on patients' recovery from critical illness. With this background information, strategies to optimize sleep in the ICU are also discussed. PMID:21220271

  1. Sleep deprivation in critical illness: its role in physical and psychological recovery.

    PubMed

    Kamdar, Biren B; Needham, Dale M; Collop, Nancy A

    2012-01-01

    Critically ill patients frequently experience poor sleep, characterized by frequent disruptions, loss of circadian rhythms, and a paucity of time spent in restorative sleep stages. Factors that are associated with sleep disruption in the intensive care unit (ICU) include patient-ventilator dysynchrony, medications, patient care interactions, and environmental noise and light. As the field of critical care increasingly focuses on patients' physical and psychological outcomes following critical illness, understanding the potential contribution of ICU-related sleep disruption on patient recovery is an important area of investigation. This review article summarizes the literature regarding sleep architecture and measurement in the critically ill, causes of ICU sleep fragmentation, and potential implications of ICU-related sleep disruption on patients' recovery from critical illness. With this background information, strategies to optimize sleep in the ICU are also discussed. PMID:21220271

  2. Sleep and sleep disorders in Don Quixote.

    PubMed

    Iranzo, Alex; Santamaria, Joan; de Riquer, Martín

    2004-01-01

    In Don Quijote de la Mancha, Miguel de Cervantes presents Don Quixote as an amazing character of the 17th century who suffers from delusions and illusions, believing himself to be a medieval knight errant. Besides this neuropsychiatric condition, Cervantes included masterful descriptions of several sleep disorders such as insomnia, sleep deprivation, disruptive loud snoring and rapid eye movement sleep behaviour disorder. In addition, he described the occurrence of physiological, vivid dreams and habitual, post-prandial sleepiness--the siesta. Cervantes' concept of sleep as a passive state where all cerebral activities are almost absent is in conflict with his description of abnormal behaviours during sleep and vivid, fantastic dreams. His concept of sleep was shared by his contemporary, Shakespeare, and could have been influenced by the reading of the classical Spanish book of psychiatry Examen de Ingenios (1575).

  3. 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

  4. Roles of hypothalamic subgroup histamine and orexin neurons on behavioral responses to sleep deprivation induced by the treadmill method in adolescent rats.

    PubMed

    Xu, Ajing; Sakurai, Eiko; Kuramasu, Atsuo; Zhang, Jian; Li, Jiyu; Okamura, Nobuyuki; Zhang, Dongying; Yoshikawa, Takeo; Watanabe, Takehiko; Yanai, Kazuhiko

    2010-01-01

    Sleep deprivation induces several negative effects on behavior, emotion, attention, and learning ability. Sleep appears to be particularly important during adolescent brain development. In the present study, we examined the effects of sleep deprivation on behavior and hypothalamic neurotransmission including histamine and orexin neurons in adolescent rats using the treadmill method. Adolescent male rats were divided into three groups: treadmill sleep-deprived, treadmill control, and cage control groups. Energy expenditure, anxiety-like behavior, and locomotor activity were examined among the three groups. Histamine concentration in the cortex and diencephalon and the number of c-Fos-positive neurons in the hypothalamus were also examined. In addition, histamine and orexin neurons in the hypothalamus were simultaneously identified using rat histidine decarboxylase and orexin-A immunohistochemistry, respectively. Both energy expenditure and anxiety-related behavior significantly increased by the experimental 3-day sleep deprivation, while exploratory locomotor activity significantly decreased. Histamine contents did not change in the cortex, but significantly decreased in the diencephalon of sleep-deprived rats. Increased expression of c-Fos-positive neurons, including subgroup histamine and orexin neurons, was observed in the hypothalamus. These findings indicate that sleep deprivation increases energy expenditure and anxiety in adolescent rats and provide evidence for the pivotal role of hypothalamus subgroup histamine and orexin neurons in the behavioral response to sleep deprivation.

  5. Adjunctive Triple Chronotherapy (Combined Total Sleep Deprivation, Sleep Phase Advance, and Bright Light Therapy) Rapidly Improves Mood and Suicidality in Suicidal Depressed Inpatients: An Open Label Pilot Study

    PubMed Central

    Sahlem, Gregory L.; Kalivas, Benjamin; Fox, James B.; Lamb, Kayla; Roper, Amanda; Williams, Emily N.; Williams, Nolan R.; Korte, Jeffrey E.; Zuschlag, Zachary D.; El Sabbagh, Salim; Guille, Constance; Barth, Kelly S.; Uhde, Thomas W.; George, Mark S.; Short, E.Baron

    2014-01-01

    Previous studies have demonstrated that combined total sleep deprivation (Wake therapy), sleep phase advance, and bright light therapy (Triple Chronotherapy) produce a rapid and sustained antidepressant effect in acutely depressed individuals. To date no studies have explored the impact of the intervention on unipolar depressed individuals with acute concurrent suicidality. Participants were suicidal inpatients (N=10, Mean age=44±16.4SD, 6F) with unipolar depression. In addition to standard of care, they received open label Triple Chronotherapy. Participants underwent one night of total sleep deprivation (33–36 hours), followed by a three-night sleep phase advance along with four 30-minute sessions of bright light therapy (10,000 lux) each morning. Primary outcome measures included the 17 item Hamilton depression scale (HAM17), and the Columbia Suicide Severity Rating Scale (CSSRS), which were recorded at baseline prior to total sleep deprivation, and at protocol completion on day five. Both HAM17, and CSSRS scores were greatly reduced at the conclusion of the protocol. HAM17 scores dropped from a mean of 24.7±4.2SD at baseline to a mean of 9.4±7.3SD on day five (p=.002) with six of the ten individuals meeting criteria for remission. CSSRS scores dropped from a mean of 19.5±8.5SD at baseline to a mean of 7.2±5.5SD on day five (p=.01). The results of this small pilot trial demonstrate that adjunctive Triple Chronotherapy is feasible and tolerable in acutely suicidal and depressed inpatients. Limitations include a small number of participants, an open label design, and the lack of a comparison group. Randomized controlled studies are needed. PMID:25231629

  6. Adjunctive triple chronotherapy (combined total sleep deprivation, sleep phase advance, and bright light therapy) rapidly improves mood and suicidality in suicidal depressed inpatients: an open label pilot study.

    PubMed

    Sahlem, Gregory L; Kalivas, Benjamin; Fox, James B; Lamb, Kayla; Roper, Amanda; Williams, Emily N; Williams, Nolan R; Korte, Jeffrey E; Zuschlag, Zachary D; El Sabbagh, Salim; Guille, Constance; Barth, Kelly S; Uhde, Thomas W; George, Mark S; Short, E Baron

    2014-12-01

    Previous studies have demonstrated that combined total sleep deprivation (Wake therapy), sleep phase advance, and bright light therapy (Triple Chronotherapy) produce a rapid and sustained antidepressant effect in acutely depressed individuals. To date no studies have explored the impact of the intervention on unipolar depressed individuals with acute concurrent suicidality. Participants were suicidal inpatients (N = 10, Mean age = 44 ± 16.4 SD, 6F) with unipolar depression. In addition to standard of care, they received open label Triple Chronotherapy. Participants underwent one night of total sleep deprivation (33-36 h), followed by a three-night sleep phase advance along with four 30-min sessions of bright light therapy (10,000 lux) each morning. Primary outcome measures included the 17 item Hamilton depression scale (HAM17), and the Columbia Suicide Severity Rating Scale (CSSRS), which were recorded at baseline prior to total sleep deprivation, and at protocol completion on day five. Both HAM17, and CSSRS scores were greatly reduced at the conclusion of the protocol. HAM17 scores dropped from a mean of 24.7 ± 4.2 SD at baseline to a mean of 9.4 ± 7.3 SD on day five (p = .002) with six of the ten individuals meeting criteria for remission. CSSRS scores dropped from a mean of 19.5 ± 8.5 SD at baseline to a mean of 7.2 ± 5.5 SD on day five (p = .01). The results of this small pilot trial demonstrate that adjunctive Triple Chronotherapy is feasible and tolerable in acutely suicidal and depressed inpatients. Limitations include a small number of participants, an open label design, and the lack of a comparison group. Randomized controlled studies are needed.

  7. Metabolic consequences of sleep and sleep loss

    PubMed Central

    Van Cauter, Eve; Spiegel, Karine; Tasali, Esra; Leproult, Rachel

    2015-01-01

    Reduced sleep duration and quality appear to be endemic in modern society. Curtailment of the bedtime period to minimum tolerability is thought to be efficient and harmless by many. It has been known for several decades that sleep is a major modulator of hormonal release, glucose regulation and cardiovascular function. In particular, slow wave sleep (SWS), thought to be the most restorative sleep stage, is associated with decreased heart rate, blood pressure, sympathetic nervous activity and cerebral glucose utilization, compared with wakefulness. During SWS, the anabolic growth hormone is released while the stress hormone cortisol is inhibited. In recent years, laboratory and epidemiologic evidence have converged to indicate that sleep loss may be a novel risk factor for obesity and type 2 diabetes. The increased risk of obesity is possibly linked to the effect of sleep loss on hormones that play a major role in the central control of appetite and energy expenditure, such as leptin and ghrelin. Reduced leptin and increased ghrelin levels correlate with increases in subjective hunger when individuals are sleep restricted rather than well rested. Given the evidence, sleep curtailment appears to be an important, yet modifiable, risk factor for the metabolic syndrome, diabetes and obesity. The marked decrease in average sleep duration in the last 50 years coinciding with the increased prevalence of obesity, together with the observed adverse effects of recurrent partial sleep deprivation on metabolism and hormonal processes, may have important implications for public health. PMID:18929315

  8. Systemic amitriptyline administration does not prevent the increased thermal response induced by paradoxical sleep deprivation.

    PubMed

    Damasceno, Fabio; Skinner, Gabriela O; Gomes, Aline; Araújo, Paulo C; de Almeida, Olga M M S

    2009-11-01

    Sleep deprivation has been associated with hyperalgesia in humans and in animal models. The tricyclic antidepressant amitriptyline is used as an analgesic drug in patients and in animal models of chronic pain, including that associated with spinal nerve injury. Pain hypersensitivity following paradoxical sleep deprivation (PSD) and that following peripheral nerve injury seem to share common spinal mechanisms. Accordingly, we evaluated the effects of amitriptyline (acutely and chronically administered) on the increased thermal response observed in PSD rats (72 or 96 h). Rats were evaluated for thermal sensitivity using a hot plate (52 degrees C or 46 degrees C) at 1 or 24 h after the last administration of the drug. Following the hot plate test, motor behavior was analyzed in an open field arena for a period of 5 min. Paw withdrawal latency response to temperatures of 46 degrees C and 52 degrees C was significantly lower in PSD and in 24-hour post-PSD rats than in controls and it was not modified by amitriptyline (3, 10 and 30 mg/kg). Analgesic effects and reduced motor behavior were only observed in control groups. Overall, these findings indicate that a period of PSD can influence pain modulatory mechanisms, and that amitriptyline action is insufficient to reduce PSD-enhanced thermal sensitivity.

  9. Modafinil treatment prevents REM sleep deprivation-induced brain function impairment by increasing MMP-9 expression.

    PubMed

    He, Bin; Peng, Hua; Zhao, Ying; Zhou, Hui; Zhao, Zhongxin

    2011-12-01

    Previous work showed that sleep deprivation (SD) impairs hippocampal-dependent cognitive function and synaptic plasticity, and a novel wake-promoting agent modafinil prevents SD-induced memory impairment in rat. However, the mechanisms by which modafinil prevented REM-SD-induced impairment of brain function remain poorly understood. In the present study, rats were sleep-deprived by using the modified multiple platform method and brain function was detected. The results showed that modafinil treatment prevented REM-SD-induced impairment of cognitive function. Modafinil significantly reduced the number of errors compared to placebo and upregulated synapsin I expression in the dorsal hippocampal CA3 region. A synaptic plasticity-related gene, MMP-9 expression was also upregulated in modafinil-treated rats. Importantly, downregulation of MMP-9 expression by special siRNA decreased synapsin I protein levels and synapse numbers. Therefore, we demonstrated that modafinil increased cognition function and synaptic plasticity, at least in part by increasing MMP-9 expression in REM-SD rats.

  10. Post-learning REM sleep deprivation impairs long-term memory: reversal by acute nicotine treatment.

    PubMed

    Aleisa, A M; Alzoubi, K H; Alkadhi, K A

    2011-07-15

    Rapid eye movement sleep deprivation (REM-SD) is associated with spatial learning and memory impairment. During REM-SD, an increase in nicotine consumption among habitual smokers and initiation of tobacco use by non-smokers have been reported. We have shown recently that nicotine treatment prevented learning and memory impairments associated with REM-SD. We now report the interactive effects of post-learning REM-SD and/or nicotine. The animals were first trained on the radial arm water maze (RAWM) task, then they were REM-sleep deprived using the modified multiple platform paradigm for 24h. During REM-SD period, the rats were injected with saline or nicotine (1mg/kg s.c. every 12h: a total of 3 injections). The animals were tested for long-term memory in the RAWM at the end of the REM-SD period. The 24h post-learning REM-SD significantly impaired long-term memory. However, nicotine treatment reversed the post-learning REM-SD-induced impairment of long-term memory. On the other hand, post-learning treatment of normal rats with nicotine for 24h enhanced long-term memory. These results indicate that post-learning acute nicotine treatment prevented the deleterious effect of REM-SD on cognitive abilities.

  11. The effects of total and REM sleep deprivation on laser-evoked potential threshold and pain perception.

    PubMed

    Azevedo, Eduardo; Manzano, Gilberto M; Silva, Andressa; Martins, Raquel; Andersen, Monica L; Tufik, Sergio

    2011-09-01

    We investigated the effects of total and rapid eye movement (REM) sleep deprivation on the thermal nociceptive threshold and pain perception using the objective laser-evoked potential (LEP) and the subjective visual analogue scale (VAS). Twenty-eight male adult volunteers were assigned into Control (CTRL), Total (T-SD), and REM (REM-SD) Sleep Deprivation groups. The T-SD and REM-SD volunteers were totally or selectively deprived of sleep for 2 and 4 consecutive nights, respectively. Pain parameters were measured daily during the experimental period. Volunteers were stimulated on the back of the hand by blocks of 50 diode laser pulses. Intensities increased between successive blocks, ranging from nonnoxious to noxious levels, and the LEP threshold was identified based on the evoked-response onset. Both the LEP threshold and VAS ratings were significantly increased after the second night of T-SD. No significant variations were observed in the REM-SD group, suggesting a predominant role for slow wave sleep rather than selective REM-SD in pain perception. Also, for both sleep-deprived groups, the mean values of the LEP threshold and VAS ratings showed a gradual increase that was proportional to the SD deprivation time, followed by a decrease after 1 night of sleep restoration. These findings demonstrate a hyperalgesic modification to pain perception (as reflected by the augmented VAS) and a concomitant increase in the LEP threshold following T-SD, an apparently contradictory effect that can be explained by differences in the ways that attention affects these pain measurements.

  12. Type of diet modulates the metabolic response to sleep deprivation in rats

    PubMed Central

    2011-01-01

    Background Evidence suggests that sleep loss is associated with an increased risk of obesity and diabetes; however, animal models have failed to produce weight gain under sleep deprivation (SD). Previous studies have suggested that this discrepancy could be due to more extreme SD conditions in experimental animals, their higher resting metabolic rate than that of humans, and the decreased opportunity for animals to ingest high-calorie foods. Thus, our objective was to determine whether diets with different textures/compositions could modify feeding behavior and affect the metabolic repercussions in SD in rats. Methods Three groups of male rats were used: one was designated as control, one was sleep deprived for 96 h by the platform technique (SD-96h) and one was S