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Sample records for sleep sleep deprivation

  1. Sleep Deprivation.

    PubMed

    Abrams, Robert M

    2015-09-01

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

  2. SLEEP DEPRIVATION,

    DTIC Science & Technology

    This report was confined to considering the effects of sleep deprivation , in man, with particular reference to studies of the resulting biochemical...have a limited value when taken separately: the biochemical and physiological changes that occur in response to sleep deprivation may depend...three separate heads: first, the biochemical changes resulting from sleep deprivation ; secondly, the physiological ones; and last, the changes in performance and behaviour. (Author)

  3. Sleep

    MedlinePlus

    ... is REM sleep? What is the effect of sleep deprivation? What are sleep myths? What are sleep disorders? ... is REM sleep? What is the effect of sleep deprivation? What are sleep myths? What are sleep disorders? ...

  4. 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.

  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. Health Effects of Sleep Deprivation,

    DTIC Science & Technology

    1990-06-01

    to get full antidepressant benefit from sleep deprivation. Cole and Muller 63 reported that when elderly depressives (57-79 years old, average age 69...Cole MG, Miller HF: Sleep deprivation in the treatment of elderly depressed patients. J Am Geriatr Soc 243:308-313, 1976. 64. Collins WE: Some effects...1:207-216, 1972. 259. Salin-Pascual RJ, Ortega-Soto H, Huerto-Delgadillo L, et al: The effect of total sleep deprivation on plasma melatonin and

  7. 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

  8. PHYSIOLOGICAL RESPONSES OF MEN DURING SLEEP DEPRIVATION,

    DTIC Science & Technology

    The effects of 84 hours of sleep deprivation were examined in a group of six young men and compared with a group of six controls. Subjects were... sleep deprivation , physiological regulating systems are relatively unaffected by sleep loss. (Author)

  9. 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.

  10. Recovery sleep and performance following sleep deprivation with dextroamphetamine.

    PubMed

    Caldwell, J L; Caldwell, J A

    1997-06-01

    Twelve subjects were studied to determine the after-effects of using three 10-mg doses of dextroamphetamine to sustain alertness during sleep deprivation. Sleep architecture during recovery sleep was evaluated by comparing post-deprivation sleep after placebo. Performance and mood recovery were assessed by comparing volunteers who received dextroamphetamine first (during sleep deprivation) to those who received placebo first. Stages 1 and 2 sleep, movement time, REM latency, and sleep latency increased on the night after sleep deprivation with dextroamphetamine vs. placebo. Stage 4 was unaffected. Comparisons to baseline revealed more stage 1 during baseline than during either post-deprivation sleep period and more stage 2 during baseline than during sleep following placebo. Stage 4 sleep was lower during baseline and after dextroamphetamine than after placebo. Sleep onset was slowest on the baseline night. Next-day performance and mood were not different as a function of whether subjects received dextroamphetamine or placebo during deprivation. These data suggest dextroamphetamine alters post-deprivation sleep architecture when used to sustain alertness during acute sleep loss, but next-day performance and subjective mood ratings are not substantially affected. A recovery sleep period of only 8 h appears to be adequate to regain baseline performance levels after short-term sleep deprivation.

  11. 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+ ...

  12. 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

  13. Sleep deprivation increases cigarette smoking.

    PubMed

    Hamidovic, Ajna; de Wit, Harriet

    2009-09-01

    Loss of sleep may impair the ability to abstain from drug use, through any of a number of mechanisms. Sleep loss may increase drug use by impairing attention and inhibitory control, increasing the value of drug rewards over other rewards, or by inducing mood states that facilitate use of a drug. In the present study, we examined whether sleep deprivation (SD) would increase smoking in cigarette smokers, and whether it would do so by impairing attention or inhibitory control. Healthy cigarette smokers (N=14) were tested in a two-session within subject study, after overnight SD or after a normal night's sleep. Subjects were tested in both conditions in randomized order, after abstaining from cigarettes for 48 hours. The procedure was designed to model the human relapse situation. On each 6-h laboratory session after sleep or no sleep, subjects completed mood and craving questionnaires, tasks measuring behavioral inhibition and attention, and a choice procedure in which they chose between money and smoking cigarettes. SD increased self-reported fatigue and decreased arousal, it increased the number of cigarettes subjects chose to smoke, impaired behavioral inhibition and attention. However, the impairments in inhibition or attention were not related to the increase in smoking. It is possible that SD increases smoking because smokers expect that it will reduce sleepiness. Thus, the findings suggest that sleep loss may increase the likelihood of smoking during abstinence not through inhibitory or attentional mechanisms but because of the potential of nicotine to reduce subjective sleepiness.

  14. 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

  15. Sleep deprivation induced anxiety and anaerobic performance.

    PubMed

    Vardar, Selma Arzu; Oztürk, 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.

  16. Sleep deprivation and antidepressant treatment

    PubMed Central

    Voderholzer, Ulrich

    2003-01-01

    The mood-improving effect of sleep deprivation (SD) in depression is even today still not fully understood. Despite the fact that mood and cognitive functions are lowered by prolonged sleep loss and despite convincing data that insomnia is a strong risk factor for subsequent depression,1 acute SD for one night or even partial SD in the second half of the night improves mood in about 60% of depressed patients the day after.2,3 In this respect, among alt types of antidepressant treatments, SD elicits the fastest results, faster even than electroconvulsive therapy. Many authors correlate the likelihood of responding to SD with clinical variables. A summary of predictors is listed in Table I. PMID:22033748

  17. Sleep, sleep deprivation, autonomic nervous system and cardiovascular diseases.

    PubMed

    Tobaldini, Eleonora; Costantino, Giorgio; Solbiati, Monica; Cogliati, Chiara; Kara, Tomas; Nobili, Lino; Montano, Nicola

    2017-03-01

    Sleep deprivation (SD) has become a relevant health problem in modern societies. We can be sleep deprived due to lifestyle habits or due to sleep disorders, such as insomnia, obstructive sleep apnea (OSA) and neurological disorders. One of the common element of sleep disorders is the condition of chronic SD, which has complex biological consequences. SD is capable of inducing different biological effects, such as neural autonomic control changes, increased oxidative stress, altered inflammatory and coagulatory responses and accelerated atherosclerosis. All these mechanisms links SD and cardiovascular and metabolic disorders. Epidemiological studies have shown that short sleep duration is associated with increased incidence of cardiovascular diseases, such as coronary artery disease, hypertension, arrhythmias, diabetes and obesity, after adjustment for socioeconomic and demographic risk factors and comorbidities. Thus, an early assessment of a condition of SD and its treatment is clinically relevant to prevent the harmful consequences of a very common condition in adult population.

  18. Sleep deprivation and neurobehavioral functioning in children.

    PubMed

    Maski, Kiran P; Kothare, Sanjeev V

    2013-08-01

    Sleep deprivation can result in significant impairments in daytime neurobehavioral functioning in children. Neural substrates impacted by sleep deprivation include the prefrontal cortex, basal ganglia and amygdala and result in difficulties with executive functioning, reward anticipation and emotional reactivity respectively. In everyday life, such difficulties contribute to academic struggles, challenging behaviors and public health concerns of substance abuse and suicidality. In this article, we aim to review 1) core neural structures impacted by sleep deprivation; 2) neurobehavioral problems associated with sleep deprivation; 3) specific mechanisms that may explain the relationship between sleep disturbances and neurobehavioral dysfunction; and 4) sleep problems reported in common neurodevelopmental disorders including attention deficit hyperactivity disorder (ADHD) and autistic spectrum disorders (ASDs).

  19. 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…

  20. 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

  1. Sleep deprivation in the rat: III. Total sleep deprivation.

    PubMed

    Everson, C A; Bergmann, B M; Rechtschaffen, A

    1989-02-01

    Ten rats were subjected to total sleep deprivation (TSD) by the disk apparatus. All TSD rats died or were sacrificed when death seemed imminent within 11-32 days. No anatomical cause of death was identified. All TSD rats showed a debilitated appearance, lesions on their tails and paws, and weight loss in spite of increased food intake. Their yoked control (TSC) rats remained healthy. Since dehydration was ruled out and several measures indicated accelerated use rather than failure to absorb nutrients, the food-weight changes in TSD rats were attributed to increased energy expenditure (EE). The measurement of EE, based upon caloric value of food, weight, and wastes, indicated that all TSD rats increased EE, with mean levels reaching more than twice baseline values.

  2. Loss of negative priming following sleep deprivation.

    PubMed

    Harrison, Yvonne; Espelid, Erik

    2004-04-01

    It has been argued that one night of sleep loss in young healthy adults produces changes similar to that associated with normal, healthy ageing--in particular, that young sleep-deprived adults perform similarly to 60-year-old sleep-satiated adults on some tasks of frontal lobe function. This proposition was examined using a protocol viewed by many to be a direct probe of nonvolitional attention mechanisms associated with frontal lobe function. A negative priming (NP) procedure was used to compare performance between non-sleep-deprived (NSD) and sleep-deprived (SD, 34 hr) young, healthy adults. This protocol allowed for exploration of two theories of the NP effect based on inhibitory or memorial processes. Under conditions believed to facilitate inhibitory processes a normal NP effect was found for NSD(16 ms) and SD (9 ms) participants. Under conditions believed to rely on memorial processes there was no NP effect following SD, compared with a normal NP effect for NSD participants (11 ms). Distractor interference was also greater following SD. These findings do not suggest a similar pattern of change following sleep loss in healthy young adults to that of normal, healthy, non-sleep-deprived aged groups.

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

    PubMed

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

    1998-06-01

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

  4. 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

  5. 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

  6. Sleep Deprivation: A Cause of High Blood Pressure?

    MedlinePlus

    ... High blood pressure (hypertension) Is it true that sleep deprivation can cause high blood pressure? Answers from Sheldon ... Cirelli C, et al. Definition and consequences of sleep deprivation. http://www.uptodate.com/home. Accessed March 24, ...

  7. The role of thyroid hormone in sleep deprivation.

    PubMed

    Pereira, José Carlos; Andersen, Mônica Levy

    2014-03-01

    Sleep deprivation is a stressful condition, as the subject experiences feelings of inadequate well-being and exhibits impairments in his/her functioning. However, in some circumstances sleep deprivation may be crucial for survival of the individual. Most likely, complex neural circuits and hormones play a role in allowing sleep deprivation to occur. For instance, thyroid hormone activity sharply increases when an individual is in a state of sleep deprivation. We believe that this increase is central to sleep deprivation physiology. During sleep deprivation, the hypothalamic-pituitary-thyroid axis initially increases as a consequence of increased release of thyroid stimulating hormone from the pituitary. Subsequently, as sleep deprivation continues, the sympathetic nervous system is recruited through its anatomical connection with the thyroid gland. While thyroid stimulating hormone levels markedly increase during sleep deprivation, it has been suggested that these increases are secondary to sleep deprivation. However, there is little evidence to support this assumption. We believe that the physiology of the thyroid axis during sleep deprivation and the actions of the effector hormone thyroid hormone suggest that thyroid hormone inhibits sleep and not the contrary. To our knowledge, few studies have addressed the possible neural functions that enable sleep deprivation. In this article, we discuss the hypothesis that an augmentation in the thyroid hormone axis is central to a subject's ability to curtail sleep.

  8. BINOCULAR FUSION TIME IN SLEEP-DEPRIVED SUBJECTS,

    DTIC Science & Technology

    fatigue induced by sleep deprivation on the binocular fusion reflex. Binocular fusion times were measured morning and evening in six subjects during 86...hours of sleep deprivation and in six control subjects. The binocular fusion reflex under the experimental conditions employed appeared to be resistant to fatigue incident to sleep - deprivation . (Author)

  9. Sleep Deprivation and Exercise Tolerance.

    DTIC Science & Technology

    1986-01-01

    thermoneutral environment) is alike unchanged by loss of sleep. 5) Seven subjects were allowed to exercise to thermal comfort in a very cold (OC, 2.5...Subjects selected identical work loads for thermal comfort , and became exhausted/miserable after similar period of exposure. Physiologi- cal response and

  10. 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.

  11. 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

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

    PubMed Central

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

    2013-01-01

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

  13. 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 ...

  14. Gene Networks Underlying Chronic Sleep Deprivation in Drosophila

    DTIC Science & Technology

    2014-06-15

    SECURITY CLASSIFICATION OF: Studies of the gene network affected by sleep deprivation and stress in the fruit fly Drosophila have revealed the...transduction pathways are affected. Subseuqent tests of mutants in these pathways demonstrated a strong effect on sleep maintenance. Further...15-Apr-2009 14-Apr-2013 Approved for Public Release; Distribution Unlimited Gene Networks Underlying Chronic Sleep Deprivation in Drosophila The

  15. 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

  16. Sleep deprivation and the effect on exercise performance.

    PubMed

    VanHelder, T; Radomski, M W

    1989-04-01

    Sleep deprivation or partial sleep loss are common in work conditions as rotating shifts and prolonged work hours, in sustained military operations and in athletes competing in events after crossing several time zones or engaged in ultramarathon or triathlon events. Although it is well established that sleep loss has negative effects on mental performance, its effects on physical performance are equivocal. This review examines the latter question in light of recent studies published on this problem. Sleep deprivation of 30 to 72 hours does not affect cardiovascular and respiratory responses to exercise of varying intensity, or the aerobic and anaerobic performance capability of individuals. Muscle strength and electromechanical responses are also not affected. Time to exhaustion, however, is decreased by sleep deprivation. Although ratings of perceived exertion always increased during exercise in sleep-deprived (30 to 60 hours) subjects compared with normal sleep, this is not a reliable assessment of a subject's ability to perform physical work as the ratings of perceived exertion are dissociated from any cardiovascular changes in sleep deprivation. Examination of the various hormonal and metabolic parameters which have been measured in the studies reviewed reveals that the major metabolic perturbations accompanying sleep deprivation in humans are an increase in insulin resistance and a decrease in glucose tolerance. This may explain the reduction in observed time to exhaustion in sleep-deprived subjects. The role of growth hormone in mediating altered carbohydrate metabolism may be of particular relevance as to how sleep deprivation alters the supply of energy substrate to the muscle.

  17. Changes in the waking EEG as a consequence of sleep and sleep deprivation.

    PubMed

    Corsi-Cabrera, M; Ramos, J; Arce, C; Guevara, M A; Ponce-de León, M; Lorenzo, I

    1992-12-01

    Electroencephalographic (EEG) activity was monopolarly recorded during resting wakefulness in 10 volunteers under the following conditions: at night before going to sleep, at night before total sleep deprivation, in the morning after waking, in the morning after sleep deprivation and at night after having slept during the day. Absolute and relative power and inter- and intrahemispheric correlation were established. After diurnal and nocturnal sleep as compared to sleep deprivation, we obtained the following significant results: interhemispheric correlations were higher; intrahemispheric correlations were lower; absolute power of alpha 2, beta 1 and beta 2 was lower; and relative power of alpha 2 and beta 2 was lower. EEG changes as a consequence of sleep or lack of sleep are dependent on prior sleep and/or wakefulness and not on circadian phase. EEG activity during wakefulness is a sensitive parameter and a useful tool to assess the consequences of sleep on brain functional organization.

  18. 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.

  19. 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.

  20. 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

  1. 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.

  2. 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.

  3. 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.

  4. 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

  5. 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.

  6. Effect of sleep deprivation on the human metabolome.

    PubMed

    Davies, Sarah K; Ang, Joo Ern; Revell, Victoria L; Holmes, Ben; Mann, Anuska; Robertson, Francesca P; Cui, Nanyi; Middleton, Benita; Ackermann, Katrin; Kayser, Manfred; Thumser, Alfred E; Raynaud, Florence I; Skene, Debra J

    2014-07-22

    Sleep restriction and circadian clock disruption are associated with metabolic disorders such as obesity, insulin resistance, and diabetes. The metabolic pathways involved in human sleep, however, have yet to be investigated with the use of a metabolomics approach. Here we have used untargeted and targeted liquid chromatography (LC)/MS metabolomics to examine the effect of acute sleep deprivation on plasma metabolite rhythms. Twelve healthy young male subjects remained in controlled laboratory conditions with respect to environmental light, sleep, meals, and posture during a 24-h wake/sleep cycle, followed by 24 h of wakefulness. Two-hourly plasma samples collected over the 48 h period were analyzed by LC/MS. Principal component analysis revealed a clear time of day variation with a significant cosine fit during the wake/sleep cycle and during 24 h of wakefulness in untargeted and targeted analysis. Of 171 metabolites quantified, daily rhythms were observed in the majority (n = 109), with 78 of these maintaining their rhythmicity during 24 h of wakefulness, most with reduced amplitude (n = 66). During sleep deprivation, 27 metabolites (tryptophan, serotonin, taurine, 8 acylcarnitines, 13 glycerophospholipids, and 3 sphingolipids) exhibited significantly increased levels compared with during sleep. The increased levels of serotonin, tryptophan, and taurine may explain the antidepressive effect of acute sleep deprivation and deserve further study. This report, to our knowledge the first of metabolic profiling during sleep and sleep deprivation and characterization of 24 h rhythms under these conditions, offers a novel view of human sleep/wake regulation.

  7. Increased voluntary alcohol drinking concurrent with REM-sleep deprivation.

    PubMed

    Aalto, J; Kiianmaa, K

    1984-01-01

    The alcohol intake of twenty adult Long-Evans male rats was recorded before, during and after rapid eye movement sleep (REM) deprivation produced with the flowerpot technique modified by using a cuff pedestal and an electrified grid floor instead of water. The alcohol intake reached a steady level of 2.8 g/kg/day in the 3 weeks before REM deprivation. During seven REM-sleep deprivation days the alcohol intake was significantly elevated, finally increasing to 3.7 g/kg/day. A rebound decrease in alcohol drinking was then observed during the "REM-rebound" phase immediately after the termination of REM-sleep deprivation. The results suggest a possible vicious circle of REM-sleep deprivation increasing alcohol drinking and alcohol intake causing REM-sleep deprivation.

  8. 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.

  9. Sleep deprivation and sleep recovery modifies connexin36 and connexin43 protein levels in rat brain.

    PubMed

    Franco-Pérez, Javier; Ballesteros-Zebadúa, Paola; Fernández-Figueroa, Edith A; Ruiz-Olmedo, Isabel; Reyes-Grajeda, Pablo; Paz, Carlos

    2012-01-25

    Gap junctional communication is mainly mediated by connexin36 and connexin43 in neurons and astrocytes, respectively. It has been suggested that connexin36 allows electrical coupling between neurons whereas connexin43 participates in several process including release of ATP. It was recently reported that blockage of gap junctional communication mediated by connexin36 can disrupt the sleep architecture of the rat. However, there is no experimental approach about effects of sleep deprivation on connexins expression. Therefore, we examined in adult male Wistar rats whether protein levels of connexin36 and connexin43 change in pons, hypothalamus, and frontal cortex after 24 h of total sleep deprivation and 4 h of sleep recovery. Western blot revealed that total sleep deprivation significantly decreases the levels of connexin36 in the hypothalamus and this decrease maintains after sleep recovery. Meanwhile, connexin43 is not altered by total sleep deprivation but interestingly the sleep recovery period induces an increase of this connexin. These results suggest that electrical coupling between hypothalamic neurons could be altered by sleep deprivation and that sleep recovery drives changes in connexin43 expression probably as a mechanism related to ATP release and energy regulation during sleep.

  10. Spatial reversal learning is robust to total sleep deprivation.

    PubMed

    Leenaars, Cathalijn H C; Joosten, Ruud N J M A; Kramer, Michiel; Post, Ger; Eggels, Leslie; Wuite, Mark; Dematteis, Maurice; Feenstra, Matthijs G P; Van Someren, Eus J W

    2012-04-21

    Sleep deprivation affects cognitive functions that depend on the prefrontal cortex (PFC) such as cognitive flexibility, and the consolidation of newly learned information. The identification of cognitive processes that are either robustly sensitive or robustly insensitive to the same experimental sleep deprivation procedure, will allow us to better focus on the specific effects of sleep on cognition, and increase understanding of the mechanisms involved. In the present study we investigate whether sleep deprivation differentially affects the two separate cognitive processes of acquisition and consolidation of a spatial reversal task. After training on a spatial discrimination between two levers in a Skinner box, male Wistar rats were exposed to a reversal of the previously learned stimulus-response contingency. We first evaluated the effect of sleep deprivation on the acquisition of reversal learning. Performance on reversal learning after 12h of sleep deprivation (n=12) was compared to performance after control conditions (n=12). The second experiment evaluated the effect of sleep deprivation on the consolidation of reversal learning; the first session of reversal learning was followed by 3h of nap prevention (n=8) or undisturbed control conditions (n=8). The experiments had sufficient statistical power (0.90 and 0.81, respectively) to detect differences with medium effect sizes. Neither the acquisition, nor the consolidation, of reversal learning was affected by acute sleep deprivation. Together with previous findings, these results help to further delineate the role of sleep in cognitive processing.

  11. 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.

  12. 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…

  13. 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.

  14. The Effect of Total Sleep Deprivation and Recovery Sleep on Cognitive on Performance and Brain Function

    DTIC Science & Technology

    2005-08-01

    State University/University of California, San Diego, San Diego, CA, USA Introduction: It has been documented that REM sleep recovers later than NREM ...AD Award Number: DAMD1I7-02-1-0201 TITLE: The Effect of Total Sleep Deprivation and Recovery Sleep on Cognitive on Performance and Brain Function...changes in the brain substrate underlying the behavioral effects, and even less is known about the cerebral effects of recovery sleep . The overarching

  15. 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

  16. 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.

  17. Impact of Acute Sleep Deprivation on Sarcasm Detection.

    PubMed

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

    2015-01-01

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

  18. 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

  19. 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

  20. Melatonin improves experimental colitis with sleep deprivation.

    PubMed

    Park, Young-Sook; Chung, Sook-Hee; Lee, Seong-Kyu; Kim, Ja-Hyun; Kim, Jun-Bong; Kim, Tae-Kyun; Kim, Dong-Shin; Baik, Haing-Woon

    2015-04-01

    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

  1. 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.

  2. 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

  3. Reduced visual processing capacity in sleep deprived persons.

    PubMed

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

    2011-03-15

    Multiple experiments have found sleep deprivation to lower task-related parietal and extrastriate visual activation, suggesting a reduction of visual processing capacity in this state. The perceptual load theory of attention (Lavie, 1995) predicts that our capacity to process unattended distractors will be reduced by increasing perceptual difficulty of task-relevant stimuli. Here, we evaluated the effects of sleep deprivation and perceptual load on visual processing capacity by measuring neural repetition-suppression to unattended scenes while healthy volunteers attended to faces embedded in face-scene pictures. Perceptual load did not affect repetition suppression after a normal night of sleep. Sleep deprivation reduced repetition suppression in the parahippocampal place area (PPA) in the high but not low perceptual load condition. Additionally, the extent to which task-related fusiform face area (FFA) activation was reduced after sleep deprivation correlated with behavioral performance and lowered repetition suppression in the PPA. The findings concerning correct responses indicate that a portion of stimulus related activation following a normal night of sleep contributes to potentially useful visual processing capacity that is attenuated following sleep deprivation. Finally, when unattended stimuli are not highly intrusive, sleep deprivation does not appear to increase distractibility.

  4. 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.

  5. 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

  6. Cardiovascular, Inflammatory and Metabolic Consequences of Sleep Deprivation

    PubMed Central

    Mullington, Janet M.; Haack, Monika; Toth, Maria; Serrador, Jorge; Meier-Ewert, Hans

    2009-01-01

    That insufficient sleep is associated with poor attention and performance deficits is becoming widely recognized. Fewer people are aware that chronic sleep complaints in epidemiological studies have also been associated with an increase in overall mortality and morbidity. This article summarizes findings of known effects of insufficient sleep on cardiovascular risk factors including blood pressure, glucose metabolism, hormonal regulation and inflammation with particular emphasis on experimental sleep loss, using models of total and partial sleep deprivation, in healthy individuals who normally sleep in the range of 7-8 hours and have no sleep disorders. These studies show that insufficient sleep alters established cardiovascular risk factors in a direction that is known to increase the risk of cardiac morbidity. PMID:19110131

  7. 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

  8. 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

  9. 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.

  10. Regional differences of the human sleep electroencephalogram in response to selective slow-wave sleep deprivation.

    PubMed

    Ferrara, Michele; De Gennaro, Luigi; Curcio, Giuseppe; Cristiani, Riccardo; Corvasce, Chiara; Bertini, Mario

    2002-07-01

    The purpose of this study was to assess the topographic changes in sleep recuperative processes in response to selective slow-wave sleep (SWS) deprivation. SWS was suppressed on two consecutive nights by means of acoustic stimulation. The electroencephalogram (EEG) power of baseline, deprivation and recovery nights was analysed in 1 Hz bins. During the SWS deprivation nights, large decreases of EEG power were found at frontopolar, central and parietal derivations encompassing the delta, theta and alpha range, while only slow delta (0.5-2 Hz) was affected at the frontal derivation. Recovery sleep was characterized by a generalized increase of power during non-REM sleep encompassing the delta, theta and alpha bands, with a clear antero-posterior gradient. The coherent behaviour of different EEG bands with traditionally different electrophysiological meanings during non-REM sleep suggests that, in light of the recent advances in sleep neurophysiology, a re-examination of the functional role of EEG rhythms during sleep is needed. The 'resistance' to selective SWS deprivation of the frontal area, together with its larger increase of EEG power during recovery, may be interpreted as a sign of a greater sleep need of the frontal cortical areas, confirming that some aspects of the regulatory processes of human sleep are local in nature and may show use-dependent characteristics.

  11. [Sleep deprivation and pain: a review of the newest literature].

    PubMed

    Karmann, A J; Kundermann, B; Lautenbacher, S

    2014-04-01

    It has now been established that sleep deprivation or fragmentation causes hyperalgesia which cannot be explained by a general change in somatosensory perception. However, it has not yet been clarified which of the sleep stages are most relevant for this effect. The seemingly paradoxical effects of sleep deprivation on pain-evoked brain potentials on the one hand and the subjective pain report on the other hand suggest complex changes in gating mechanisms. As the effects on pain and affect can be dissociated a common mechanism of action seems unlikely. Data from animal studies suggest that hyperalgesia due to sleep deprivation might be particularly strong under preexisting neuropathic conditions. Together with results from animal research the finding that endogenous pain modulation (CPM) is impaired by sleep deprivation suggests that the serotoninergic system mediates the effect of sleep deprivation on pain perception. However, other neurotransmitters and neuromodulators still have to be considered. The clinically relevant question arises why sleep deprivation induces hyperalgesia more easily in certain individuals than in others and why this effect then has a longer duration?

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

    DTIC Science & Technology

    1985-09-29

    performance levels. ... ’.I •.5 PROJECT SUMMARY This research studied changes in event-related brain potentials (ERPs) in sleep -deprived subjects over...sleepiness involves monitoring ongoing electroencephalographic (EEG) activity . EEG activity changes with wakefulness, drowsiness and sleep and investigators...rapid-eye- movement ( NREM ) sleep , the amplitude of certain components of the ERPs (P1 and N2) increased while the amplitude of other compone’nts (Ni

  13. 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)

  14. 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

  15. 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…

  16. Binocular and monocular/unihemispheric sleep in the domestic chick (Gallus gallus) after a moderate sleep deprivation.

    PubMed

    Bobbo, Daniela; Nelini, Cristian; Mascetti, Gian G

    2008-03-01

    Binocular (Bin-sleep) and monocular/unihemispheric sleep (Mo-Un sleep) were studied in domestic chicks (Gallus gallus) after an 8 h period of sleep deprivation. Eleven-day-old chicks were divided into three groups: two non-deprived (N-DEP1 and N-DEP2) and one deprived for 8 h (DEP-8H). Deprivation was performed by placing chicks on a treadmill on which they were forced to walk continuously. Sleep behaviour was recorded for 6 h consecutively immediately after the end of sleep deprivation. During the recovery period, sleep-deprived chicks slept for a longer duration, spent significantly more time in binocular sleep and slept for significantly longer episodes that did control chicks. Regarding Mo-Un sleep, sleep deprivation seems to affect the right hemisphere by reducing the number of episodes and the time spent sleeping with the left eye closed. These results suggest that sleep-deprivation significantly influences the pattern of sleep in domestic chicks allowing for a better recovery.

  17. 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.

  18. 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

  19. 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

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

    NASA Technical Reports Server (NTRS)

    Carskadon, Mary A.

    1997-01-01

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

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

    NASA Technical Reports Server (NTRS)

    Carskadon, Mary A.

    1997-01-01

    Previous work has indicated that a small but significant number of participants in sleep deprivation studies or in simulated shift work experiments manifests an exaggerated performance decrement when they reach a critical point in the experiment, usually near the trough of the circadian cycle or the middle of the night. Those who show this exaggerated response do not appear to differ from other 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

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

    NASA Technical Reports Server (NTRS)

    Carskadon, Mary A.

    1997-01-01

    Previous work has indicated that a small but significant number of participants in sleep deprivation studies or in simulated shift work experiments manifests an exaggerated performance decrement when they reach a critical point in the experiment, usually near the trough of the circadian cycle or the middle of the night. Those who show this exaggerated response do not appear to differ from other 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

  3. 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.

  4. [A world record in marathon tennis: sleep deprivation and performance].

    PubMed

    Tafti, M; Vergé, M; Besset, A; Billiard, M

    1989-01-01

    We studied the effects of marked sleep deprivation on the EEG patterns and performance of a physically fit man (age 26) on the occasion of the world record continuous marathon tennis play (147 hours, 20 minutes). Before and immediately after the marathon, the sleep patterns of the player were recorded in our laboratory. After playing for 40 and 80 hours and within 24 hours, the performance changes were evaluated each hour. Amounts of the different sleep stages during the first recovery night compared with those of the baseline indicate an increase of 56% for total sleep time, 54% for stages 1 and 2, 154% for stages 3 and 4 and 20% for REM sleep. During the second recovery night, only REM sleep showed an increase. Activity index showed a marked decrease after 80 hours of sleep deprivation compared with that after 40 hours and was dramatically worsened during nighttime. The number of faults and pauses was also increased after 80 hours, suggesting a clear performance deterioration. Our results confirmed the effects of sleep deprivation on the recovery and performance deterioration.

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

    PubMed

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

    2011-01-01

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

  6. Chronic sleep deprivation and seasonality: Implications for the obesity epidemic

    PubMed Central

    Cizza, G.; Requena, M.; Galli, G.; de Jonge, L.

    2012-01-01

    Sleep duration has progressively fallen over the last 100 years while obesity has increased in the past 30 years. Several studies have reported an association between chronic sleep deprivation and long-term weight gain. Increased energy intake due to sleep loss has been listed as the main mechanism. The consequences of chronic sleep deprivation on energy expenditure have not been fully explored. Sleep, body weight, mood and behavior are subjected to circannual changes. However, in our modern environment seasonal changes in light and ambient temperature are attenuated. Seasonality, defined as cyclic changes in mood and behavior, is a stable personality trait with a strong genetic component. We hypothesize that the attenuation in seasonal changes in the environment may produce negative consequences, especially in individuals more predisposed to seasonality, such as women. Seasonal affective disorder, a condition more common in women and characterized by depressed mood, hypersomnia, weight gain, and carbohydrate craving during the winter, represents an extreme example of seasonality. One of the postulated functions of sleep is energy preservation. Hibernation, a phenomenon characterized by decreased energy expenditure and changes in the state of arousal, may offer useful insight into the mechanisms behind energy preservation during sleep. The goals of this article are to: a) consider the contribution of changes in energy expenditure to the weight gain due to sleep loss; b) review the phenomena of seasonality, hibernation, and their neuroendocrine mechanisms as they relate to sleep, energy expenditure, and body weight regulation. PMID:21720205

  7. Effects of sleep deprivation on short-term recognition memory.

    PubMed

    Polzella, D J

    1975-03-01

    A probe-recognition short-term memory paradigm was used to inquire into the precise effects of sleep deprivation on human memory. It was found that recognition performance, as measured by d', was generally impaired for each subjects after 24 hr of sleep deprivation. While d' was shown to decrease exponentially as the number of items intervening between the target and the probe increased, this decay rate was not affected by sleep loss. In addition there was confirmation of a previously observed increase in the positive skewness of reaction times after wakefulness. The data were consistent with the hypothesis that sleep deprivation increases the occurrence of lapses, periods of lowered reactive capacity, which prevent the encoding of items in short-term memory.

  8. Salivary Biomarkers of Physical Fatigue as Markers of Sleep Deprivation

    PubMed Central

    Michael, Darren J.; Valle, Bianca; Cox, Jennifer; Kalns, John E.; Fogt, Donovan L.

    2013-01-01

    Study Objective: Determine whether a salivary biomarker of physical fatigue, referred to as the fatigue biomarker index (FBI), can discriminate a control group from a sleep deprived group when saliva is collected under controlled conditions. The study expands on previous work examining changes in the composition of saliva during periods of prolonged exercise. Methods: Thirty (30) young adults (14 Control [CON]; 16 Sleep Deprived [SDEP]) were monitored for mood state (Profile of Mood States [POMS]), cognitive performance (Stroop Color-Conflict Tests), and salivary biomarkers of physical fatigue over a 48-h period with sampling at 3-h intervals. Trials lasted from 06:00 on day 1 (time = -3 h) to 09:00 on day 3 (time = 48 h). Levels of salivary biomarkers were calculated from liquid chromatography-mass spectrometry (LC-MS) data. Statistical comparisons were made using Wilcoxon rank sum tests with a Bonferroni correction to limit type 1 error. Receiver-operator characteristic (ROC) analysis was used to evaluate the ability of the various parameters to distinguish the SDEP population from the CON population. Results: Longitudinal analysis demonstrated significant between-group differences in all three parameters. ROC analysis demonstrated that cognitive performance tests and salivary biomarkers of physical fatigue distinguish the SDEP population from the CON population. Conclusions: A previously identified salivary biomarker of physical fatigue may provide an alternative method for discriminating sleep deprived from rested individuals. The salivary biomarker of physical fatigue holds promise as an objective measure of sleep deprivation, perhaps eventually removing the reliance on self-reported sleep diaries and/or repeated polysomnographs for longitudinal tracking of sleep quality and/or diagnosis of sleep disorders. Citation: Michael DJ; Valle B; Cox J; Kalns JE; Fogt DL. Salivary biomarkers of physical fatigue as markers of sleep deprivation. J Clin Sleep Med 2013

  9. [Circadian fluctuations in the muscular efficiency of athletes: with sleep versus sleep deprivation].

    PubMed

    Callard, D; Gauthier, A; Maffiuletti, N; Davenne, D; Van Hoecke, J

    2000-01-01

    The influence of time of day on muscular performance was studied. From part of the results of two different studies (EAS et EPS), the effects of sleep deprivation were appreciated. Seven times over the 24-h period, developed torque and myoelectric activity were estimated during maximal isometric voluntary contractions using an isokinetic dynamometer: elbow flexion for EAS in standardised sleep, and knee extension for EPS in complete sleep deprivation. The results showed nycthemeral changes in torque in both conditions (p < 0.005), with maximal values recorded at the beginning of night. Although during sleep deprivation (EPS) the rhythm followed neurophysiological factors, during EAS, this rhythm was accounted for by the variations in the contractile state of muscle.

  10. 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.

  11. Sleep deprivation and its effects on object-selective attention.

    PubMed

    Chee, Michael W L; Tan, Jiat Chow; Parimal, Sarayu; Zagorodnov, Vitali

    2010-01-15

    Sleep deprivation (SD) affects attention but it is an open question as to whether all subtypes of attention are similarly affected. We investigated the effects of 24 h of total SD on object-selective attention. 26 healthy, young adults viewed quartets of alternating faces or place scenes and performed selective judgments on faces only, scenes only or both faces and scenes. Volunteers underwent fMRI following a normal night of sleep and again following approximately 24 h of total sleep deprivation in a counterbalanced fashion. Sleep deprivation resulted in slower and less accurate picture classification as well as poorer recognition memory for scenes. Attention strongly modulated activation in the Parahippocampal Place Area (PPA). Task-related activation in the fronto-parietal cortex and PPA was reduced in SD, but the relative modulation of PPA activation by attention was preserved. Psychophysiological interaction between the left intra-parietal sulcus and the PPA that was clearly present after a normal night of sleep was reduced below threshold following SD suggesting that PPI may be a more sensitive method of detecting change in selective attention. Sleep deprivation may affect object-selective attention in addition to exerting a task-independent deficit in attention.

  12. 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

  13. Effects of cocaine, methamphetamine and modafinil challenge on sleep rebound after paradoxical sleep deprivation in rats.

    PubMed

    Martins, R C S; Andersen, M L; Shih, M C; Tufik, S

    2008-01-01

    Sleep loss is both common and critically relevant to our society and might lead to the abuse of psychostimulants such as amphetamines, cocaine and modafinil. Since psychoactive substance abuse often occurs within a scenario of sleep deficit, the purpose of this investigation was to compare the sleep patterns of rats challenged with cocaine (7 mg/kg, ip), methamphetamine (7 mg/kg, ip), or modafinil (100 mg/kg, ip) subsequent to paradoxical sleep deprivation (PSD) for 96 h. Our results show that, immediately after 96 h of PSD, rats (10 per group) that were injected with a psychostimulant presented lower percentages of paradoxical sleep compared to those injected with saline (P < 0.01). Regarding slow wave sleep (SWS), rats injected with psychostimulants after PSD presented a late rebound (on the second night subsequent to the injection) in the percentage of this phase of sleep when compared to PSD rats injected with saline (P < 0.05). In addition, the current study has produced evidence of the characteristic effect of each drug on sleep architecture. Home cage control rats injected with modafinil and methamphetamine showed a reduction in SWS compared with the saline group. Methamphetamine affected sleep patterns most, since it significantly reduced paradoxical sleep, SWS and sleep efficiency before and after PSD compared to control (P < 0.05). Cocaine was the psychostimulant causing the least changes in sleep pattern in relation to those observed after saline injection. Therefore, our results suggest that abuse of these psychostimulants in a PSD paradigm aggravates their impact on sleep patterns.

  14. 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.

  15. Prolonged Eyelid Closure Episodes during Sleep Deprivation in Professional Drivers

    PubMed Central

    Alvaro, Pasquale K.; Jackson, Melinda L.; Berlowitz, David J.; Swann, Philip; Howard, Mark E.

    2016-01-01

    Study Objectives: Real life ocular measures of drowsiness use average blink duration, amplitude and velocity of eyelid movements to reflect drowsiness in drivers. However, averaged data may conceal the variability in duration of eyelid closure episodes, and more prolonged episodes that indicate higher levels of drowsiness. The current study aimed to describe the frequency and duration of prolonged eyelid closure episodes during acute sleep deprivation. Methods: Twenty male professional drivers (mean age ± standard deviation = 41.9 ± 8.3 years) were recruited from the Transport Workers Union newsletter and newspaper advertisements in Melbourne, Australia. Each participant underwent 24 hours of sleep deprivation and completed a simulated driving task (AusEd), the Psychomotor Vigilance Task, and the Karolinska Sleepiness Scale. Eyelid closure episodes during the driving task were recorded and analyzed manually from digital video recordings. Results: Eyelid closure episodes increased in frequency and duration with a median of zero s/h of eyelid closure after 3 h increasing to 34 s/h after 23 h awake. Eyelid closure episodes were short and infrequent from 3 to 14 h of wakefulness. After 17 h of sleep deprivation, longer and more frequent eyelid closure episodes began to occur. Episodes lasting from 7 seconds up to 18 seconds developed after 20 h of wakefulness. Length of eyelid closure episodes was moderately to highly correlated with the standard deviation of lateral lane position, braking reaction time, crashes, impaired vigilance, and subjective sleepiness. Conclusions: The frequency and duration of episodes of prolonged eyelid closure increases during acute sleep deprivation, with very prolonged episodes after 17 hours awake. Automated devices that assess drowsiness using averaged measures of eyelid closure episodes need to be able to detect prolonged eyelid closure episodes that occur during more severe sleep deprivation. Citation: Alvaro PK, Jackson ML

  16. Role of Sleep Deprivation in Fear Conditioning and Extinction: Implications for Treatment of PTSD

    DTIC Science & Technology

    2013-10-01

    of the model is the impact on sleep . In animals, fear conditioning disrupts sleep , especially REM sleep . Sleep deprivation, in whole or just of REM ...was tested. We examined the effects of initial learning on REM sleep and whether REM sleep subsequent to learning facilitated memory consolidation of...threat and safety. Results showed increased safety learning was associated with increased consolidation of REM sleep the subsequent night. Increased

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

    PubMed Central

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

    2015-01-01

    Objective Changes in slow waves during non-rapid eye movement (NREM) sleep in response to acute total sleep deprivation are well-established measures of sleep homeostasis. This investigation utilized high-density electroencephalography (hdEEG) to examine topographic changes in slow waves during repeated partial sleep deprivation. Methods Twenty-four participants underwent a 6-day sleep restriction protocol. Spectral and period-amplitude analyses of sleep hdEEG data were used to examine changes in slow wave energy, count, amplitude, and slope relative to baseline. Results Changes in slow wave energy were dependent on the quantity of NREM sleep utilized for analysis, with widespread increases during sleep restriction and recovery when comparing data from the first portion of the sleep period, but restricted to recovery sleep if the entire sleep episode was considered. Period-amplitude analysis was less dependent on the quantity of NREM sleep utilized, and demonstrated topographic changes in the count, amplitude, and distribution of slow waves, with frontal increases in slow wave amplitude, numbers of high-amplitude waves, and amplitude/slopes of low amplitude waves resulting from partial sleep deprivation. Conclusions Topographic changes in slow waves occur across the course of partial sleep restriction and recovery. Significance These results demonstrate a homeostatic response to partial sleep loss in humans. PMID:26596212

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

    PubMed

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

    2017-01-01

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

  19. 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

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

    PubMed

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

    2017-02-01

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

  1. Rapid eye movement sleep deprivation affects sleep similarly in castrated and noncastrated rats.

    PubMed

    Peder, M

    1987-03-01

    Twenty-four-hour recordings of electrophysiological correlates of the sleep-waking cycle in castrated and noncastrated Wistar rats were performed to validate the cuff pedestal technique in the deprivation of rapid eye movement sleep. An undisturbed pattern of sleep was found in both castrated and noncastrated rats when the cuffs were in the raised position. The lowering of the cuff for 4 days virtually abolished REMs in both groups of rats. During neither the dark nor the light period was there any difference between the castrated and noncastrated rats in the total amount of REMs rebound. The results accord with the data obtained by the conventional flowerpot procedure and show that castration does not influence the amount of REMs before, during, and after REMs deprivation in the rat. It is suggested that testicular testosterone, contrary to growth hormone, is not essential for the triggering of REMs sleep, although both have anabolic actions.

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

    PubMed

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

    1988-08-01

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

  3. Changes in brain glycogen after sleep deprivation vary with genotype.

    PubMed

    Franken, Paul; Gip, Phung; Hagiwara, Grace; Ruby, Norman F; Heller, H Craig

    2003-08-01

    Sleep has been functionally implicated in brain energy homeostasis in that it could serve to replenish brain energy stores that become depleted while awake. Sleep deprivation (SD) should therefore lower brain glycogen content. We tested this hypothesis by sleep depriving mice of three inbred strains, i.e., AKR/J (AK), DBA/2J (D2), and C57BL/6J (B6), that differ greatly in their sleep regulation. After a 6-h SD, these mice and their controls were killed by microwave irradiation, and glycogen and glucose were quantified in the cerebral cortex, brain stem, and cerebellum. After SD, both measures significantly increased by approximately 40% in the cortex of B6 mice, while glycogen significantly decreased by 20-38% in brain stem and cerebellum of AK and D2 mice. In contrast, after SD, glucose content increased in all three structures in AK mice and did not change in D2 mice. The increase in glycogen after SD in B6 mice persisted under conditions of food deprivation that, by itself, lowered cortical glycogen. Furthermore, the strains that differ most in their compensatory response to sleep loss, i.e., AK and D2, did not differ in their glycogen response. Thus glycogen content per se is an unlikely end point of sleep's functional role in brain energy homeostasis.

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

    PubMed

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

    2012-05-15

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

  5. 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…

  6. Effects of 72-Hour Partial Sleep Deprivation on Human Behavioral and Physiological Response Measures.

    DTIC Science & Technology

    Ten adult males were subjected to partial sleep deprivation experiments in order to study the effects of progressive sleep deprivation on the basic...progressive loss of performance capability. Power spectral data also show changes as a function of sleep deprivation , indicating that one feature of this type of stress may be an alteration of basic human biorhythms. (Author)

  7. Sleep active cortical neurons expressing neuronal nitric oxide synthase are active after both acute sleep deprivation and chronic sleep restriction.

    PubMed

    Zielinski, M R; Kim, Y; Karpova, S A; Winston, S; McCarley, R W; Strecker, R E; Gerashchenko, D

    2013-09-05

    Non-rapid eye movement (NREM) sleep electroencephalographic (EEG) delta power (~0.5-4 Hz), also known as slow wave activity (SWA), is typically enhanced after acute sleep deprivation (SD) but not after chronic sleep restriction (CSR). Recently, sleep-active cortical neurons expressing neuronal nitric oxide synthase (nNOS) were identified and associated with enhanced SWA after short acute bouts of SD (i.e., 6h). However, the relationship between cortical nNOS neuronal activity and SWA during CSR is unknown. We compared the activity of cortical neurons expressing nNOS (via c-Fos and nNOS immuno-reactivity, respectively) and sleep in rats in three conditions: (1) after 18-h of acute SD; (2) after five consecutive days of sleep restriction (SR) (18-h SD per day with 6h ad libitum sleep opportunity per day); (3) and time-of-day matched ad libitum sleep controls. Cortical nNOS neuronal activity was enhanced during sleep after both 18-h SD and 5 days of SR treatments compared to control treatments. SWA and NREM sleep delta energy (the product of NREM sleep duration and SWA) were positively correlated with enhanced cortical nNOS neuronal activity after 18-h SD but not 5days of SR. That neurons expressing nNOS were active after longer amounts of acute SD (18h vs. 6h reported in the literature) and were correlated with SWA further suggest that these cells might regulate SWA. However, since these neurons were active after CSR when SWA was not enhanced, these findings suggest that mechanisms downstream of their activation are altered during CSR.

  8. 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.

  9. 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

  10. Effects of a selective sleep deprivation on subsequent anaerobic performance.

    PubMed

    Mougin, F; Bourdin, H; Simon-Rigaud, M L; Didier, J M; Toubin, G; Kantelip, J P

    1996-02-01

    The aim of the study was to investigate the effects of a partial sleep deprivation on a subsequent supramaximal exercise evaluated from the 30 second Wingate test, and on the following recovery. To take into account the active muscle mass, the Wingate test was performed against a constant braking force related to the data of a force-velocity test conducted on a Monark cycle ergometer (Model 814 E with weights) one week before the experimental test. Eight highly trained athletes were enrolled for this study. The changes in ventilatory and metabolic responses were analyzed during and upon completion of physical 30 second exercise, taking place after two nights, in other words, after a reference night and after a night with reduced sleep. Partial sleep deprivation was obtained by delaying bedtime until 3 a.m. The 30 second Wingate test was performed between 9 a.m. and noon the following days, using a Monark ergometer (Model 814 F). The analyses of change scores disclosed that there were no main significant effects for measures of ventilation, lactates and pH(v) levels under the two experimental conditions. The peak power, the mean power output and the peak velocity recorded after partial sleep deprivation were not modified in comparison with the values obtained after the reference night. These findings suggest that acute sleep loss did not contribute to alterations in supramaximal exercise.

  11. 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.

  12. 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

  13. 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.

  14. 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.

  15. 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

  16. Aging does not affect the sleep endocrine response to total sleep deprivation in humans.

    PubMed

    Murck, H; Antonijevic, I A; Schier, T; Frieboes, R M; Barthelmes, J; Steiger, A

    1999-01-01

    Aging is associated with decreased sleep continuity, slow wave sleep (SWS), growth hormone (GH) release and an increased hypothalamo-pituitary-adrenocortical (HPA) system activity. Total sleep deprivation (TSD) is a strong stimulus for sleep. To determine if aging affects the response to TSD, for the first time the combined effects of TSD on conventional and spectral sleep electroencephalographic (EEG) parameters and GH, cortisol and prolactin secretion were compared in elderly (60-80 years; n = 7) vs. younger subjects (20-30 years; n = 7). MANOVA revealed a reduction of SWS in the elderly. TSD led to an increase in SWS, a decrease in sleep onset latency, rapid eye movement (REM) density and by trend REM-latency without a global group difference. GH was reduced, whereas prolactin was enhanced in the elderly. After TSD GH was unchanged and prolactin secretion was enhanced without group difference. Thus, the plasticity of the sleep-endocrine system in response to TSD is sustained during aging. The possible involvement of the GABAergic system, that seems not to be severely impaired with age, is proposed.

  17. 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

  18. Exercise-Induced growth hormone during acute sleep deprivation.

    PubMed

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

    2014-10-01

    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.

  19. 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

  20. 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.

  1. 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.

  2. Small platform sleep deprivation selectively increases the average duration of rapid eye movement sleep episodes during sleep rebound.

    PubMed

    Kitka, Tamas; Katai, Zita; Pap, Dorottya; Molnar, Eszter; Adori, Csaba; Bagdy, Gyorgy

    2009-12-28

    The single platform-on-water (flower pot) method is extensively used for depriving rapid eye movement sleep (REMS). Detailed comparison of sleep-wake architecture, recorded during the rebound period after spending three days on either a small or large platform, could separate the effects of REMS deficit from other stress factors caused by the procedure. A further aim of the study was to find the most characteristic REMS parameter of the rebound originating from REMS deficit. Rats were kept on a small or large platform for 72 h. Their fronto-parietal electroencephalogram, electromyogram and motility were recorded during the 24 h rebound at the beginning of the passive phase. A similar period of a home cage group was also recorded. The most typical differences between the two rebound groups were the increased cumulative time and longer average duration of REMS episodes without significant change in the number of these episodes of the small platform animals during the passive phase. Results obtained by cosinor analysis were in accordance with the findings above. Since we did not find any difference in the average duration of REMS episodes comparing the large platform rebound group and the home cage group, we concluded that the increased mean duration of REMS episodes is a selective marker for the rebound caused by small platform sleep deprivation, while other changes in sleep architecture may be the consequence of stress and also some sleep deficit.

  3. The Effects of Two Types of Sleep Deprivation on Visual Working Memory Capacity and Filtering Efficiency

    PubMed Central

    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). PMID

  4. 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…

  5. 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…

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

    DTIC Science & Technology

    2002-11-01

    modafinil on plasma melatonin , cortisol and growth hormone rhythms, rectal temperature and performance in healthy subjects during 36h sleep deprivation...UNCLASSIFIED Defense Technical Information Center Compilation Part Notice ADP013763 TITLE: An Overview of Sleep Deprivation and The Ameliorative...Effects of Modafinil DISTRIBUTION: Approved for public release, distribution unlimited rhis paper is part of the following report: TITLE: Sleep

  7. 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

  8. Effects of sleep deprivation on measures of the febrile reaction and the recovery of somatovisceral functions and sleep in endotoxemia.

    PubMed

    Lapshina, K V; Ekimova, I V

    2010-05-01

    Electroencephalographic methods were used to study the effects of total sleep deprivation on thermoregulatory measures of the fever response in pigeons (Columba livia): brain temperature, peripheral vasomotor reactions, thoracic muscle contractile activity, and the recovery of somatic functions and the time characteristics of waking and sleep in lipopolysaccharide (LPS)-induced endotoxemia. Sleep deprivation during the period in which the quantity of slow-wave sleep increased on administration of LPS induced decreases in the latent period of fever onset and in the duration of fever, along with more significant increases in brain temperature and the level of muscle contractile activity as compared with the effects of LPS alone. The period after sleep deprivation was characterized by more prolonged recovery of muscle contractile activity and the time characteristics of sleep and waking states, along with more prolonged compensatory "rebound" of slow-wave sleep as compared with the effects of sleep deprivation alone. Thus, sleep deprivation in endotoxemia led to decreases in the latent period of fever onset, exacerbation of fever, and increases in the latent period of recovery of physiological functions.

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

    PubMed

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

    2014-03-01

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

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

    PubMed Central

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

    2014-01-01

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

  11. 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

  12. 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…

  13. 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).

  14. A Time for Learning and a Time for Sleep: The Effect of Sleep Deprivation on Contextual Fear Conditioning at Different Times of the Day

    PubMed Central

    Hagewoud, Roelina; Whitcomb, Shamiso N.; Heeringa, Amarins N.; Havekes, Robbert; Koolhaas, Jaap M.; Meerlo, Peter

    2010-01-01

    Study Objectives: Sleep deprivation negatively affects memory consolidation, especially in the case of hippocampus-dependent memories. Studies in rodents have shown that 5 hours of sleep deprivation immediately following footshock exposure selectively impairs the formation of a contextual fear memory. In these studies, both acquisition and subsequent sleep deprivation were performed in the animals' main resting phase. However, in everyday life, subjects most often learn during their active phase. Design: Here we examined the effects of sleep deprivation on memory consolidation for contextual fear in rats when the task was performed at different times of the day, particularly, at the beginning of the resting phase or right before the onset of the active phase. Measurements and Results: Results show that sleep deprivation immediately following training affects consolidation of contextual fear, independent of time of training. However, in the resting phase memory consolidation was impaired by 6 hours of posttraining sleep deprivation, whereas, in the active phase, the impairment was only seen after 12 hours of sleep deprivation. Since rats sleep at least twice as much during the resting phase compared with the active phase, these data suggest that the effect of sleep deprivation depends on the amount of sleep that was lost. Also, control experiments show that effects of sleep deprivation were not related to the amount of stimulation the animals received and were therefore not likely an indirect effect of the sleep-deprivation method. Conclusion: These results support the notion that sleep immediately following acquisition, independent of time of day, promotes memory consolidation and that sleep deprivation may disrupt this process depending on the amount of sleep that is lost. Citation: Hagewoud R; Whitcomb SN; Heeringa AN; Havekes R; Koolhaas JM; Meerlo P. A time for learning and a time for sleep: the effect of sleep deprivation on contextual fear conditioning at

  15. Proteomic changes in rat hippocampus and adrenals following short-term sleep deprivation

    PubMed Central

    Poirrier, Jean-Etienne; Guillonneau, François; Renaut, Jenny; Sergeant, Kjell; Luxen, Andre; Maquet, Pierre; Leprince, Pierre

    2008-01-01

    Background To identify the biochemical changes induced by sleep deprivation at a proteomic level, we compared the hippocampal proteome of rats either after 4 hours of sleep or sleep deprivation obtained by gentle handling. Because sleep deprivation might induce some stress, we also analyzed proteomic changes in rat adrenals in the same conditions. After sleep deprivation, proteins from both tissues were extracted and subjected to 2D-DIGE analysis followed by protein identification through mass spectrometry and database search. Results In the hippocampus, 87 spots showed significant variation between sleep and sleep deprivation, with more proteins showing higher abundance in the latter case. Of these, 16 proteins were present in sufficient amount for a sequencing attempt and among the 12 identified proteins, inferred affected cellular functions include cell metabolism, energy pathways, transport and vesicle trafficking, cytoskeleton and protein processing. Although we did not observe classical, macroscopic effect of stress in sleep-deprived rats, 47 protein spots showed significant variation in adrenal tissue between sleep and sleep deprivation, with more proteins showing higher abundance following sleep. Of these, 16 proteins were also present in sufficient amount for a sequencing attempt and among the 13 identified proteins, the most relevant cellular function that was affected was cell metabolism. Conclusion At a proteomic level, short term sleep deprivation is characterized by a higher expression of some proteins in the hippocampus and a lower abundance of other proteins in the adrenals (compared to normal sleep control). Altogether, this could indicate a general activation of a number of cellular mechanisms involved in the maintenance of wakefulness and in increased energy expenditure during sleep deprivation. These findings are relevant to suggested functions of sleep like energy repletion and the restoration of molecular stocks or a more global homeostasis of

  16. 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.

  17. 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

  18. Individualising EEG frequency bands for sleep deprivation studies.

    PubMed

    Henelius, Andreas; Korpela, Jussi; Huotilainen, Minna

    2011-01-01

    A method for determining individualised frequency bands from electroencephalographic (EEG) power spectral density (PSD) plots is presented. EEG was collected during the performance of a computerised multitask test from 21 healthy male subjects, of which an experimental group of 14 subjects underwent sleep deprivation and 7 subjects formed the control group. EEG PSD plots were compared between the groups and were used to determine individual theta, alpha and beta bands for the subjects by studying the points of intersection between the individual subjects' normalised spectra and the normalised average spectrum of the control group. The results show that the frontal and occipital locations are best suited for the determination of individualised frequency bands. The proposed method can be used to enhance EEG spectral analysis of task-induced cognitive effort during sleep deprivation.

  19. Degradation of Cortical Representations during Encoding following Sleep Deprivation.

    PubMed

    Poh, Jia-Hou; Chee, Michael W L

    2017-02-01

    A night of total sleep deprivation (TSD) reduces task-related activation of fronto-parietal and higher visual cortical areas. As this reduction in activation corresponds to impaired attention and perceptual processing, it might also be associated with poorer memory encoding. Related animal work has established that cortical columns stochastically enter an 'off' state in sleep deprivation, leading to predictions that neural representations are less stable and distinctive following TSD. To test these predictions participants incidentally encoded scene images while undergoing fMRI, either during rested wakefulness (RW) or after TSD. In scene-selective PPA, TSD reduced stability of neural representations across repetition. This was accompanied by poorer subsequent memory. Greater representational stability benefitted subsequent memory in RW but not TSD. Even for items subsequently recognized, representational distinctiveness was lower in TSD, suggesting that quality of encoding is degraded. Reduced representational stability and distinctiveness are two novel mechanisms by which TSD can contribute to poorer memory formation.

  20. A comparison of tyrosine against placebo, phentermine, caffeine, and D-amphetamine during sleep deprivation.

    PubMed

    Waters, William F; Magill, Richard A; Bray, George A; Volaufova, Julia; Smith, Steven R; Lieberman, Harris R; Rood, Jennifer; Hurry, Mark; Anderson, Tai; Ryan, Donna H

    2003-08-01

    Sleep deprivation can impair alertness and cognitive and motor performance. We hypothesized that the amino acid tyrosine might reduce deleterious effects of sleep deprivation. Seventy-six healthy males, age 18-35 years, participated in a four-day protocol that included a habituation night, a baseline night, a 40.5 h period without sleep, and a recovery night. Tyrosine 150 mg/kg, caffeine 300 mg/70 kg, phentermine 37.5 mg, D-amphetamine 20 mg and placebo were administered in a double-blind, randomized fashion to compare their effects on the time it took to fall asleep, on endocrine responses during sleep deprivation, and on sleep quantity, quality and architecture as measured by polysomnography during recovery sleep. When given after 36 h without sleep, tyrosine had no significant effect on any parameter of sleep. D-amphetamine produced marked decrease in sleep drive but caused deleterious effects on many aspects of recovery sleep. Still, D-amphetamine was associated with increased alertness on the first recovery day. Phentermine and caffeine both decreased sleep drive during sleep deprivation, but phentermine impaired rapid-eye-movement (REM) recovery sleep. Tyrosine (when compared to placebo) had no effect on any sleep related measure, but it did stimulate prolactin release.

  1. 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.

  2. 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.

  3. 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.

  4. 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

  5. Auditory and Visual Evoked Potentials as a Function of Sleep Deprivation and Irregular Sleep

    DTIC Science & Technology

    1989-08-15

    Broughton, 1968). If the cyclicity of REM sleep is a sleep -dependent phenomenon as purported by Moses et al. (1977), rather than the sleeping ...1977). The auditory evoked brain response during adult human sleep . Waking and Sleeping , 1, 189-194. Aserinsky, E., & Kleitman, N. (1953). Regularly...wave versus REM sleep . Psychophysiology, 5, 231. Globus, G.G., Drury, R. L., Phoebus, E.C., & Boyd, R. (1971). Ultradian rhythms in human performance

  6. The effects of sleep and sleep deprivation on task-switching performance.

    PubMed

    Couyoumdjian, Alessandro; Sdoia, Stefano; Tempesta, Daniela; Curcio, Giuseppe; Rastellini, Elisabetta; DE Gennaro, Luigi; Ferrara, Michele

    2010-03-01

    Neural systems of the prefrontal cortex (PFC) involved in executive functions are particularly vulnerable to sleep deprivation (SD). In this study, we investigated whether SD selectively affects specific components of the executive control processes involved in task-switching performance. Two different tasks are performed in rapid and random succession in this procedure, so that the to-be-executed task may change from one trial to the next (switch trial), or may be repeated (repetition trial). Task-switches are usually slower than task repetitions, giving way to the 'switch cost'. One hundred and eight university students were assigned randomly to the sleep (S) or the SD group. Each of them was tested on a task-switching paradigm before and after an experimental night (S or SD), and after one recovery night. SD impaired both task-switching accuracy and speed. A higher proportion of errors and increased switch costs after SD have been observed, compared to normal sleep. Control analyses on switch and repetition trials showed that the SD group was significantly worse only on the switch trials. The effects of SD are reverted by one night of recovery sleep. It is concluded that the ability to adjust behaviour rapidly and flexibly to changing environmental demands, which relies on the functional integrity of the PFC, is impacted negatively by sleep loss.

  7. 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.

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

    PubMed

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

    2017-03-01

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

  9. Role of Sleep Deprivation in Fear Conditioning and Extinction: Implications for Treatment of PTSD

    DTIC Science & Technology

    2014-10-01

    Groeger JA, Santhi N, Arbon EL, Lazar AS, Hasan S, et al. Effects of partial and acute total sleep deprivation on performance across cognitive...Acheson, D., Risbrough, V., Drummond, S., Geyer, M., Young, J. Sleep deprivation impairs performance in the 5-choice continuous performance test...examining the effects of our sleep deprivation manipulation on attention with animal model data from Dr. Risbrough’s lab also examining the effects of

  10. High-Throughput Analysis of Dynamic Gene Expression Associated with Sleep Deprivation and Recovery Sleep in the Mouse Brain

    DTIC Science & Technology

    2006-12-01

    Gene Expression Associated with Sleep Deprivation and Recovery Sleep in the Mouse Brain PRINCIPAL INVESTIGATOR: Ed Lein, Ph.D...CONTRACTING ORGANIZATION: Allen Institute for Brain Science Seattle, WA 98103 REPORT DATE...Recovery Sleep in the Mouse Brain 5b. GRANT NUMBER W81XWH-06-1-0131 5c. PROGRAM ELEMENT NUMBER 6. AUTHOR(S) 5d. PROJECT NUMBER Ed Lein, Ph.D

  11. Sleep Deprivation Increases Cerebral Serotonin 2A Receptor Binding in Humans

    PubMed Central

    Elmenhorst, David; Kroll, Tina; Matusch, Andreas; Bauer, Andreas

    2012-01-01

    Study Objectives: Serotonin and its cerebral receptors play an important role in sleep-wake regulation. The aim of the current study is to investigate the effect of 24-h total sleep deprivation on the apparent serotonin 2A receptor (5-HT2AR) binding capacity in the human brain to test the hypothesis that sleep deprivation induces global molecular alterations in the cortical serotonergic receptor system. Design: Volunteers were tested twice with the subtype-selective radiotracer [18F]altanserin and positron emission tomography (PET) for imaging of 5-HT2ARs at baseline and after 24 h of sleep deprivation. [18F]Altanserin binding potentials were analyzed in 13 neocortical regions of interest. The efficacy of sleep deprivation was assessed by questionnaires, waking electroencephalography, and cognitive performance measurements. Setting: Sleep laboratory and neuroimaging center. Patients or Participants: Eighteen healthy volunteers. Interventions: Sleep deprivation. Measurements and Results: A total of 24 hours of sleep deprivation led to a 9.6% increase of [18F]altanserin binding on neocortical 5-HT2A receptors. Significant region-specific increases were found in the medial inferior frontal gyrus, insula, and anterior cingulate, parietal, sensomotoric, and ventrolateral prefrontal cortices. Conclusions: This study demonstrates that a single night of total sleep deprivation causes significant increases of 5-HT2AR binding potentials in a variety of cortical regions although the increase declines as sleep deprivation continued. It provides in vivo evidence that total sleep deprivation induces adaptive processes in the serotonergic system of the human brain. Citation: Elmenhorst D; Kroll T; Matusch A; Bauer A. Sleep Deprivation Increases Cerebral Serotonin 2A Receptor Binding in Humans. SLEEP 2012;35(12):1615-1623. PMID:23204604

  12. 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.

  13. 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.

  14. 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.

  15. 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.

  16. 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

  17. Total sleep deprivation decreases immobility in the forced-swim test.

    PubMed

    Lopez-Rodriguez, Faustino; Kim, Joseph; Poland, Russell E

    2004-06-01

    Sleep deprivation can exert antidepressant effects in humans in less than 24 h, making it the fastest acting antidepressant treatment. However, it is rarely used clinically because the effect disappears once the subject goes back to sleep. An understanding of the neurobiological mechanisms underlying the antidepressant effect of sleep deprivation should help to develop new rapidly acting antidepressant strategies. In the present report, an animal model of depression (the forced-swim test) was used to determine whether the effects of total sleep deprivation parallel those obtained with antidepressant drugs. Using the disk-over-water method, rats deprived of sleep for 24 h exhibited increased swimming behavior when compared to cage control rats, mimicking the effects of serotonergic antidepressants. After 48 h, sleep-deprived rats exhibited increased swimming when compared to both cage control and stimulus control rats, demonstrating that the effect is due to sleep deprivation per se, and not to extraneous factors inherent in the sleep deprivation protocol (such as stress and movement). We believe that this paradigm can be used to study the neurobiological mechanisms of rapid antidepressant effects induced by sleep deprivation.

  18. 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.

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

    ERIC Educational Resources Information Center

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

    2017-01-01

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

  20. Mood, alertness, and performance in response to sleep deprivation and recovery sleep in experienced shiftworkers versus non-shiftworkers.

    PubMed

    Wehrens, Sophie M T; Hampton, Shelagh M; Kerkhofs, Myriam; Skene, Debra J

    2012-06-01

    Previous studies have shown increased sleepiness and mood changes in shiftworkers, which may be due to sleep deprivation or circadian disruption. Few studies, however, have compared responses of experienced shiftworkers and non-shiftworkers to sleep deprivation in an identical laboratory setting. The aim of this laboratory study, therefore, was to compare long-term shiftworkers and non-shiftworkers and to investigate the effects of one night of total sleep deprivation (30.5 h of continuous wakefulness) and recovery sleep on psychomotor vigilance, self-rated alertness, and mood. Eleven experienced male shiftworkers (shiftwork ≥5 yrs) were matched with 14 non-shiftworkers for age (mean ± SD: 35.7 ± 7.2 and 32.5 ± 6.2 yrs, respectively) and body mass index (BMI) (28.7 ± 3.8 and 26.6 ± 3.4 kg/m(2), respectively). After keeping a 7-d self-selected sleep/wake cycle (7.5/8 h nocturnal sleep), both groups entered a laboratory session consisting of a night of adaptation sleep and a baseline sleep (each 7.5/8 h), a sleep deprivation night, and recovery sleep (4-h nap plus 7.5/8 h nighttime sleep). Subjective alertness and mood were assessed with the Karolinska Sleepiness Scale (KSS) and 9-digit rating scales, and vigilance was measured by the visual psychomotor vigilance test (PVT). A mixed-model regression analysis was carried out on data collected every hour during the sleep deprivation night and on all days (except for the adaptation day), at .25, 4.25, 5.25, 11.5, 12.5, and 13.5 h after habitual wake-up time. Despite similar circadian phase (melatonin onset), demographics, food intake, body posture, and environmental light, shiftworkers felt significantly more alert, more cheerful, more elated, and calmer than non-shiftworkers throughout the laboratory study. In addition, shiftworkers showed a faster median reaction time (RT) compared to non-shiftworkers, although four other PVT parameters did not differ between the groups. As expected, both groups showed a

  1. 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.

  2. 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.

  3. 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

  4. 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.

  5. 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.

  6. Recovery after prolonged sleep deprivation: residual effects of slow-release caffeine on recovery sleep, sleepiness and cognitive functions.

    PubMed

    Beaumont, Maurice; Batéjat, Denise; Coste, Olivier; Doireau, Philippe; Chauffard, Françoise; Enslen, Marc; Lagarde, Didier; Pierard, Christophe

    2005-01-01

    A long work schedule often results in sleep deprivation, sleepiness, impaired performance and fatigue. We investigated the residual effects of slow-release caffeine (SRC) on sleep, sleepiness and cognitive performance during a 42-hour recovery period following a 64-hour continuous wakefulness period in 16 healthy males, according to a double-blind, randomised, placebo-controlled, crossover study. Three hundred milligrams of SRC or placebo was given twice a day at 21:00 and 9:00 during the first 48 h of wakefulness. Recovery sleep was analysed with electroencephalography (EEG) and wrist actigraphy, daytime sleepiness with continuous EEG, sleep latency tests and actigraphy and cognitive functions with computerized tests from the NATO AGARD STRES battery. Both drug groups exhibited almost the same sleep architecture with a rebound of slow-wave sleep during both recovery nights and of REM sleep during the second night. Wakefulness level and cognitive functions were similarly impaired in both groups on the first day of recovery and partially returned to baseline on the second. To conclude, SRC appears to have no unwanted side-effects on recovery sleep, wakefulness and cognitive performance after a long period of sleep deprivation and might therefore be a useful choice over other psychostimulants for a long work schedule.

  7. 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

  8. [Effect of paradoxical sleep deprivation on elaboration and differentiation of alimentary conditioned reflexes].

    PubMed

    Koridze, M G; Nemsadze, N D

    1980-01-01

    Paradoxical sleep deprivation of cats by means of awakening them without any significant emotional stress does not affect the acquisition of sound discrimination. Paradoxical sleep deprivation by Jouvet's method producing emotional stress impairs the acquisition of sound discrimination. However, it fails to affect the reproduction of preliminary elaborated sound discrimination.

  9. Sleep deprivation affects inflammatory marker expression in adipose tissue

    PubMed Central

    2010-01-01

    Sleep deprivation has been shown to increase inflammatory markers in rat sera and peripheral blood mononuclear cells. Inflammation is a condition associated with pathologies such as obesity, cancer, and cardiovascular diseases. We investigated changes in the pro and anti-inflammatory cytokines and adipokines in different depots of white adipose tissue in rats. We also assessed lipid profiles and serum levels of corticosterone, leptin, and adiponectin after 96 hours of sleep deprivation. Methods The study consisted of two groups: a control (C) group and a paradoxical sleep deprivation by 96 h (PSD) group. Ten rats were randomly assigned to either the control group (C) or the PSD. Mesenteric (MEAT) and retroperitoneal (RPAT) adipose tissue, liver and serum were collected following completion of the PSD protocol. Levels of interleukin (IL)-6, interleukin (IL)-10 and tumour necrosis factor (TNF)-α were analysed in MEAT and RPAT, and leptin, adiponectin, glucose, corticosterone and lipid profile levels were analysed in serum. Results IL-6 levels were elevated in RPAT but remained unchanged in MEAT after PSD. IL-10 protein concentration was not altered in either depot, and TNF-α levels decreased in MEAT. Glucose, triglycerides (TG), VLDL and leptin decreased in serum after 96 hours of PSD; adiponectin was not altered and corticosterone was increased. Conclusion PSD decreased fat mass and may modulate the cytokine content in different depots of adipose tissue. The inflammatory response was diminished in both depots of adipose tissue, with increased IL-6 levels in RPAT and decreased TNF-α protein concentrations in MEAT and increased levels of corticosterone in serum. PMID:21034496

  10. 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.

  11. 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

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

    PubMed

    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.

  13. 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 ...

  14. The tired hippocampus: the molecular impact of sleep deprivation on hippocampal function.

    PubMed

    Havekes, Robbert; Abel, Ted

    2017-02-27

    Memory consolidation, the process by which information is stored following training, consists of synaptic consolidation and systems consolidation. It is widely acknowledged that sleep deprivation has a profound effect on synaptic consolidation, particularly for memories that require the hippocampus. It is unclear, however, which of the many molecular changes associated with sleep deprivation directly contribute to memory deficits. In this review, we highlight recent studies showing that sleep deprivation impairs hippocampal cAMP and mTOR signaling, and ultimately causes spine loss in CA1 neurons in a cofilin-dependent fashion. Reversing these molecular alterations made memory consolidation resistant to the negative impact of sleep deprivation. Together, these studies have started to identify the molecular underpinnings by which sleep deprivation impairs synaptic consolidation.

  15. Effect of 72 h of Sleep Deprivation on the Iowa Gambling Task

    PubMed Central

    LIU, Lei; ZHOU, Renlai

    2016-01-01

    Introduction Sleep deprivation has detrimental effects on cognitive processes, including decision making. The present study investigated how 72 h of sleep deprivation influenced individual neural performance in the Iowa gambling task using event-related potential technology. Methods Eleven healthy male adults who participated in our study were randomized to be either in group with 72 h of social isolation condition or 72 h of sleep deprivation condition. Results Results showed that, in the feedback stage, the N250–400 amplitude was smaller in post-test than in pre-test for the sleep deprivation condition, especially in the frontal cortex. No significant difference between the pre-test and post-test condition was found in the social isolation condition. Conclusion These results suggested that 72 h of sleep deprivation affected an individual’s response to feedback stimuli, causing the individual to evaluate the stimuli slowly. PMID:28360813

  16. 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

  17. Effect of rapid eye movement sleep deprivation on rat brain monoamine oxidases.

    PubMed

    Thakkar, M; Mallick, B N

    1993-08-01

    Monoamine oxidase, monoamine oxidase-A, and monoamine oxidase-B activities were compared in free moving, rapid eye movement sleep-deprived, recovered, and control rat brains. The activities were estimated in the whole brain, cerebrum, cerebellum, whole brainstem, medulla, pons, and midbrain. The flowerpot method was used for continuing deprivation for one, two, or four days. Monoamine oxidase activity decreased significantly in the cerebrum and the cerebellum of the sleep-deprived rats, whereas monoamine oxidase-A and monoamine oxidase-B were differentially affected. Medullary MAO-A was the first to be affected, showing an increase after just one day of rapid eye movement sleep deprivation, while longer deprivation decreased its activity. The activity of monoamine oxidase-B was not significantly affected in any brain areas of the deprived rats until after two days of rapid eye movement sleep deprivation. All the altered enzyme activities returned to control levels after recovery. Control experiments suggest that the decrease was primarily caused by the rapid eye movement sleep deprivation and was not due to nonspecific effects. These findings are consistent with past studies and may help to explain earlier observations. The results support the involvement of aminergic mechanisms in rapid eye movement sleep. The plausible reasons for the changes in the activities of monoamine oxidases, after rapid eye movement sleep deprivation, are discussed.

  18. 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.

  19. 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

  20. 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…

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

    MedlinePlus

    ... restless legs syndrome narcolepsy (extreme daytime sleepiness), and parasomnias (abnormal sleep behaviors). Michael J. Twery, Ph.D., ... that the symptoms of a sleep problem in children can be complicated. Some children may show signs ...

  2. 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.

  3. Sleep deprivation induces abnormal bone metabolism in temporomandibular joint

    PubMed Central

    Geng, Wei; Wu, Gaoyi; Huang, Fei; Zhu, Yong; Nie, Jia; He, Yuhong; Chen, Lei

    2015-01-01

    Background: The purpose of this study was to explore the effect of experimental sleep deprivation (SD) on the temporomandibular joint (TMJ) of rats and the possible mechanism related to abnormal bone metabolism. Material and methods: SD was induced by a modified multiple platform method and assessed by serum adrenocorticotropic hormone (ACTH) level. TMJs were detached and stained with hematoxylin and eosin (H&E). Expression of interleukin-1β (IL-1β), tumor necrosis factor alpha (TNF-α), osteoprotegerin (OPG) and receptor activator of nuclear factor kappa B ligand (RANKL) was evaluated by quantitative reverse transcription polymerase chain reaction, H&E staining, immunohistochemical staining and enzyme linked immunosorbent assay. Results: Compared with controls, SD significantly increased serum ACTH, indicating that the SD model was successful. In the SD group, H&E staining revealed greater vessel hyperplasia in the synovial membrane and thicker hypertrophic layers in condylar cartilages. Compared with controls, RNA and protein expression of the inflammatory factors IL-1β and TNF-α and the bone metabolism-related factor RANKL increased in condylar cartilage in the SD group, whereas OPG and the OPG/RANKL ratio decreased. Immunohistochemical staining revealed that OPG/RANKL immunopositive cells were mainly located in hypertrophic layers. Conclusions: These results suggest that sleep deprivation might play an important role in the occurrence and development of temporomandibular disorders, which may occur through abnormal secretion of inflammatory and bone metabolism-related factors. PMID:25785010

  4. The impact of sleep deprivation on food desire in the human brain.

    PubMed

    Greer, Stephanie M; Goldstein, Andrea N; Walker, Matthew P

    2013-01-01

    Epidemiological evidence supports a link between sleep loss and obesity. However, the detrimental impact of sleep deprivation on central brain mechanisms governing appetitive food desire remains unknown. Here we report that sleep deprivation significantly decreases activity in appetitive evaluation regions within the human frontal cortex and insular cortex during food desirability choices, combined with a converse amplification of activity within the amygdala. Moreover, this bi-directional change in the profile of brain activity is further associated with a significant increase in the desire for weight-gain promoting high-calorie foods following sleep deprivation, the extent of which is predicted by the subjective severity of sleep loss across participants. These findings provide an explanatory brain mechanism by which insufficient sleep may lead to the development/maintenance of obesity through diminished activity in higher-order cortical evaluation regions, combined with excess subcortical limbic responsivity, resulting in the selection of foods most capable of triggering weight-gain.

  5. Circadian rhythm in plasma noradrenaline of healthy sleep-deprived subjects.

    PubMed

    Candito, M; Pringuey, D; Jacomet, Y; Souêtre, E; Salvati, E; Ardisson, J L; Chambon, P; Darcourt, G

    1992-12-01

    Under normal sleep-wake conditions, noradrenaline (NA) secretions in supine subjects exhibit a weak circadian variation with a peak that occurs around noon; the sleep span is characterized by reduced NA secretion. Some investigators have reported that the circadian NA rhythm is completely obliterated during sleep deprivation. In our laboratory, plasma NA was assayed every hour for 24 h in nine healthy men 20-23 years of age. All men were deprived of sleep and were required to eat and walk around every hour to prevent sleep. However, subjects remained supine for 20 min before blood samples were collected to eliminate the effect of activity. Persistence of a slight decrease in the night concentration in several subjects, despite sleep deprivation, suggests that NA secretion may be influenced by a biological clock whose activity becomes visible when the influence of posture is removed.

  6. REM-sleep deprivation-induced increase in ethanol intake: role of brain monoaminergic neurons.

    PubMed

    Aalto, J; Kiianmaa, K

    1986-01-01

    The ethanol intake of Long-Evans male rats was recorded before, during and after deprivation of rapid eye movement (REM) sleep produced with the flowerpot technique modified by using a cuff pedestal and electrified grid floor instead of water. Ethanol intake increased significantly during REM-sleep deprivation. A rebound decrease in ethanol drinking was then observed during the REM-rebound phase immediately after the termination of REM-sleep deprivation. Because REM-sleep deprivation has been reported to impair the function of central monoamine neuronal systems and because some studies have implicated these systems in the control of voluntary ethanol intake, we studied whether different monoamine uptake blocking agents could antagonize the increase in ethanol intake caused by REM-sleep deprivation. After three days of REM-sleep deprivation, the rats were given uptake blocking agents for serotonin (citalopram, 5, 10 and 20 mg/kg/day, IP), dopamine (GBR 12909, 5 mg/kg/day, IP) and noradrenaline (talsupram, 1, 5 and 10 mg/kg/day, IP). Citalopram and GBR 12909 did not modify the increased level of ethanol intake, but talsupram decreased ethanol intake to the levels seen prior to deprivation, and during the REM-rebound phase amplified the decrease found. These effects of talsupram could be antagonized by blocking mg/kg/day, IP). Prazosin alone tended to increase ethanol consumption. These findings suggest that functional alterations in central noradrenergic neurons during REM-sleep deprivation may contribute to the concurrent increase in ethanol intake.

  7. 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

  8. Acute total sleep deprivation potentiates cocaine-induced hyperlocomotion in mice.

    PubMed

    Berro, L F; Santos, R; Hollais, A W; Wuo-Silva, R; Fukushiro, D F; Mári-Kawamoto, E; Costa, J M; Trombin, T F; Patti, C L; Grapiglia, S B; Tufik, S; Andersen, M L; Frussa-Filho, R

    2014-09-05

    Sleep deprivation is common place in modern society. Nowadays, people tend to self-impose less sleep in order to achieve professional or social goals. In the social context, late-night parties are frequently associated with higher availability of recreational drugs with abuse potential. Physiologically, all of these drugs induce an increase in dopamine release in the mesolimbic dopaminergic system, which leads to hyperlocomotion in rodents. Sleep deprivation also seems to play an important role in the events related to the neurotransmission of the dopaminergic system by potentiating its behavioral effects. In this scenario, the aim of the present study was to investigate the effects of total sleep deprivation (6h) on the acute cocaine-induced locomotor stimulation in male mice. Animals were sleep deprived or maintained in their home cages and subsequently treated with an acute i.p. injection of 15mg/kg cocaine or saline and observed in the open field. Total sleep deprivation for 6h potentiated the hyperlocomotion induced by acute cocaine administration. In addition, the cocaine sleep deprived group showed a decreased ratio central/total locomotion compared to the cocaine control group, which might be related to an increase in the impulsiveness of mice. Our data indicate that acute periods of sleep loss should be considered risk factors for cocaine abuse.

  9. 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

  10. 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.

  11. 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.

  12. 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.

  13. 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

  14. Effects of sleep deprivation and exercise on cognitive, motor performance and mood.

    PubMed

    Scott, Jonathon P R; McNaughton, Lars R; Polman, Remco C J

    2006-02-28

    This study examined the effect of 30 h of sleep deprivation and intermittent physical exercise, on both cognitive and psychomotor function as well subjective ratings of mood. Six subjects with the following physical characteristics participated in the study (Mean +/- S.D.): age 22 +/- 0.3 years, height 180 +/- 5 cm, body mass: 77 +/- 5 kg, VO2peak 44 +/- 5 ml kg(-1) min(-1). Three subjects engaged in normal sedentary activities while three others cycled on a cycle ergometer at 50% VO2peak for 20 min out of every 2 h during 30 h of sleep deprivation. One week later sleep deprivation was repeated with a cross over of subjects. Every 4 h, subjects completed simple and two-choice reaction time tasks at both rest and during exercise, a computerized tracking task, a number cancellation task, and an assessment of subjective mood state as measured by the POMS questionnaire. A 3 x 4 repeated measures ANOVA revealed that resting but not exercising reaction times were significantly slower with sleep deprivation. Sleep deprivation was also associated with significantly greater negative disturbances to subjective vigour, fatigue and depression assessed by the Profile of Mood States questionnaire. Compared to those who have been deprived of sleep alone, individuals that performed 5 h of intermittent moderate exercise during 30 h of sleep deprivation appeared to be more vulnerable to negative mood disturbances and impairment in reaction times. This could result in greater risk of accident due to a reduced capacity to respond quickly.

  15. 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

  16. 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.

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

    PubMed Central

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

    2010-01-01

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

  18. Intensive Sleep Deprivation and Cognitive Behavioral Therapy for Pharmacotherapy Refractory Insomnia in a Hospitalized Patient

    PubMed Central

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

    2014-01-01

    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. Citation: Breitstein J, Penix B, Roth BJ, Baxter T, Mysliwiec V. Intensive sleep deprivation and cognitive behavioral therapy for pharmacotherapy refractory insomnia in a hospitalized patient. J Clin Sleep Med 2014;10(6):689-690. PMID:24932151

  19. Effect of sleep deprivation on tolerance of prolonged exercise.

    PubMed

    Martin, B J

    1981-01-01

    Acute loss of sleep produces few apparent physiological effects at rest. Nevertheless, many anecdotes suggest that adequate sleep is essential for optimum endurance athletic performance. To investigate this question, heavy exercise performance after 36 h without sleep was compared with that after normal sleep in eight subjects. During prolonged treadmill walking at about 80% of the VO2 max, sleep loss reduced work time to exhaustion by an average of 11% (p = 0.05). This decrease occurred despite doubling monetary incentives for subjects during work after sleeplessness. Subjects appeared to fall into "resistant" and "susceptible" categories: four showed less than a 5% change in performance after sleep loss, while four others showed decrements in exercise tolerance ranging from 15 to 40%. During the walk, sleep loss resulted in significantly greater perceived exertion (p less than 0.05), even though exercise heart rate and metabolic rate (VO2 and VCO2) were unchanged. Minute ventilation was significantly elevated during exercise after sleep loss ( p less than 0.05). Sleep loss failed to alter the continuous slow rises in VE and heart rate that occurred as work was prolonged. These findings suggest that the psychological effects of acute sleep loss may contribute to decreased tolerance of prolonged heavy exercise.

  20. 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

  1. 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.

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

    PubMed

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

    2011-06-01

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

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

    PubMed

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

    2010-08-01

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

  4. 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.

  5. 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

  6. 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

  7. 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.

  8. 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.

  9. Effects of 24-h and 36-h sleep deprivation on human postural control and adaptation.

    PubMed

    Patel, M; Gomez, S; Berg, S; Almbladh, P; Lindblad, J; Petersen, H; Magnusson, M; Johansson, R; Fransson, P A

    2008-02-01

    This study investigated whether human postural stability and adaptation were affected by sleep deprivation and the relationship between motor performance and subjective scores of sleepiness (visuo-anlogue sleepiness scores, VAS). Postural stability and subjective sleepiness were examined in 18 healthy subjects (mean age 23.8 years) following 24 and 36 h of continued wakefulness, ensured by portable EEG recordings, and compared to a control test where the assessments were made after a normal night of sleep. The responses were assessed using posturography with eyes open and closed, and vibratory proprioceptive stimulations were used to challenge postural control. Postural control was significantly affected after 24 h of sleep deprivation both in anteroposterior and in lateral directions, but less so after 36 h. Subjective VAS scores showed poor correlation with indicators of postural control performance. The clearest evidence that sleep deprivation decreased postural control was the reduction of adaptation. Also several near falls after 2-3 min during the posturographic tests showed that sleep deprivation might affect stability through momentary lapses of attention. Access to vision, somewhat, but not entirely reduced the effect of sleep deprivation. In conclusion, sleep deprivation can be a contributing factor to decreased postural control and falls.

  10. 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.

  11. Lack of estradiol modulation of sleep deprivation-induced c-Fos in the rat brain.

    PubMed

    Mashoodh, Rahia; Stamp, Jennifer A; Wilkinson, Michael; Rusak, Benjamin; Semba, Kazue

    2008-11-28

    Women recover from sleep deprivation more efficiently than men, but the mechanism for this difference is unknown. Effects of estrogen on sleep suggest that it could play a role, but the brain targets on which estrogen may act to have this effect have not been identified. Sleep deprivation increases levels of the immediate-early gene protein c-Fos in selected brain regions, but it is unknown whether estrogen modulates this response. We investigated the influence of different levels of exogenous estradiol on the c-Fos response to sleep deprivation in ovariectomized female rats. Female rats were treated with low or high levels of estradiol (mimicking diestrous and proestrous levels, respectively) delivered via subcutaneous silastic tubes. Control ovariectomized females and sham-operated males were implanted with tubes filled with cholesterol. One week after surgery, half of the rats underwent a 3 h period of sleep deprivation during the light phase in a motorized Wahmann activity wheel that rotated constantly at a slow speed, while half were confined to fixed wheels. Immediately after sleep deprivation, animals were killed and their brains processed to detect c-Fos using immunohistochemistry. Sleep deprivation increased the number of c-Fos positive cells in a number of brain areas, including the caudate putamen, medial preoptic area, perifornical hypothalamus, and anterior paraventricular thalamic nucleus. Other areas, including the suprachiasmatic nucleus, posterior paraventricular hypothalamic nucleus, posterior paraventricular thalamic nucleus, arcuate nucleus, and central amygdala, did not respond to 3 h sleep deprivation with a significant increase in c-Fos levels. Levels of c-Fos induced in the selected brain regions by sleep deprivation were not modulated by estrogen levels, nor by sex.

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

    PubMed Central

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

    2010-01-01

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

  13. Hormone treatment gives no benefit against cognitive changes caused by acute sleep deprivation in postmenopausal women.

    PubMed

    Karakorpi, Maija; Alhola, Paula; Urrila, Anna Sofia; Kylmälä, Mervi; Portin, Raija; Kalleinen, Nea; Polo-Kantola, Päivi

    2006-09-01

    The objective was to evaluate whether hormone therapy (HT) gives any benefit against the possible impairment of cognitive performance when challenged by acute sleep deprivation. Twenty postmenopausal women volunteered (age range 59-72 years, mean=64.4 years, SD=4.4): 10 HT users and 10 nonusers. Eleven young women served as a control group for the cognitive age effect (age range 20-26 years, mean age 23.1 years, SD=1.6). The subjects spent four consecutive nights at the sleep laboratory and were exposed to acute sleep deprivation of 40 h. Measures of attention (reaction speed and vigilance), alertness, and mood were administered every 2 h during the daytime and every hour during the sleep deprivation night. Postmenopausal women performed slower than young controls, whereas young controls made more errors. In HT users, the recovery night did not fully restore the performance in the simple and two-choice reaction time tasks, but in nonusers it did so. Sleep deprivation had a detrimental, yet reversible effect on vigilance in all groups. In all groups, sleepiness started to increase after 15 h of sleep deprivation and remained elevated in the morning after the recovery night. Prolonged wakefulness or HT had no effect on mood. In conclusion, sleep deprivation impaired cognitive performance in postmenopausal as well as young women. Postmenopausal women kept up their performance at the expense of reaction speed and young women at the expense of accuracy. One night was not enough for HT users to recover from sleep deprivation. Thus, HT gave no benefit in maintaining the attention and alertness during sleep deprivation.

  14. Some measures to reduce effects of prolonged sleep deprivation.

    PubMed

    Lagarde, D; Batejat, D

    1995-01-01

    Prolonged sleep deprivation is an exceptional situation, encountered in special environments such as sports, civilian and military, and which induces deficits in vigilance and performance. Among the array of measures which may be used to counteract these effects, the authors described a protocol using the combination of small naps, and administration of a pharmacological aid. A detailed description of advantages and drawbacks of each one of these measures is given, illustrated by several examples extracted from different studies. Four aspects of pharmacological aid are reviewed: the effects of amphetamines and amphetamine-like substances, caffeine, eugregoric substances, and the effect of the association small nap + eugregoric substances. The use of these various aids is discussed, and findings show that each one of them finds an application in a specific context.

  15. Effect of sleep deprivation on rhythms of clock gene expression and melatonin in humans.

    PubMed

    Ackermann, Katrin; Plomp, Rosina; Lao, Oscar; Middleton, Benita; Revell, Victoria L; Skene, Debra J; Kayser, Manfred

    2013-08-01

    This study investigated the impact of sleep deprivation on the human circadian system. Plasma melatonin and cortisol levels and leukocyte expression levels of 12 genes were examined over 48 h (sleep vs. no-sleep nights) in 12 young males (mean±SD: 23±5 yrs). During one night of total sleep deprivation, BMAL1 expression was suppressed, the heat shock gene HSPA1B expression was induced, and the amplitude of the melatonin rhythm increased, whereas other high-amplitude clock gene rhythms (e.g., PER1-3, REV-ERBα) remained unaffected. These data suggest that the core clock mechanism in peripheral oscillators is compromised during acute sleep deprivation.

  16. 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.

  17. Pemoline and Methylphenidate: Interaction With Mood, Sleepiness, and Cognitive Performance During 64 Hours of Sleep Deprivation

    DTIC Science & Technology

    1992-07-07

    AD-A256 601 PEMOLINE AND METHYLPHENIDATE : INTERACTION WITH MOOD, SLEEP:7NESS, AND COGNITIVE PERFORMANCE DURING 64 HOURS OF SLEEP DEPRIVATION H...COMMAND BETHESDA, MARYLAND Pemoline and Methylphenidate : Interaction with Mood, Sleepiness, and Cognitive Performance During 64 Hours of Sleep...Report No. 90-41. ABSTRACT Moderate doses of the stimulant drugs methylphenidate (10 mg every 6 hr x 8 doses) or pemoline (37.5 mg every 12 hr x 4 doses

  18. 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.

  19. 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

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

    PubMed

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

    2014-11-19

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

  1. 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

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

    PubMed

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

    2013-09-05

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

  3. 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.

  4. Increased ultrasonic vocalizations and risk-taking in rat pups of sleep-deprived dams.

    PubMed

    Gulia, Kamalesh K; Patel, Niraj; Kumar, Velayudhan Mohan

    2015-02-01

    Ultrasonic vocalizations (USVs) in rodent pups are analogous to cries in human babies. There is reduction in USVs in pups after experimental deprivation of rapid eye movement sleep of dams during pregnancy. However, the effects of total sleep deprivation on the USVs of newborns and their emotional development are not documented. Male pups born to the rats that underwent total sleep deprivation for 5h during the third trimester made higher vocalizations, when tested on early postnatal days (pnds) in an isolation-paradigm. Their anxiety-related behaviors during pnds 25-28, were tested using elevated plus maze (EPM). In comparison to the control pups, weanlings of sleep-deprived dams made increased entries into the open arms and higher mobility in the EPM. Enhanced distress calls during early pnds and reduction in risk assessment in weanlings indicate a link between the two behaviors. The USVs during ontogeny may provide early signals about altered emotional development.

  5. How does one night of sleep deprivation affect the internal clock?

    PubMed

    Casini, Laurence; Ramdani-Beauvir, Céline; Burle, Boris; Vidal, Franck

    2013-01-01

    Twelve subjects performed two temporal tasks, one explicit (Experiment 1) and one implicit (Experiment 2) after one night of sleep deprivation and after one night of normal rest. Experiment 1 involved a 1100-ms duration production task, and in Experiment 2 subjects performed a word identification task requiring implicit estimation of vowel duration (around 150 ms). One night of sleep deprivation had the same pattern of effect on explicit timing in the suprasecond range and implicit timing in the millisecond range. Specifically, sleep deprivation induced productions of shorter intervals in the duration production task and estimation of segmental durations as being longer in the word identification task. Both results are consistent with an acceleration of pacemaker rate.Moreover, in both experiments, we found a correlation between the alertness level of participants and the size of the effect. Therefore, sleep deprivation, which physiologically manipulates cortical arousal level, produced similar performance modulation in suprasecond explicit and subsecond implicit tasks suggesting a common mechanism.

  6. 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

  7. Sleep deprivation impairs the extinction of cocaine-induced environmental conditioning in mice.

    PubMed

    Berro, L F; Hollais, A W; Patti, C L; Fukushiro, D F; Mári-Kawamoto, E; Talhati, F; Costa, J M; Zanin, K A; Lopes-Silva, L B; Ceccon, L M; Santos, R; Procópio-Souza, R; Trombin, T F; Yokoyama, T S; Wuo-Silva, R; Tufik, S; Andersen, M L; Frussa-Filho, R

    2014-09-01

    Persistence of a drug-environment conditioning induced by repeated psychostimulant treatment is thought to play a key role in the addictive cycle. In addition, sleep disorders are a common feature in patients with addictive disorders. Sleep deprivation shares similar neurobiological effects with psychostimulants. Therefore, we investigated whether sleep deprivation would impair the extinction of previously established conditioning between the drug effect and the environmental cues. Four cohorts of male adult mice underwent a behavioral sensitization procedure pairing drug (cocaine at 15 mg/kg, i.p.) or saline with environment (open-field apparatus). The extinction of conditioned locomotion was evaluated after control (home-cage maintained) or sleep deprivation (gentle handling method for 6h) conditions. Sleep deprivation both postponed the initiation and impaired the completeness of extinction of the conditioned locomotion promoted by previous drug-environment conditioning in cocaine-sensitized animals. While the cocaine control group required 5 free-drug sessions of exposure to the open-field apparatus to complete extinction of conditioned locomotion, the cocaine pre-treated group that experienced sleep deprivation before each extinction session still significantly differed from its respective control group on Day 5 of extinction. The possibility that the sleep condition can influence the extinction of a long-lasting association between drug effects and environmental cues can represent new outcomes for clinically relevant phenomena.

  8. 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.

  9. 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.

  10. 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

  11. Effect of sleep deprivation on response threshold for signal detectability parameter, beta.

    PubMed

    Polzella, D J

    1978-12-01

    In contrast to a previous study (Deaton, Tobias, & Wilkinson, 1971), data are presented which demonstrate significant decreases in response bias (beta) as well as sensitivity (d') following one night of sleep deprivation. It is argued that previous failures to observe significant decreases in beta may be related to the disparity in the number of noise and signal-plus-noise trials in these experiments. The use of parametric analysis to test the effect of sleep deprivation on d' and beta is recommended.

  12. 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.

  13. 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.

  14. 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

  15. Influence of sleep deprivation coupled with administration of melatonin on the ultrastructure of rat pineal gland.

    PubMed

    Lan, C T; Hsu, J C; Ling, E A

    2001-08-10

    The effects of sleep deprivation with or without melatonin treatment on the pineal morphology in rats were studied. Five days after sleep deprivation and using electron microscopy, many of the pinealocytes exhibited structural alterations including dilation of the cisternae of the rough/smooth endoplasmic reticulum, Golgi saccules and mitochondria, and an increase in the numbers of lipid droplets, vacuoles and dense-core vesicles. These features were considered as morphological evidence of increased synthesis or secretion by the pineal gland. In addition, numerous membranous profiles, considered to be degraded cellular organelles, were observed in some pinealocytes and sympathetic nerve terminals. It is suggested that the occurrence of degenerating organelles had resulted from the deleterious effect of sleep deprivation. This may be attributed to an overload of secretory activity of the pineal gland during stress elicited by the long-term sleep deprivation, leading to functional exhaustion and irreversible damage of the oxidation-related organelles. In sleep-deprived rats receiving a single injection of melatonin (10 mg/kg) for 5 consecutive days, the above features indicative of pinealocytic activation were attenuated. In fact, all signs of degeneration of cellular organelles were rarely found. These results suggest that the pineal gland is itself a target for exogenously administered melatonin. Thus, melatonin when administered systemically may be used as a potential neuroprotective drug against neuronal damage induced by sleep deprivation.

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

    PubMed

    Singh, Anant; Kumar, Anil

    2008-04-01

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

  17. Tempol Protects Sleep-deprivation Induced Behavioral Deficits in Aggressive Male Long-Evans Rats

    PubMed Central

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

    2016-01-01

    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 (24 h) 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 (24 h) 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

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

    PubMed

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

    2014-09-01

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

  19. 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.

  20. 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

  1. 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

  2. Dopamine Transporter Regulation during Four Nights of REM Sleep Deprivation Followed by Recovery – An in vivo Molecular Imaging Study in Humans

    PubMed Central

    Martins, RCS; Andersen, ML; Garbuio, SA; Bittencourt, LR; Guindalini, C; Shih, MC; Hoexter, MQ; Bressan, RA; Castiglioni, MLV; Tufik, S

    2010-01-01

    Objectives: To assess the influence of total or selective REM sleep deprivation on the dopamine transporter (DAT) densities and sleep patterns of healthy volunteers. Design: Prospective study. Setting: Evaluation of polysomnography recordings and DAT density after 4 nights of selective REM sleep deprivation followed by 3 nights of sleep recovery compared to a control group and a group that was subjected to 2 nights of total sleep deprivation. Single positron emission computed tomography and [99mTc]TRODAT-1 were used to assess the cerebral DAT density in the striatum at baseline, after REM sleep deprivation and total sleep deprivation as well as after sleep recovery. Blood was collected daily to examine prolactin and estradiol levels, which were correlated with dopaminergic activity. Patients or Participants: Thirty healthy male volunteers ranging from 19 to 29 years of age were randomly assigned to one of three experimental groups after giving written informed consent (10 non-sleep deprived, 10 total sleep deprived, and 10 REM sleep deprived). Measurements and Results: Four nights of REM sleep deprivation and 2 nights of total sleep deprivation induced distinct and heterogeneous patterns of sleep recovery. No significant modulation of DAT availability was observed within groups. In the recovery nights, changes in cortisol, prolactin and estradiol concentrations were significantly correlated with specific sleep stages in the total and REM sleep deprived groups. In addition, DAT density was positively correlated with estradiol concentration and inversely associated with SWS latency only after total sleep deprivation. Conclusion: Our study demonstrates that although sleep deprivation did not promote significant alterations in DAT density within the striatum, there were significant correlations among transporter availability, hormonal concentrations and sleep parameters. Citation: Martins, RCS; Andersen ML; Garbuio SA; Bittencourt LR: Guindalini C; Shih MC; Hoexter MQ

  3. 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

  4. 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

  5. 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.

  6. The impact of sleep deprivation on neuronal and glial signalling pathways important for memory and synaptic plasticity

    PubMed Central

    Havekes, Robbert; Vecsey, Christopher G.; Abel, Ted

    2012-01-01

    Sleep deprivation is a common feature in modern society, and one of the consequences of sleep loss is the impairment of cognitive function. Although it has been widely accepted that sleep deprivation affects learning and memory, only recently has research begun to address which molecular signalling pathways are altered by sleep loss and, more importantly, which pathways can be targeted to reverse the memory impairments resulting from sleep deprivation. In this review, we discuss the different methods used to sleep deprive animals and the effects of different durations of sleep deprivation on learning and memory with an emphasis on hippocampus-dependent memory. We then review the molecular signalling pathways that are sensitive to sleep loss, with a focus on those thought to play a critical role in the memory and synaptic plasticity deficits observed after sleep deprivation. Finally, we highlight several recent attempts to reverse the effects of sleep deprivation on memory and synaptic plasticity. Future research building on these studies promises to contribute to the development of novel strategies to ameliorate the effects of sleep loss on cognition. PMID:22570866

  7. Influence of locus of control on mood state disturbance after short-term sleep deprivation.

    PubMed

    Hill, D W; Welch, J E; Godfrey, J A

    1996-01-01

    Twenty-eight healthy university students were classified as having either an internal (n = 14) or external (n = 14) locus of control. Before and after 26-30 hours of sleep deprivation, their mood state was evaluated using the Profile of Mood States questionnaire. There was a significant sleep status x locus of control interaction effect on mood state disturbance (p = 0.049). In the individuals with an external locus of control, there was an increase (p < 0.001) in total mood disturbance from (mean +/- standard deviation) 115 +/- 23 during baseline testing to 148 +/- 22 after sleep loss (effect size = 1.4). Sleep loss did not significantly affect total mood disturbance in the subjects with an internal locus of control (115 +/- 26 vs. 128 +/- 34). These results suggest that locus of control is a factor that influences the degree of mood state disturbance caused by short-term sleep deprivation.

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

    PubMed

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

    2016-12-01

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

  9. A tryptophan-rich protein diet efficiently restores sleep after food deprivation in the rat.

    PubMed

    Minet-Ringuet, J; Le Ruyet, P M; Tomé, D; Even, P C

    2004-07-09

    Sleep depends on the quantity and quality of the diet. Several studies have shown that food deprivation results in a reduction in sleep duration. It has also been demonstrated that in the newborn, the supply of certain essential amino acids improves sleep through their action on the synthesis of specific neurotransmitters. The aim of the present study was to test if the quantity and/or quality of dietary protein could improve the recovery of sleep during re-feeding after caloric deprivation. Sleep parameters were compared in rats fed ad libitum, food restricted during 4 days, or reefed isocalorically after food restriction with three dietary regimens varying in terms of the amount (14% versus 30%) or quality (milk protein or alpha-lactalbumin) of protein. The results showed that sleep recovery, in particular slow-wave sleep, was improved in rats re-fed with alpha-lactalbumin. This result confirms the close relationship between feeding and sleep and suggest that alpha-lactabumin could be used to improve sleep in adult submitted to nutritional disturbances such as food restriction, shift work, Ramadan.

  10. Effects of Sleep Deprivation on U.S. Navy Watchstander Performance Onboard the Independence Class Littoral Combat Ship (LCS 2)

    DTIC Science & Technology

    2013-09-01

    Shipboard Operations: A Guide for Commanders Yokeley 2012 Effects of Sleep Deprivation on U.S. Navy Surface Ship Watchstander Performance using... Effects of sleep deprivation on U.S. Navy surface ship watchstander performance using alternative watch schedules (master’s thesis). Naval Postgraduate... SLEEP DEPRIVATION ON U.S. NAVY WATCHSTANDER PERFORMANCE ONBOARD THE INDEPENDENCE CLASS LITTORAL COMBAT SHIP (LCS 2) James D. Davey Lieutenant

  11. 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

  12. The Effect of Sleep Deprivation on Choice Reaction Time and Anaerobic Power of College Student Athletes

    PubMed Central

    Taheri, Morteza; Arabameri, Elaheh

    2012-01-01

    Purpose The aim of this study was to determine the effect of one night's sleep deprivation on anaerobic performance and Reaction time of subjects in the morning of the following day. Methods Eighteen male college student athletes were studied twice in a balanced, randomized design. Subjects were measured for peak power, mean power and Reaction time. Results The performance showed no significant difference in both tests of anaerobic power (peak power, mean power) over the sleep deprivation period (P= 0.3; P= 0.4 respectively), but reaction time differed significantly from baseline (P=0.003). Results support the hypothesis that sleep serves a function of cognitive restitution, particularly in the maintenance of attentional mechanisms. In the light of the above considerations. Conclusions It was concluded that short-term sleep deprivation is not effective on anaerobic performance, but adversely affects cognitive function such as Reaction Time. PMID:22461961

  13. Time-on-task and sleep deprivation effects are evidenced in overlapping brain areas.

    PubMed

    Asplund, Christopher L; Chee, Michael W L

    2013-11-15

    Both sleep deprivation and extended task engagement (time-on-task) have been shown to degrade performance in tasks evaluating sustained attention. Here we used pulsed arterial spin labeling (pASL) to study participants engaged in a demanding selective attention task. The participants were imaged twice, once after a normal night of sleep and once after approximately 24h of total sleep deprivation. We compared task-related changes in BOLD signal alongside ASL-based cerebral blood flow (CBF) changes. We also collected resting baseline CBF data prior to and following task performance. Both BOLD fMRI and ASL identified spatially congruent task activation in ventral visual cortex and fronto-parietal regions. Sleep deprivation and time-on-task caused a decline of both measures in ventral visual cortex. BOLD fMRI also revealed such declines in fronto-parietal cortex. Only early visual cortex showed a significant upward shift in resting baseline CBF following sleep deprivation, suggesting that the neural consequences of both SD and ToT are primarily evident in task-evoked signals. We conclude that BOLD fMRI is preferable to pASL in studies evaluating sleep deprivation given its better signal to noise characteristics and the relative paucity of state differences in baseline CBF.

  14. Influence of sleep deprivation on expression of MKK4 and c-fos in the mandibular condylar cartilage of rats.

    PubMed

    Chen, Jinlong; Wu, Gaoyi; Zhu, Guoxiong; Wang, Peihuan; Chen, Hongyu; Zhao, Huaqiang

    2013-12-01

    The aim of this study was to investigate the changes in expression of mitogen-activated protein kinase kinase 4 (MKK4) and c-fos in the mandibular condylar cartilage of rats that had been subjected to sleep deprivation. One hundred and twenty female Wistar rats were randomly divided into 6 groups with 20 in each: sleep deprivation for 2 days, 4 days, 6 days, and 8 days, large-platform controls, and cage controls. After sleep deprivation by the modified multiple platform method the sleep-deprived rats were killed. The large-platform and cage control rats were killed at the same time as the rats deprived of sleep for 8 days. Haematoxylin and eosin were used to record the morphological changes in cartilage, and immunohistochemistry and real-time quantitative polymerase chain reaction (PCR) were used to detect the expression of MKK4 and c-fos. Pathological alterations were apparent after 6 and 8 days of sleep deprivation. Compared with control groups, the expression of MKK4 in the sleep-deprived groups was lower, while that of c-fos was higher. As the duration of sleep deprivation increased, the expression of MKK4 decreased. These results indicate that the variation in expression of MKK4 and c-fos may be correlated with pathological changes induced by sleep deprivation in mandibular condylar cartilage in rats.

  15. Role of REM Sleep, Melanin Concentrating Hormone and Orexin/Hypocretin Systems in the Sleep Deprivation Pre-Ischemia

    PubMed Central

    Pace, Marta; Adamantidis, Antoine; Facchin, Laura; Bassetti, Claudio

    2017-01-01

    Study Objectives Sleep reduction after stroke is linked to poor recovery in patients. Conversely, a neuroprotective effect is observed in animals subjected to acute sleep deprivation (SD) before ischemia. This neuroprotection is associated with an increase of the sleep, melanin concentrating hormone (MCH) and orexin/hypocretin (OX) systems. This study aims to 1) assess the relationship between sleep and recovery; 2) test the association between MCH and OX systems with the pathological mechanisms of stroke. Methods Sprague-Dawley rats were assigned to four experimental groups: (i) SD_IS: SD performed before ischemia; (ii) IS: ischemia; (iii) SD_Sham: SD performed before sham surgery; (iv) Sham: sham surgery. EEG and EMG were recorded. The time-course of the MCH and OX gene expression was measured at 4, 12, 24 hours and 3, 4, 7 days following ischemic surgery by qRT-PCR. Results A reduction of infarct volume was observed in the SD_IS group, which correlated with an increase of REM sleep observed during the acute phase of stroke. Conversely, the IS group showed a reduction of REM sleep. Furthermore, ischemia induces an increase of MCH and OX systems during the acute phase of stroke, although, both systems were still increased for a long period of time only in the SD_IS group. Conclusions Our data indicates that REM sleep may be involved in the neuroprotective effect of SD pre-ischemia, and that both MCH and OX systems were increased during the acute phase of stroke. Future studies should assess the role of REM sleep as a prognostic marker, and test MCH and OXA agonists as new treatment options in the acute phase of stroke. PMID:28061506

  16. Socially isolated mice exhibit a blunted homeostatic sleep response to acute sleep deprivation compared to socially paired mice.

    PubMed

    Kaushal, Navita; Nair, Deepti; Gozal, David; Ramesh, Vijay

    2012-05-15

    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 6h and telemetric polygraphic recordings were conducted, including 18 h 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.

  17. Sleep Does Not Enhance the Recovery of Deprived Eye Responses in Developing Visual Cortex

    PubMed Central

    Dadvand, Laila; Stryker, Michael P.; Frank, Marcos G.

    2007-01-01

    Monocular deprivation (MD) during a critical period of visual development triggers a rapid remodeling of cortical responses in favor of the open eye. We have previously shown that this process is enhanced by sleep and is inhibited when the sleeping cortex is reversibly inactivated. A related but distinct form of cortical plasticity is evoked when the originally deprived eye (ODE) is reopened, and the non-deprived eye is closed during the critical period (reverse monocular deprivation (RMD)). Recent studies suggest that different mechanisms regulate the initial loss of deprived eye responses following MD and the recovery of deprived eye responses following RMD. In this study we investigated whether sleep also enhances RMD plasticity in critical period cats. Using polysomnography combined with microelectrode recordings and intrinsic signal optical imaging in visual cortex we show that sleep does not enhance the recovery of ODE responses following RMD. These findings add to the growing evidence that different forms of plasticity in vivo are regulated by distinct mechanisms and that sleep has divergent roles upon different types of experience-dependent cortical plasticity. PMID:17000056

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

    PubMed Central

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

    2017-01-01

    Sleep deprivation impairs cognitive performance and reliably alters brain activation in wakefulness and sleep. Nevertheless, the molecular regulators of prolonged wakefulness remain poorly understood. Evidence from genetic, behavioral, pharmacologic and imaging studies suggest that dopaminergic signaling contributes to the behavioral and electroencephalographic (EEG) consequences of sleep loss, although direct human evidence thereof is missing. We tested whether dopamine neurotransmission regulate sustained attention and evolution of EEG power during prolonged wakefulness. Here, we studied the effects of functional genetic variation in the dopamine transporter (DAT1) and the dopamine D2 receptor (DRD2) genes, on psychomotor performance and standardized waking EEG oscillations during 40 hours of wakefulness in 64 to 82 healthy volunteers. Sleep deprivation consistently enhanced sleepiness, lapses of attention and the theta-to-alpha power ratio (TAR) in the waking EEG. Importantly, DAT1 and DRD2 genotypes distinctly modulated sleep loss-induced changes in subjective sleepiness, PVT lapses and TAR, according to inverted U-shaped relationships. Together, the data suggest that genetically determined differences in DAT1 and DRD2 expression modulate functional consequences of sleep deprivation, supporting the hypothesis that striato-thalamo-cortical dopaminergic pathways modulate the neurobehavioral and neurophysiological consequences of sleep loss in humans. PMID:28393838

  19. 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

  20. 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.

  1. 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

  2. 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

  3. 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

  4. EphA4 is Involved in Sleep Regulation but Not in the Electrophysiological Response to Sleep Deprivation

    PubMed Central

    Freyburger, Marlène; Pierre, Audrey; Paquette, Gabrielle; Bélanger-Nelson, Erika; Bedont, Joseph; Gaudreault, Pierre-Olivier; Drolet, Guy; Laforest, Sylvie; Blackshaw, Seth; Cermakian, Nicolas; Doucet, Guy; Mongrain, Valérie

    2016-01-01

    Study Objectives: Optimal sleep is ensured by the interaction of circadian and homeostatic processes. Although synaptic plasticity seems to contribute to both processes, the specific players involved are not well understood. The EphA4 tyrosine kinase receptor is a cell adhesion protein regulating synaptic plasticity. We investigated the role of EphA4 in sleep regulation using electrocorticography in mice lacking EphA4 and gene expression measurements. Methods: EphA4 knockout (KO) mice, ClockΔ19/Δ19 mutant mice and littermates, C57BL/6J and CD-1 mice, and Sprague-Dawley rats were studied under a 12 h light: 12 h dark cycle, under undisturbed conditions or 6 h sleep deprivation (SLD), and submitted to a 48 h electrophysiological recording and/or brain sampling at different time of day. Results: EphA4 KO mice showed less rapid eye movement sleep (REMS), enhanced duration of individual bouts of wakefulness and nonrapid eye movement sleep (NREMS) during the light period, and a blunted daily rhythm of NREMS sigma activity. The NREMS delta activity response to SLD was unchanged in EphA4 KO mice. However, SLD increased EphA4 expression in the thalamic/hypothalamic region in C57BL/6J mice. We further show the presence of E-boxes in the promoter region of EphA4, a lower expression of EphA4 in Clock mutant mice, a rhythmic expression of EphA4 ligands in several brain areas, expression of EphA4 in the suprachiasmatic nuclei of the hypothalamus (SCN), and finally an unchanged number of cells expressing Vip, Grp and Avp in the SCN of EphA4 KO mice. Conclusions: Our results suggest that EphA4 is involved in circadian sleep regulation. Citation: Freyburger M, Pierre A, Paquette G, Bélanger-Nelson E, Bedont J, Gaudreault PO, Drolet G, Laforest S, Blackshaw S, Cermakian N, Doucet G, Mongrain V. EphA4 is involved in sleep regulation but not in the electrophysiological response to sleep deprivation. SLEEP 2016;39(3):613–624. PMID:26612390

  5. 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.

  6. Reductions in circulating anabolic hormones induced by sustained sleep deprivation in rats.

    PubMed

    Everson, Carol A; Crowley, William R

    2004-06-01

    The main systemic disorders resulting from prolonged sleep deprivation in laboratory animals are a negative energy balance, low circulating thyroid hormones, and host defense impairments. Low thyroid hormones previously have been found caused by altered regulation at the level of the hypothalamus with possible pituitary involvement. The present studies investigated the effects of sleep deprivation on other major anabolic hormonal systems. Plasma growth hormone (GH) concentrations and major secretory bursts were characterized. Insulin-like growth factor I (IGF-I) was evaluated as an integrative marker of peripheral GH effector activity. Prolactin (PRL) was assessed by basal concentrations and by stimulating the pituitary with exogenous thyrotropin-releasing hormone. Leptin was studied for its linkage to metabolic signs of sleep loss and its correspondence to altered neuroendocrine regulation in other disease states. Last, plasma corticosterone was measured to investigate the degree of hypothalamic-pituitary-adrenal activation. Sleep deprivation was produced by the disk-over-water method, a well-established means of selective deprivation of sleep and noninterference with normal waking behaviors. Hormone concentrations were determined in sham comparisons and at intervals during baseline and experimental periods lasting at least 15 days in partially and totally sleep-deprived rats. The results indicate that high-amplitude pulses of GH were nearly abolished and that concentrations of GH, IGF-I, PRL, and leptin all were suppressed by sleep deprivation. Corticosterone concentration was relatively unaffected. Features of these results, such as low GH and low IGF-I, indicate failed negative feedback and point to hypothalamic mechanisms as containing the foci responsible for peripheral signs.

  7. 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.

  8. 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.

  9. 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

  10. 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.

  11. 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.

  12. Paradoxical Sleep Deprivation Causes Cardiac Dysfunction and the Impairment Is Attenuated by Resistance Training

    PubMed Central

    Giampá, Sara Quaglia de Campos; Mônico-Neto, Marcos; de Mello, Marco Tulio; Souza, Helton de Sá; Tufik, Sergio; Lee, Kil Sun; Koike, Marcia Kiyomi; dos Santos, Alexandra Alberta; Antonio, Ednei Luiz; Serra, Andrey Jorge; Tucci, Paulo José Ferreira

    2016-01-01

    Background Paradoxical sleep deprivation activates the sympathetic nervous system and the hypothalamus-pituitary-adrenal axis, subsequently interfering with the cardiovascular system. The beneficial effects of resistance training are related to hemodynamic, metabolic and hormonal homeostasis. We hypothesized that resistance training can prevent the cardiac remodeling and dysfunction caused by paradoxical sleep deprivation. Methods Male Wistar rats were distributed into four groups: control (C), resistance training (RT), paradoxical sleep deprivation for 96 hours (PSD96) and both resistance training and sleep deprivation (RT/PSD96). Doppler echocardiograms, hemodynamics measurements, cardiac histomorphometry, hormonal profile and molecular analysis were evaluated. Results Compared to the C group, PSD96 group had a higher left ventricular systolic pressure, heart rate and left atrium index. In contrast, the left ventricle systolic area and the left ventricle cavity diameter were reduced in the PSD96 group. Hypertrophy and fibrosis were also observed. Along with these alterations, reduced levels of serum testosterone and insulin-like growth factor-1 (IGF-1), as well as increased corticosterone and angiotensin II, were observed in the PSD96 group. Prophylactic resistance training attenuated most of these changes, except angiotensin II, fibrosis, heart rate and concentric remodeling of left ventricle, confirmed by the increased of NFATc3 and GATA-4, proteins involved in the pathologic cardiac hypertrophy pathway. Conclusions Resistance training effectively attenuates cardiac dysfunction and hormonal imbalance induced by paradoxical sleep deprivation. PMID:27880816

  13. Evaluation of the effect of pentoxifylline on sleep-deprivation induced memory impairment.

    PubMed

    Alzoubi, Karem H; Khabour, Omar F; Tashtoush, Noor H; Al-Azzam, Sayer I; Mhaidat, Nizar M

    2013-09-01

    In this study, we examined the ability of Pentoxifylline (PTX) to prevent sleep deprivation induced memory impairment probably through decreasing oxidative stress. Sleep deprivation was chronically induced 8 h/day for 6 weeks in rats using modified multiple platform model. Concurrently, PTX (100 mg/kg) was administered to animals on daily basis. After 6 weeks of treatment, behavioral studies were conducted to test the spatial learning and memory using the Radial Arm Water Maze. Additionally, the hippocampus was dissected; and levels/activities of antioxidant defense biomarkers glutathione reduced (GSH), glutathione oxidized (GSSG), GSH/GSSG ratio, glutathione peroxidase (GPx), catalase, and superoxide dismutase (SOD), were assessed. The results show that chronic sleep deprivation impaired short- and long-term memories, which was prevented by chronic treatment with PTX. Additionally, PTX normalized sleep deprivation-induced reduction in the hippocampus GSH/GSSG ratio (P < 0.05), and activities of GPx, catalase, and SOD (P < 0.05). In conclusion, chronic sleep deprivation induces memory impairment, and treatment with PTX prevented this impairment probably through normalizing antioxidant mechanisms in the hippocampus.

  14. 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.

  15. Chronic sleep deprivation alters the myosin heavy chain isoforms in the masseter muscle in rats.

    PubMed

    Cao, Ruihua; Huang, Fei; Wang, Peihuan; Chen, Chen; Zhu, Guoxiong; Chen, Lei; Wu, Gaoyi

    2015-05-01

    To investigate the changes in myosin heavy chain (MyHC) isoforms of rat masseter muscle fibres caused by chronic sleep deprivation and a possible link with the pathogenesis of disorders of the temporomandibular joint (TMJ). A total of 180 male rats were randomly divided into three groups (n=60 in each): cage controls, large platform controls, and chronic sleep deprivation group. Each group was further divided into three subgroups with different observation periods (7, 14, and 21 days). We investigated he expression of MyHC isoforms in masseter muscle fibres by real-time quantitative polymerase chain reaction (PCR), Western blotting, and immunohistochemical staining. In rats with chronic sleep deprivation there was increased MyHC-I expression in layers of both shallow and deep muscles at 7 and 21 days compared with the control groups, whereas sleep deprivation was associated with significantly decreased MyHC-II expression. At 21 days, there were no differences in MyHC-I or MyHC-II expression between the groups and there were no differences between the two control groups at any time point. These findings suggest that chronic sleep deprivation alters the expression of MyHC isoforms, which may contribute to the pathogenesis of disorders of the TMJ.

  16. The effects of sleep deprivation on brain functioning in older adults.

    PubMed

    Almklov, Erin L; Drummond, Sean P A; Orff, Henry; Alhassoon, Omar M

    2015-01-01

    Few studies have examined the effects of total sleep deprivation (TSD) on cognitive performance and brain activation using functional MRI (fMRI) in older adults. The current study examines blood oxygen level-dependent (BOLD) activation in older adults and younger adults during the sustained attention (GO) and response inhibition (NOGO) portions of a GO-NOGO cognitive task following 36 hr of total sleep deprivation. No significant performance differences were observed between the groups on the behavioral outcome measures of total hits and false alarms. Neuroimaging results, however, revealed a significant interaction between age-group and sleep-deprivation status. Specifically, older adults showed greater BOLD activation as compared to younger adults after 36 hours total sleep deprivation in brain regions typically associated with attention and inhibitory processes. These results suggest in order for older adults to perform the GO-NOGO task effectively after sleep deprivation, they rely on compensatory recruitment of brain regions that aide in the maintenance of cognitive performance.

  17. Parametric analysis of thermal preference following sleep deprivation in the rat.

    PubMed

    Harvey, Mark T; Kline, Robert H; May, Michael E; Roberts, A Celeste; Valdovinos, Maria G; Wiley, Ronald G; Kennedy, Craig H

    2010-11-19

    A thermal preference task was used to assess the effects of sleep deprivation on nociceptive behavior using hot and cool stimuli. The thermal preference apparatus allowed male rats to move freely from a hot thermal plate (44.7°C) to an adjacent plate at neutral (33.5°C) or cold temperatures (1.3-11°C). Investigators recorded occupancy on the colder side, frequency of movements between the 2 compartments, and first escape latency from the cold side. Parametric analysis of thermal preference indicated that behavioral allocation was related to temperature ranges previously associated with activation of thermal nociceptors. A 50% occupancy rate was determined from a stimulus-response function identifying 1.3°C vs. 44.7°C as optimal temperatures. This temperature combination was then used to test the effects of sleep deprivation for 48h using the pedestal-over-water method on response allocation to the 2 temperature zones. Sleep deprivation decreased time spent on the cooled plate. Cumulative occupancy indicated differential effects for sleep deprivation with the rats preferring to remain on the hot side vs. the cold side, suggesting that sleep deprivation increased the nociceptive properties of the cold stimulus.

  18. 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.

  19. 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.

  20. Sleep walking

    MedlinePlus

    ... sleep cycle has stages, from light drowsiness to deep sleep. During the stage called rapid eye movement ( ... REM sleep. Sleepwalking (somnambulism) most often occurs during deep, non-REM sleep (called N3 sleep) early in ...

  1. 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.

  2. The effect of partial sleep deprivation on weight-lifting performance.

    PubMed

    Reilly, T; Piercy, M

    1994-01-01

    This study examined the effects of partial sleep deprivation on submaximal and maximal weight-lifting tasks and on subjective states pre- and post-activity. Eight male subjects (aged 18-24 years) were restricted to a nightly ration of 3 h sleep for 3 successive nights after baseline measures on the first day. A 4 day period where normal sleep was permitted fulfilled a control condition, the normal and sleep-deprived conditions being counterbalanced and separated by 10 days. The weight-lifting tasks consisted of biceps curl, bench press, leg press, and dead lift. For each exercise a submaximal load, corresponding to a fixed value on a category ratio scale of exertion, was determined for 20 repetitions; the maximal lift for that exercise was then obtained. A profile of mood states and subjective sleepiness were determined at each test occasion, tests being conducted in the evening of each day. There was no significant effect of sleep loss on performance of maximal biceps curl (p < 0.05) but a significant effect was noted on maximal bench press, leg press, and dead lift (p < 0.001). Trend analysis indicated decreased performance in submaximal lifts for all the 4 tasks: the deterioration was significant after the second night of sleep loss (p < 0.01). Performing the lifts had little influence on sleepiness ratings which increased linearly with successive days of sleep loss. Mood states of confusion, vigour, and fatigue were affected significantly by the sleep deprivation regimen (p < 0.001), but there was no significant effect of sleep loss or anger, tension, and depression (p > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

  3. 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

  4. 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.

  5. Withania somnifera as a potential anxiolytic and immunomodulatory agent in acute sleep deprived female Wistar rats.

    PubMed

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

    2017-03-01

    Sleep is a profound regulator of cellular immunity, and the curtailment of sleep in present day lifestyle leads to disruption of neuro-immune-endocrine interactions. No therapeutic remedy is yet known for the amelioration of detrimental effects caused by sleep deprivation (SD). The current study was aimed to elucidate the effects of acute SD on immune function and its modulation by water extract from leaves of Withania somnifera (ASH-WEX). Three groups of animals, i.e. Vehicle-Undisturbed sleep (VUD), Vehicle-Sleep deprived (VSD) and ASH-WEX fed sleep deprived (WSD) rats were tested for their anxiety-like behaviour and further used for the study of inflammatory and apoptotic markers expression in piriform cortex and hippocampus regions of the brain. VSD animals showed high level of anxiety in elevated plus maze test, which was ameliorated in WSD group. The stress induced expression of inflammatory and immune response markers GFAP, TNFα, IL-6, OX-18 and OX-42 in VSD animals was found to be modulated by ASH-WEX. Further, the stress induced apoptosis was suppressed in WSD group as indicated by expression of NF-κB, AP-1, Bcl-xL and Cytochrome c. This study provides scientific validation to the anxiolytic, anti-inflammatory and anti-apoptotic properties of ASH-WEX, which may serve as an effective dietary supplement for management of SD induced stress and associated functional impairments.

  6. 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.…

  7. On-line analysis of biosignals for the automation of total and specific sleep deprivation in the rat.

    PubMed

    Vivaldi, Ennio A; Bassi, Alejandro; Estrada, Jorge; Garrido, Ignacio; Díaz, Javier; Ocampo-Garcés, Adrián

    2008-01-01

    A computer-based system that automates sleep studies, including sleep deprivation paradigms, is described. The system allows for total or REM-specific sleep deprivation and is based on a reliable, fast-responding, on-line state detection algorithm linked to a dependable intervention device. Behavioral state detection is achieved by dimension reduction of short-term EEG power spectrum. Interventions are made by serial outputs to servomotors that move a cage with different patterns and variable intensity. The system can adapt itself to individual characteristics and to changes in recording conditions. Customized protocols can be designed by defining the states or stages to be deprived, including scheduling temporal patterns. A detailed analysis of the relevant signals during and after deprivation is readily available. Data is presented from two experimental designs in rats. One consisted of specific REM-sleep short-term deprivation and the other of 10-hour total sleep deprivation. An outline of conceptual and practical considerations involved in the automation of laboratory set-ups oriented to biosignal analysis is provided. Careful monitoring of sleep EEG variables during sleep deprivation suggests peculiarities of brain functioning in that condition. A corollary is that sleep deprivation should not be considered to be merely a forced prolonged wakefulness.

  8. 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

  9. 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.

  10. Effects of caffeine on electrophysiological and neuropsychological indices after sleep deprivation.

    PubMed

    Deslandes, Andréa; Ferreira, Camila; Veiga, Heloisa; Cagy, Maurício; Piedade, Roberto; Pompeu, Fernando; Ribeiro, Pedro

    2006-01-01

    Caffeine is regarded as a central nervous system (CNS) stimulant. The goal of this study was to analyze electrophysiological, motor, cognitive and behavioral changes produced by caffeine ingestion after sleep deprivation. Ten subjects were evaluated after sleep deprivation, comparing the ingestion of either 400 mg of caffeine or placebo, in a double-blind randomized study. The variables analyzed were: quantitative EEG, the event-related potential (ERP-P300) and cognitive responses. The most significant quantitative EEG results, which were characterized by moment x treatment interactions, were seen in alpha and theta relative power variables. A significant decrease in relative alpha and theta was observed in the caffeine group after sleep deprivation. In relation to caffeine stimulant effects, there were no significant differences in the other parameters.

  11. 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.

  12. Sleep deprivation effects on growth factor expression in neonatal rats: a potential role for BDNF in the mediation of delta power.

    PubMed

    Hairston, Ilana S; Peyron, Christelle; Denning, Daniel P; Ruby, Norman F; Flores, Judith; Sapolsky, Robert M; Heller, H Craig; O'Hara, Bruce F

    2004-04-01

    The sleeping brain differs from the waking brain in its electrophysiological and molecular properties, including the expression of growth factors and immediate early genes (IEG). Sleep architecture and homeostatic regulation of sleep in neonates is distinct from that of adults. Hence, the present study addressed the question whether the unique homeostatic response to sleep deprivation in neonates is reflected in mRNA expression of the IEG cFos, brain-derived nerve growth factor (BDNF), and basic fibroblast growth factor (FGF2) in the cortex. As sleep deprivation is stressful to developing rats, we also investigated whether the increased levels of corticosterone would affect the expression of growth factors in the hippocampus, known to be sensitive to glucocorticoid levels. At postnatal days 16, 20, and 24, rats were subjected to sleep deprivation, maternal separation without sleep deprivation, sleep deprivation with 2 h recovery sleep, or no intervention. mRNA expression was quantified in the cortex and hippocampus. cFos was increased after sleep deprivation and was similar to control level after 2 h recovery sleep irrespective of age or brain region. BDNF was increased by sleep deprivation in the cortex at P20 and P24 and only at P24 in the hippocampus. FGF2 increased during recovery sleep at all ages in both brain regions. We conclude that cortical BDNF expression reflects the onset of adult sleep-homeostatic response, whereas the profile of expression of both growth factors suggests a trophic effect of mild sleep deprivation.

  13. 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.

  14. 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

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

    PubMed

    Aguiar, Stefane A; Barela, José A

    2014-06-27

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

  16. Effect of Sleep Extension on the Subsequent Testosterone, Cortisol and Prolactin Responses to Total Sleep Deprivation and Recovery.

    PubMed

    Arnal, P J; Drogou, C; Sauvet, F; Regnauld, J; Dispersyn, G; Faraut, B; Millet, G Y; Leger, D; Gomez-Merino, D; Chennaoui, M

    2016-02-01

    Total sleep deprivation (TSD) in humans is associated with altered hormonal levels, which may have clinical relevance. Less is known about the effect of an extended sleep period before TSD on these hormonal changes. Fourteen subjects participated in two experimental counterbalanced conditions (randomised cross-over design): extended sleep (21.00-07.00 h time in bed, EXT) and habitual sleep (22.30-07.00 h time in bed, HAB). For each condition, subjects performed two consecutive phases: six nights of either EXT or HAB. These nights were followed by 3 days in the sleep laboratory with blood sampling at 07.00 and 17.00 h at baseline (B-07.00 and B-17.00), after 24 and 34 h of continuous awakening (24 h-CA, 34 h-CA) and after one night of recovery sleep (R-07.00 and R-17.00) to assess testosterone, cortisol, prolactin and catecholamines concentrations. At 24 h of awakening, testosterone, cortisol and prolactin concentrations were significantly lower compared to B-07.00 and recovered basal levels after recovery sleep at R-07.00 (P < 0.001 for all). However, no change was observed at 34 h of awakening compared to B-17.00. No effect of sleep extension was observed on testosterone, cortisol and catecholamines concentrations at 24 and 34 h of awakening. However, prolactin concentration was significantly lower in EXT at B-07.00 and R-07.00 compared to HAB (P < 0.05, P < 0.001, respectively). In conclusion, 24 h of awakening inhibited gonadal and adrenal responses in healthy young subjects and this was not observed at 34 h of awakening. Six nights of sleep extension is not sufficient to limit decreased concentrations of testosterone and cortisol at 24 h of awakening but may have an impact on prolactin concentration.

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

    PubMed

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

    2014-08-01

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

  18. 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

  19. Sleep: A Health Imperative

    PubMed Central

    Luyster, Faith S.; Strollo, Patrick J.; Zee, Phyllis C.; Walsh, James K.

    2012-01-01

    Chronic sleep deficiency, defined as a state of inadequate or mistimed sleep, is a growing and underappreciated determinant of health status. Sleep deprivation contributes to a number of molecular, immune, and neural changes that play a role in disease development, independent of primary sleep disorders. These changes in biological processes in response to chronic sleep deficiency may serve as etiological factors for the development and exacerbation of cardiovascular and metabolic diseases and, ultimately, a shortened lifespan. Sleep deprivation also results in significant impairments in cognitive and motor performance which increase the risk of motor vehicle crashes and work-related injuries and fatal accidents. The American Academy of Sleep Medicine and the Sleep Research Society have developed this statement to communicate to national health stakeholders the current knowledge which ties sufficient sleep and circadian alignment in adults to health. Citation: Luyster FS; Strollo PJ; Zee PC; Walsh JK. Sleep: a health imperative. SLEEP 2012;35(6):727-734. PMID:22654183

  20. Sleep deprivation impairs spatial memory and decreases extracellular signal-regulated kinase phosphorylation in the hippocampus.

    PubMed

    Guan, Zhiwei; Peng, Xuwen; Fang, Jidong

    2004-08-20

    Loss of sleep may result in memory impairment. However, little is known about the biochemical basis for memory deficits induced by sleep deprivation. Extracellular signal-regulated kinase (ERK) is involved in memory consolidation in different tasks. Phosphorylation of ERK is necessary for its activation and is an important step in mediating neuronal responses to synaptic activities. The aim of the present study was to determine the effects of total sleep deprivation (TSD) on memory and ERK phosphorylation in the brain. Rats were trained in Morris water maze to find a hidden platform (a spatial task) or a visible platform (a nonspatial task) after 6 h TSD or spontaneous sleep. TSD had no effect on spatial learning, but significantly impaired spatial memory tested 24 h after training. Nonspatial learning and memory were not impaired by TSD. Phospho-ERK levels in the hippocampus were significantly reduced after 6 h TSD compared to the controls and returned to the control levels after 2 h recovery sleep. Total ERK1 and ERK2 were slightly increased after 6 h TSD and returned to the control levels after 2 h recovery sleep. These alterations were not observed in the cortex after TSD. Protein phosphotase-1 and mitogen-activated protein kinase phosphatase-2, which dephosphorylates phospho-ERK, were also measured, but they were not altered by TSD. The impairments of both spatial memory and ERK phosphorylation indicate that the hippocampus is vulnerable to sleep loss. These results are consistent with the idea that decreased ERK activation in the hippocampus is involved in sleep deprivation-induced spatial memory impairment.

  1. 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

  2. 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.

  3. 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

  4. Extended Remediation of Sleep Deprived-Induced Working Memory Deficits Using fMRI-guided Transcranial Magnetic Stimulation

    PubMed Central

    Luber, Bruce; Steffener, Jason; Tucker, Adrienne; Habeck, Christian; Peterchev, Angel V.; Deng, Zhi-De; Basner, Robert C.; Stern, Yaakov; Lisanby, Sarah H.

    2013-01-01

    Study Objectives: We attempted to prevent the development of working memory (WM) impairments caused by sleep deprivation using fMRI-guided repetitive transcranial magnetic stimulation (rTMS). Novel aspects of our fMRI-guided rTMS paradigm included the use of sophisticated covariance methods to identify functional networks in imaging data, and the use of fMRI-targeted rTMS concurrent with task performance to modulate plasticity effects over a longer term. Design: Between-groups mixed model. Setting: TMS, MRI, and sleep laboratory study. Participants: 27 subjects (13 receiving Active rTMS, and 14 Sham) completed the sleep deprivation protocol, with another 21 (10 Active, 11 Sham) non-sleep deprived subjects run in a second experiment. Interventions: Our previous covariance analysis had identified a network, including occipital cortex, which demonstrated individual differences in resilience to the deleterious effects of sleep deprivation on WM performance. Five Hz rTMS was applied to left lateral occipital cortex while subjects performed a WM task during 4 sessions over the course of 2 days of total sleep deprivation. Measurements and Results: At the end of the sleep deprivation period, Sham sleep deprived subjects exhibited degraded performance in the WM task. In contrast, those receiving Active rTMS did not show the slowing and lapsing typical in sleep deprivation, and instead performed similarly to non- sleep deprived subjects. Importantly, the Active sleep deprivation group showed rTMS-induced facilitation of WM performance a full 18 hours after the last rTMS session. Conclusions: Over the course of sleep deprivation, these results indicate that rTMS applied concurrently with WM task performance affected neural circuitry involved in WM to prevent its full impact. Citation: Luber B; Steffener J; Tucker A; Habeck C; Peterchev AV; Deng ZD; Basner RC; Stern Y; Lisanby SH. Extended remediation of sleep deprived-induced working memory deficits using f

  5. 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

  6. 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.

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

    PubMed Central

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

    2017-01-01

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

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

    PubMed

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

    2017-03-21

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

  9. 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

  10. 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.

  11. [Sleep: regulation and phenomenology].

    PubMed

    Vecchierini, M-F

    2013-12-01

    This article describes the two-process model of sleep regulation. The 24-hour sleep-wake cycle is regulated by a homeostatic process and an endogenous, 2 oscillators, circadian process, under the influence of external synchronisers. These two processes are partially independent but influence each other, as shown in the two-sleep-process auto-regulation model. A reciprocal inhibition model of two interconnected neuronal groups, "SP on" and "SP off", explains the regular recurrence of paradoxical sleep. Sleep studies have primarily depended on observation of the subject and have determined the optimal conditions for sleep (position, external conditions, sleep duration and need) and have studied the consequences of sleep deprivation or modifications of sleep schedules. Then, electrophysiological recordings permitted the classification of sleep stages according to the observed EEG patterns. The course of a night's sleep is reported on a "hypnogram". The adult subject falls asleep in non-REM sleep (N1), then sleep deepens progressively to stages N2 and N3 with the appearance of spindles and slow waves (N2). Slow waves become more numerous in stage N3. Every 90minutes REM sleep recurs, with muscle atonia and rapid eye movements. These adult sleep patterns develop progressively during the 2 first years of life as total sleep duration decreases, with the reduction of diurnal sleep and of REM sleep. Around 2 to 4 months, spindles and K complexes appear on the EEG, with the differentiation of light and deep sleep with, however, a predominance of slow wave sleep.

  12. Habitual Sleep Deprivation is Associated with 
Type 2 Diabetes: A Case-Control Study

    PubMed Central

    Al-Abri, Mohammed A.; Jaju, Deepali; Al-Sinani, Sawsan; Al-Mamari, Ali; Albarwani, Sulayma; Al-Resadi, Khalid; Bayoumi, Riyadh; Hassan, Mohammed; Al-Hashmi, Khamis

    2016-01-01

    Objectives It is suggested that a minimum of eight hours of sleep per night is needed for metabolism to work normally. The aim of the study was to determine the association of habitual sleep deprivation and type 2 diabetes mellitus (T2DM). Methods We conducted a case-control study comparing patients with T2DM with age and sex matched healthy controls. Standard sleep questionnaires (the Berlin and Epworth Sleepiness Scale) and a weekly diary were used by patients to self-report habitual sleep. Results A total of 172 diabetics and 188 healthy controls were enrolled in the study. There was a significant difference between T2DM and healthy controls in nocturnal sleep duration (p = 0.033). There was a significant association between nocturnal sleep duration of fewer than six hours and T2DM (χ2 = 14.0; p = 0.0001). There was no significant difference in daytime sleepiness and daytime naps between the T2DM and control groups (p = 0.452; p = 0.581, respectively). Conclusions A nocturnal sleep duration < 6 hours is associated with T2DM. PMID:27974953

  13. 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.

  14. 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.

  15. 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.

  16. 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.

  17. Sleep deprivation can inhibit adult hippocampal neurogenesis independent of adrenal stress hormones.

    PubMed

    Mueller, Anka D; Pollock, Michael S; Lieblich, Stephanie E; Epp, Jonathan R; Galea, Liisa A M; Mistlberger, Ralph E

    2008-05-01

    Sleep deprivation (SD) can suppress cell proliferation in the hippocampal dentate gyrus of adult male rodents, suggesting that sleep may contribute to hippocampal functions by promoting neurogenesis. However, suppression of cell proliferation in rats by the platform-over-water SD method has been attributed to elevated corticosterone (Cort), a potent inhibitor of cell proliferation and nonspecific correlate of this procedure. We report here results that do not support this conclusion. Intact and adrenalectomized (ADX) male rats were subjected to a 96-h SD using multiple- and single-platform methods. New cells were identified by immunoreactivity for 5-bromo-2'-deoxyuridine (BrdU) or Ki67 and new neurons by immunoreactivity for BrdU and doublecortin. EEG recordings confirmed a 95% deprivation of rapid eye movement (REM) sleep and a 40% decrease of non-REM sleep. Cell proliferation in the dentate gyrus was suppressed by up to 50% in sleep-deprived rats relative to apparatus control or home cage control rats. This effect was also observed in ADX rats receiving continuous low-dose Cort replacement via subcutaneous minipumps but not in ADX rats receiving Cort replacement via drinking water. In these latter rats, Cort intake via water was reduced by 60% during SD; upregulation of cell proliferation by reduced Cort intake may obscure inhibitory effects of sleep loss on cell proliferation. SD had no effect on the percentage of new cells expressing a neuronal phenotype. These results demonstrate that the Cort replacement method is critical for detecting an effect of SD on cell proliferation and support a significant role for sleep in adult neurogenesis.

  18. 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

  19. 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.

  20. 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

  1. Comparison of sustained attention assessed by auditory and visual psychomotor vigilance tasks prior to and during sleep deprivation.

    PubMed

    Jung, Christopher M; Ronda, Joseph M; Czeisler, Charles A; Wright, Kenneth P

    2011-06-01

    To date, no detailed examination of the pattern of change in reaction time performance for different sensory modalities has been conducted across the circadian cycle during sleep deprivation. Therefore, we compared sustained auditory and visual attention performance during 40h of sleep deprivation assessing multiple metrics of auditory and visual psychomotor vigilance tasks (PVT). Forty healthy participants (14 women) aged 30.8±8.6years were studied. Subjects were scheduled for an ∼8h sleep schedule at home prior to three-six laboratory baseline days with an 8 h sleep schedule followed by 40h sleep deprivation. Visual and auditory PVTs were 10min in duration, and were administered every 2h during sleep deprivation. Data were analysed with mixed-model anova. Sleep deprivation and circadian phase increased response time, lapses, anticipations, standard deviation of response times and time on task decrements for visual and auditory PVTs. In general, auditory vigilance was faster and less variable than visual vigilance, with larger differences between auditory and visual PVT during sleep deprivation versus baseline. Failures to respond to stimuli within 10s were four times more likely to occur to visual versus auditory stimuli. Our findings highlight that lapses during sleep deprivation are more than just long responses due to eye closure or visual distraction. Furthermore, our findings imply that the general pattern of change in attention during sleep deprivation (e.g. circadian variation, response slowing, lapsing and anticipations, time on task decrements and state instability) is similar among sensory-motor behavioral response modalities.

  2. Sleep Deprivation Decreases [11C]Raclopride’s Binding to Dopamine D2/D3 Receptors in the Human Brain

    PubMed Central

    Volkow, Nora D.; Wang, Gene-Jack; Telang, Frank; Fowler, Joanna S.; Logan, Jean; Wong, Christopher; Ma, Jim; Pradhan, Kith; Tomasi, Dardo; Thanos, Peter K.; Ferré, Sergi; Jayne, Millard

    2009-01-01

    Sleep deprivation can markedly impair human performance contributing to accidents and poor productivity. The mechanisms underlying this impairment are not well understood but brain dopamine systems have been implicated. Here we test whether one night of sleep deprivation changes dopamine brain activity. We studied fifteen healthy subjects using positron emission tomography and [11C]raclopride (dopamine D2/3 receptor radioligand) and [11C]cocaine (dopamine transporter radioligand). Subjects were tested twice; after one night of rested sleep and after on night of sleep deprivation. [11C]Raclopride’s specific binding in striatum and thalamus were significantly reduced after sleep deprivation and the magnitude of this reduction correlated with increases in fatigue (tiredness and sleepiness) and with deterioration in cognitive performance (visual attention and working memory). In contrast sleep deprivation did not affect the specific binding of [11C]cocaine in striatum. Since [11C]raclopride competes with endogenous dopamine for binding to D2/D3 receptors, we interpret the decreases in binding to reflect dopamine increases with sleep deprivation. However, we can not rule out the possibility that decreased [11C]raclopride binding reflects decreases in receptor levels or affinity. Sleep deprivation did not affect dopamine transporters (target for most wake-promoting medications) and thus dopamine increases are likely to reflect increases in dopamine cell firing and/or release rather than decreases in dopamine reuptake. Inasmuch as dopamine-enhancing drugs increase wakefulness we postulate that dopamine increases after sleep deprivation is a mechanism by which the brain maintains arousal as the drive to sleep increases but one that is insufficient to counteract behavioral and cognitive impairment. PMID:18716203

  3. Circadian Variations in Performance, Psychological Ratings, Catecholamine Excretion and Urine Flow During Prolonged Sleep Deprivation,

    DTIC Science & Technology

    rhythms in a number of biochemical and psychological variables under controlled conditions. (b) changes in these variables with the duration of sleep ... deprivation . (c) temporal interrelationships between the biochemical and psychological variables. In all the above respects, the first experiment was an exploratory study, the results being further tested in the second.

  4. 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…

  5. 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…

  6. Xylaria nigripes mitigates spatial memory impairment induced by rapid eye movement sleep deprivation.

    PubMed

    Zhao, Zhengqing; Li, Yanpeng; Chen, Haiyan; Huang, Liuqing; Zhao, Fei; Yu, Qiang; Xiang, Zhenghua; Zhao, Zhongxin

    2014-01-01

    We aimed to investigate the effects of Xylaria nigripes (XN) extracts on the rapid eye movement sleep deprivation (REMSD)-induced memory impairment, and explore related mechanism. Male Sprague Dawley rats were randomly divided into 6 groups: cage control (CC)-NaCl group; tank control (TC)-NaCl group; sleep deprivation (SD)-NaCl group; CC-XN group; TC-XN group and SD-XN group. The rats were administered with intragastric XN and 0.9% of sodium chloride. SD group rats were deprived of REM sleep for 72 h. Morris water maze (MWM) was used to assess the effects of XN on spatial learning and memory. The expression of cAMP-response element binding protein (CREB) and p-CREB were also investigated in all groups. Result showed rats in SD-NaCl group had significantly longer mean escape latencies in finding the platform as compared to the control rats (p<0.05) in MWM test. The SD-NaCl group spent significantly less time in goal quadrant compared with the SD-XN group. REMSD and XN did not alter CREB expression in the hippocampus, while sleep deprivation resulted in reduced phosphorylation of CREB in the hippocampus, which was reversed by XN. XN mitigates spatial memory impairment induced by REMSD in rat. Phosphorylation of CREB in hippocampus might be one of the mechanisms.

  7. 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…

  8. Sleep deprivation impairs emotional memory retrieval in mice: influence of sex.

    PubMed

    Fernandes-Santos, Luciano; Patti, Camilla L; Zanin, Karina A; Fernandes, Helaine A; Tufik, Sergio; Andersen, Monica L; Frussa-Filho, Roberto

    2012-08-07

    The deleterious effects of paradoxical sleep deprivation on memory processes are well documented. However, non-selective sleep deprivation occurs more commonly in modern society and thus represents a better translational model. We have recently reported that acute total sleep deprivation (TSD) for 6 h immediately before testing impaired performance of male mice in the plus-maze discriminative avoidance task (PM-DAT) and in the passive avoidance task (PAT). In order to extend these findings to females, we examined the effect of (pre-test) TSD on the retrieval of different memory tasks in both male and female mice. Animals were tested using 3 distinct memory models: 1) conditioning fear context (CFC), 2) PAT and 3) PM-DAT. In all experiments, animals were totally sleep-deprived by the gentle interference method for 6h immediately before being tested. In the CFC task and the PAT, TSD induced memory impairment regardless of sex. In PM-DAT, the memory impairing effects of TSD were greater in females. Collectively, our results confirm the impairing effect of TSD on emotional memory retrieval and demonstrate that it can be higher in female mice depending on the memory task evaluated.

  9. Effects of Sleep Deprivation on Cognitive Ability and Skills of Pediatrics Residents.

    ERIC Educational Resources Information Center

    Storer, James S.; And Others

    1989-01-01

    The cognitive and skills performances of sleep-deprived pediatrics residents were measured by using questions like those on the pediatrics board certification examination and using tasks that required coordination and dexterity. Implications of findings are discussed in the context of the controversy over the structure and process of medical…

  10. Modafinil ameliorates cognitive deficits induced by maternal separation and sleep deprivation.

    PubMed

    Garcia, Vanessa Athaíde; Hirotsu, Camila; Matos, Gabriela; Alvarenga, Tathiana; Pires, Gabriel Natan; Kapczinski, Flávio; Schröder, Nadja; Tufik, Sergio; Andersen, Monica Levy

    2013-09-15

    Animals exposed to an early adverse event may be more susceptible to a second source of stress later in life, and these stressors may have additive deleterious effects. Sleep deprivation is known to be a stressor, affecting multiple body functions such as the cognition. Modafinil enhances working memory and attention in healthy non-sleep deprived subjects and in animal models of sleep deprivation. The first aim of the present study was to investigate the effects of maternal separation (MS) combined with paradoxical sleep deprivation (PSD) in adulthood on recognition memory in rats. Second, we aimed to evaluate whether the administration of modafinil would be able to ameliorate memory deficits induced by MS and PSD. Wistar rat pups were initially distributed into MS and handling (H) groups, with their litters standardized in 4 females and 4 males. In adulthood, the male rats were submitted to PSD or control condition, being redistributed afterwards in modafinil- or vehicle-treatment immediately after the training session of object recognition task. PSD did not potentiate the cognitive deficit due to MS. However, modafinil was able to recover memory impairments associated to PSD and also to MS in the neonatal period. This study demonstrates for the first time that modafinil ameliorates cognitive deficits associated to MS and to PSD in adulthood, independent from MS in the neonatal period.

  11. 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

  12. 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 ...

  13. 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 - ...

  14. 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

  15. Social and environmental contexts modulate sleep deprivation-induced c-Fos activation in rats.

    PubMed

    Deurveilher, Samuel; Ryan, Nathan; Burns, Joan; Semba, Kazue

    2013-11-01

    People often sleep deprive themselves voluntarily for social and lifestyle reasons. Animals also appear to stay awake longer as a result of their natural curiosity to explore novel environments and interact socially with conspecifics. Although multiple arousal systems in the brain are known to act jointly to promote and maintain wakefulness, it remains unclear whether these systems are similarly engaged during voluntary vs. forced wakefulness. Using c-Fos immunohistochemistry, we compared neuronal responses in rats deprived of sleep for 2 h by gentle sensory stimulation, exploration under social isolation, or exploration with social interaction, and rats under undisturbed control conditions. In many arousal, limbic, and autonomic nuclei examined (e.g., anterior cingulate cortex and locus coeruleus), the two sleep deprivation procedures involving exploration were similarly effective, and both were more effective than sleep deprivation with sensory stimulation, in increasing the number of c-Fos immunoreactive neurons. However, some nuclei (e.g., paraventricular hypothalamic nucleus and select amygdala nuclei) were more responsive to exploration with social interaction, while others (e.g., histaminergic tuberomammillary nucleus) responded more strongly to exploration in social isolation. In the rostral basal forebrain, cholinergic and GABAergic neurons responded preferentially to exploration with social interaction, whereas resident neurons in general responded most strongly to exploration without social interaction. These results indicate that voluntary exploration with/without social interaction is more effective than forced sleep deprivation with gentle sensory stimulation for inducing c-Fos in arousal and limbic/autonomic brain regions, and suggest that these nuclei participate in different aspects of arousal during sustained voluntary wakefulness.

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

    PubMed

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

    2015-12-20

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

  17. 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

  18. Dose-dependent model of caffeine effects on human vigilance during total sleep deprivation.

    PubMed

    Ramakrishnan, Sridhar; Laxminarayan, Srinivas; Wesensten, Nancy J; Kamimori, Gary H; Balkin, Thomas J; Reifman, Jaques

    2014-10-07

    Caffeine is the most widely consumed stimulant to counter sleep-loss effects. While the pharmacokinetics of caffeine in the body is well-understood, its alertness-restoring effects are still not well characterized. In fact, mathematical models capable of predicting the effects of varying doses of caffeine on objective measures of vigilance are not available. In this paper, we describe a phenomenological model of the dose-dependent effects of caffeine on psychomotor vigilance task (PVT) performance of sleep-deprived subjects. We used the two-process model of sleep regulation to quantify performance during sleep loss in the absence of caffeine and a dose-dependent multiplier factor derived from the Hill equation to model the effects of single and repeated caffeine doses. We developed and validated the model fits and predictions on PVT lapse (number of reaction times exceeding 500 ms) data from two separate laboratory studies. At the population-average level, the model captured the effects of a range of caffeine doses (50-300 mg), yielding up to a 90% improvement over the two-process model. Individual-specific caffeine models, on average, predicted the effects up to 23% better than population-average caffeine models. The proposed model serves as a useful tool for predicting the dose-dependent effects of caffeine on the PVT performance of sleep-deprived subjects and, therefore, can be used for determining caffeine doses that optimize the timing and duration of peak performance.

  19. 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

  20. Influence of food restriction on lipid profile and spontaneous glucose levels in male rats subjected to paradoxical sleep deprivation

    PubMed Central

    Alvarenga, Tathiana Aparecida; Tufik, Sergio; Pires, Gabriel Natan; Andersen, Monica Levy

    2012-01-01

    OBJECTIVES: The purpose of this study was to determine the paired consequences of food restriction and paradoxical sleep deprivation on lipid profile and spontaneous glucose levels in male rats. METHOD: Food restriction began at weaning, with 6 g of food being provided per day, which was subsequently increased by 1 g per week until reaching 15 g per day by the eighth week. At adulthood, both rats subjected to food restriction and those fed ad libitum were exposed to paradoxical sleep deprivation for 96 h or were maintained in their home-cage groups. RESULTS: Animals subjected to food restriction exhibited a significant increase in high-density lipoprotein levels compared to animals that were given free access to food. After the paradoxical sleep deprivation period, the food-restricted animals demonstrated reduced concentrations of high-density lipoprotein relative to their respective controls, although the values for the food-restricted animals after sleep deprivation were still higher than those for the ad libitum group. The concentration of low-density lipoproteins was significantly increased in sleep-deprived animals fed the ad libitum diet. The levels of triglycerides, very low-density lipoproteins, and glucose in food-restricted animals were each decreased compared to both ad libitum groups. CONCLUSION: These results may help to illustrate the mechanisms underlying the relationship between sleep curtailment and metabolism and may suggest that, regardless of sleep deprivation, dietary restriction can minimize alterations in parameters related to cardiovascular risk. PMID:22522763

  1. 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…

  2. A Unified Mathematical Model to Quantify Performance Impairment for Both Chronic Sleep Restriction and Total Sleep Deprivation

    DTIC Science & Technology

    2013-04-24

    Performance prediction models based on the classical two- process model of sleep regulation are reasonably effective at predicting alertness and...recent history exerting greater influence. This incorporation of sleep/wake history into the classical two- process model captures an individual’s...capacity to recover during sleep as a function of sleep debt and naturally bridges the continuum from CSR to TSD by reducing to the classical two- process

  3. 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.

  4. 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.

  5. Suppression of hippocampal plasticity-related gene expression by sleep deprivation in rats

    PubMed Central

    Guzman-Marin, Ruben; Ying, Zhe; Suntsova, Natalia; Methippara, Melvi; Bashir, Tariq; Szymusiak, Ronald; Gomez-Pinilla, Fernando; McGinty, Dennis

    2006-01-01

    Previous work shows that sleep deprivation impairs hippocampal-dependent learning and long-term potentiation (LTP). Brain-derived neurotrophic factor (BDNF), cAMP response-element-binding (CREB) and calcium–calmodulin-dependent protein kinase II (CAMKII) are critical modulators of hippocampal-dependent learning and LTP. In the present study we compared the effects of short- (8 h) and intermediate-term (48 h) sleep deprivation (sd) on the expression of BDNF and its downstream targets, Synapsin I, CREB and CAMKII in the neocortex and the hippocampus. Rats were sleep deprived using an intermittent treadmill system which equated total movement in the SD and control treadmill animals (CT), but permitted sustained periods of rest in CT animals. Animals were divided into SD (treadmill schedule: 3 s on/12 s off) and two treadmill control groups, CT1 (15 min on/60 min off) and CT2 (30 min on/120 min off – permitting more sustained sleep). Real-time Taqman RT-PCR was used to measure changes in mRNA; BDNF protein levels were determined using ELISA. In the hippocampus, 8 h treatments reduced BDNF, Synapsin I, CREB and CAMKII gene expression in both SD and control groups. Following 48 h of experimental procedures, the expression of all these four molecular markers of plasticity was reduced in SD and CT1 groups compared to the CT2 and cage control groups. In the hippocampus, BDNF protein levels after 8 h and 48 h treatments paralleled the changes in mRNA. In neocortex, neither 8 h nor 48 h SD or control treatments had significant effects on BDNF, Synapsin I and CAMKII mRNA levels. Stepwise regression analysis suggested that loss of REM sleep underlies the effects of SD on hippocampal BDNF, Synapsin I and CREB mRNA levels, whereas loss of NREM sleep underlies the effects on CAMKII mRNA. PMID:16825295

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

    PubMed Central

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

    2015-01-01

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

  7. Facilitation of task performance and removal of the effects of sleep deprivation by an ampakine (CX717) in nonhuman primates.

    PubMed

    Porrino, Linda J; Daunais, James B; Rogers, Gary A; Hampson, Robert E; Deadwyler, Sam A

    2005-09-01

    The deleterious effects of prolonged sleep deprivation on behavior and cognition are a concern in modern society. Persons at risk for impaired performance and health-related issues resulting from prolonged sleep loss would benefit from agents capable of reducing these detrimental effects at the time they are sleep deprived. Agents capable of improving cognition by enhancing brain activity under normal circumstances may also have the potential to reduce the harmful or unwanted effects of sleep deprivation. The significant prevalence of excitatory alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamatergic receptors in the brain provides a basis for implementing a class of drugs that could act to alter or remove the effects of sleep deprivation. The ampakine CX717 (Cortex Pharmaceuticals), a positive allosteric modulator of AMPA receptors, was tested for its ability to enhance performance of a cognitive, delayed match-to-sample task under normal circumstances in well-trained monkeys, as well as alleviate the detrimental effects of 30-36 h of sleep deprivation. CX717 produced a dose-dependent enhancement of task performance under normal alert testing conditions. Concomitant measures of regional cerebral metabolic rates for glucose (CMRglc) during the task, utilizing positron emission tomography, revealed increased activity in prefrontal cortex, dorsal striatum, and medial temporal lobe (including hippocampus) that was significantly enhanced over normal alert conditions following administration of CX717. A single night of sleep deprivation produced severe impairments in performance in the same monkeys, accompanied by significant alterations in task-related CMRglc in these same brain regions. However, CX717 administered to sleep-deprived monkeys produced a striking removal of the behavioral impairment and returned performance to above-normal levels even though animals were sleep deprived. Consistent with this recovery, CMRglc in all but one brain

  8. Effect of total sleep deprivation on reaction time and waking EEG activity in man.

    PubMed

    Lorenzo, I; Ramos, J; Arce, C; Guevara, M A; Corsi-Cabrera, M

    1995-06-01

    Nine paid volunteers were sleep deprived over a period of 40 hours. Every 2 hours during total sleep deprivation (TSD) and after recovery sleep, oral temperature (OT), reaction time (RT) in a vigilance task and electroencephalogram (EEG) with eyes open and closed (C3, C4, T3 and T4) were recorded. Ten artifact-free samples from each condition were Fourier transformed. Absolute power was calculated for six bands. Analyses of variance with deprivation and time of day as factors showed the following significant results: 1) TSD induced an increase in RT, of theta power in all derivations, of beta power in both centrals and a decrease of alpha power with eyes closed; OT was not affected. 2) All bands showed a peak of power at 1800 hours, 2 hours in advance of the OT acrophase at 2000 hours. All variables recovered baseline values after 1 night of sleep. Significant linear correlations of hours of wakefulness with EEG and RT, and of EEG power with OT and RT, were observed. The present findings show a linear increase in EEG power and RT with TSD, and a diurnal oscillation of EEG power, which is independent of TSD.

  9. Neuroimaging and genetics of antidepressant response to sleep deprivation: implications for drug development.

    PubMed

    Benedetti, Francesco; Smeraldi, Enrico

    2009-01-01

    Despite confirmed evidences about some neurochemical effects of antidepressant treatments, there is still a high level of uncertainty about which biological changes are needed to recover from a major depressive episode. Changes of monoaminergic neurotransmission are paralleled by profound changes in brain metabolism, neural responses to stimuli, sleep architecture, biological rhythms, and, at the intracellular level, neuronal signaling pathways regulating gene expression, neuroplasticity, and neurotrophic mechanisms. Sleep deprivation targets the biological mechanisms which are responsible for the possibility, unique to mood disorders, of rapid switching between depression, euthymia, and mania. The rapidity of action of sleep deprivation enables the study of the correlates of antidepressant response at close time points, providing a good model to study the biological basis of the antidepressant response and of the pathophysiology of affective illness. Current knowledge suggests that multiple neurobiological effects of sleep deprivation are responsible for the clinical mood amelioration, suggesting a multi-target mechanism of action. An impressive group of brain imaging studies using different brain imaging techniques (positron emission tomography, single photon emission tomography, functional magnetic resonance imaging, proton spectroscopy, arterial spin labeling) showed that clinical response is associated with changes in the functioning of specific brain areas. The combination of these new methodological acquisitions with the classical neurobiological and pharmacogenetic perspective provides an evolving knowledge about brain changes associated with antidepressant response, and will then help to identify the real targets of antidepressant treatment.

  10. Time estimation during prolonged sleep deprivation and its relation to activation measures.

    PubMed

    Miró, Elena; Cano, M Carmen; Espinosa-Fernández, Lourdes; Buela-Casal, Gualberto

    2003-01-01

    This is the first study to analyze variations in time estimation during 60 h of sleep deprivation and the relation between time estimation performance and the activation measures of skin resistance level, body temperature, and Stanford Sleepiness Scale (SSS) scores. Among 30 healthy participants 18 to 24 years of age, for a 10-s interval using the production method, we found a lengthening in time estimations that was modulated by circadian oscillations. No differences in gender were found in the time estimation task during sleep deprivation. The variations in time estimation correlated significantly with body temperature, skin resistance level, and SSS throughout the sleep deprivation period. When body temperature is elevated, indicating a high level of activation, the interval tends to be underestimated, and vice versa. When the skin resistance level or SSS is elevated (low activation), time estimation is lengthened, and vice versa. This lengthening is important because many everyday situations involve duration estimation under moderate to severe sleep loss. Actual or potential applications of this research include transportation systems, emergency response work, sporting activities, and industrial settings in which accuracy in anticipation or coincidence timing is important for safety or efficiency.

  11. Alerting, orienting and executive control: the effects of sleep deprivation on attentional networks.

    PubMed

    Martella, Diana; Casagrande, Maria; Lupiáñez, Juan

    2011-04-01

    Sleep deprivation alters attentional functions like vigilance or tonic alerting (i.e., sustaining an alert state over a period of time). However, the effects of sleep loss on both orienting and executive control are still not clear, and no study has assessed whether sleep deprivation might affect the relationships among these three attentional systems. In order to investigate the efficiency of the three attentional networks--alerting, orienting and executive control--within a single task, we used the Attention Network Test (ANT). Eighteen right-handed male participants took part in the experiment, which took place on two consecutive days. On the first day, each participant performed a 20 min training session of the ANT. On the second day, participants remained awake for 24 h during which time the ANT was performed once at 5:00 p.m. and once at 4:00 a.m. Results showed an overall slowing of reaction times in the nocturnal session, indicating a strong decrease in vigilance. Furthermore, sleep deprivation did affect attentional orienting and executive control. Results are consistent with the hypothesis that the tonic component of alerting interacts with both attentional orienting and executive functions.

  12. Rapid eye movement sleep deprivation does not affect fear memory reconsolidation in rats.

    PubMed

    Tian, Shaowen; Huang, Fulian; Li, Peng; Ouyang, Xinping; Li, Zengbang; Deng, Haifeng; Yang, Yufeng

    2009-09-29

    There is increasing evidence that sleep may be involved in memory consolidation. However, there remain comparatively few studies that have explored the relationship between sleep and memory reconsolidation. At present study, we tested the effects of rapid eye movement sleep deprivation (RSD) on the reconsolidation of cued (experiment 1) and contextual (experiment 2) fear memory in rats. Behaviour procedure involved four training phases: habituation, fear conditioning, reactivation and test. Rats were subjected to 6h RSD starting either immediately after reactivation or 6h later. The control rats were returned to their home cages immediately after reactivation and left undisturbed. Contrary to those hypotheses speculating a potential role of sleep in reconsolidation, we found that post-reactivation RSD whether from 0 to 6h or 6 to 12h had no effect on the reconsolidation of both cued and contextual fear memory. However, our present results did not exclude the potential roles of non-rapid eye movement sleep in the reconsolidation of fear memory or sleep in the reconsolidation of other memory paradigms.

  13. [Sleep patterns and the efficiency of the gentle methods of sleep deprivation in rats at different stages of pregnancy: behavioral study].

    PubMed

    Pigareva, M L

    2008-01-01

    In Wistar rats, pregnant or not pregnant, sleep-wakefulness parameters were registered for 2 days from 10:00 till 14:00. Later, these rats were subjected to 3-hour (11:00-14:00) daily sleep deprivation (SD) during 3 consecutive days. To prevent sleep, the following manipulations were used: acoustic stimulation from moving of the food pellets, opening or horizontal rotation of the cage and gentle handling. Control pregnant or not pregnant rats were placed in individual cages in the same room, but their sleep was not disturbed. On average, not pregnant rats spent about 65% of the time in sleep. Sleep episodes were mostly short (less than 1 min) or medium (1-15 min). After the beginning and with advance of pregnancy, the amount, deepness and duration of sleep episodes increased. With the methods of SD used, not pregnant rats did not sleep almost at all during the SD session. In pregnant rats, the quantity and intensity of stimuli used for SD increased as compared to control, which was indicatives of the growth of "sleep pressure" during pregnancy.

  14. Phenotypic Stability of Energy Balance Responses to Experimental Total Sleep Deprivation and Sleep Restriction in Healthy Adults

    PubMed Central

    Dennis, Laura E.; Spaeth, Andrea M.; Goel, Namni

    2016-01-01

    Experimental studies have shown that sleep restriction (SR) and total sleep deprivation (TSD) produce increased caloric intake, greater fat consumption, and increased late-night eating. However, whether individuals show similar energy intake responses to both SR and TSD remains unknown. A total of N = 66 healthy adults (aged 21–50 years, 48.5% women, 72.7% African American) participated in a within-subjects laboratory protocol to compare daily and late-night intake between one night of SR (4 h time in bed, 04:00–08:00) and one night of TSD (0 h time in bed) conditions. We also examined intake responses during subsequent recovery from SR or TSD and investigated gender differences. Caloric and macronutrient intake during the day following SR and TSD were moderately to substantially consistent within individuals (Intraclass Correlation Coefficients: 0.34–0.75). During the late-night period of SR (22:00–04:00) and TSD (22:00–06:00), such consistency was slight to moderate, and participants consumed a greater percentage of calories from protein (p = 0.01) and saturated fat (p = 0.02) during SR, despite comparable caloric intake (p = 0.12). Similarly, participants consumed a greater percentage of calories from saturated fat during the day following SR than TSD (p = 0.03). Participants also consumed a greater percentage of calories from protein during recovery after TSD (p < 0.001). Caloric intake was greater in men during late-night hours and the day following sleep loss. This is the first evidence of phenotypic trait-like stability and differential vulnerability of energy balance responses to two commonly experienced types of sleep loss: our findings open the door for biomarker discovery and countermeasure development to predict and mitigate this critical health-related vulnerability. PMID:27999367

  15. Sleep deprivation alters functioning within the neural network underlying the covert orienting of attention.

    PubMed

    Mander, Bryce A; Reid, Kathryn J; Davuluri, Vijay K; Small, Dana M; Parrish, Todd B; Mesulam, M-Marsel; Zee, Phyllis C; Gitelman, Darren R

    2008-06-27

    One function of spatial attention is to enable goal-directed interactions with the environment through the allocation of neural resources to motivationally relevant parts of space. Studies have shown that responses are enhanced when spatial attention is predictively biased towards locations where significant events are expected to occur. Previous studies suggest that the ability to bias attention predictively is related to posterior cingulate cortex (PCC) activation [Small, D.M., et al., 2003. The posterior cingulate and medial prefrontal cortex mediate the anticipatory allocation of spatial attention. Neuroimage 18, 633-41]. Sleep deprivation (SD) impairs selective attention and reduces PCC activity [Thomas, M., et al., 2000. Neural basis of alertness and cognitive performance impairments during sleepiness. I. Effects of 24 h of sleep deprivation on waking human regional brain activity. J. Sleep Res. 9, 335-352]. Based on these findings, we hypothesized that SD would affect PCC function and alter the ability to predictively allocate spatial attention. Seven healthy, young adults underwent functional magnetic resonance imaging (fMRI) following normal rest and 34-36 h of SD while performing a task in which attention was shifted in response to peripheral targets preceded by spatially informative (valid), misleading (invalid), or uninformative (neutral) cues. When rested, but not when sleep-deprived, subjects responded more quickly to targets that followed valid cues than those after neutral or invalid cues. Brain activity during validly cued trials with a reaction time benefit was compared to activity in trials with no benefit. PCC activation was greater during trials with a reaction time benefit following normal rest. In contrast, following SD, reaction time benefits were associated with activation in the left intraparietal sulcus, a region associated with receptivity to stimuli at unexpected locations. These changes may render sleep-deprived individuals less able

  16. A new automated method for rat sleep deprivation with minimal confounding effects on corticosterone and locomotor activity.

    PubMed

    Leenaars, Cathalijn H C; Dematteis, Maurice; Joosten, Ruud N J M A; Eggels, Leslie; Sandberg, Hans; Schirris, Mischa; Feenstra, Matthijs G P; Van Someren, Eus J W

    2011-03-15

    The function of sleep in physiology, behaviour and cognition has become a primary focus of neuroscience. Its study inevitably includes experimental sleep deprivation designs. However, concerns exist regarding confounds like stress, increased locomotor activity levels, and decreased motivation to perform operant tasks induced by the methods employed. We here propose a novel procedure for sleep deprivation in rats and evaluate how it affects sleep, corticosterone concentration profiles, locomotor activity levels, and motivation to perform an operant task. Before, during and after 12h of total sleep deprivation by means of gradually increasing the rotation variability and the speed of a novel automated, two-compartment sleep deprivation device, sleep-wake states were assessed by electroencephalography (n=21), brain extracellular corticosterone concentrations using microdialysis (n=11), locomotor activity by infrared measurements (n=8), and operant performance using a fixed-interval-fixed-ratio task (n=16). Sleep was effectively prevented during the procedure; rats on average slept less than 1% of the time (0.8±0.2%, mean±standard error). Brain corticosterone concentrations were mildly increased during the procedure, but did not exceed normal peak concentrations. Locomotor activity was not only increased during the procedure, but also did not exceed the peak levels found during undisturbed wakefulness. Food restriction to 12 g/rat/day prevented sleep deprivation from reducing the motivation to perform an operant task. This novel procedure can be applied to sleep deprive rats in a highly effective way, while keeping corticosterone and locomotor activity within the normal range.

  17. Sleep: a health imperative.

    PubMed

    Luyster, Faith S; Strollo, Patrick J; Zee, Phyllis C; Walsh, James K

    2012-06-01

    Chronic sleep deficiency, defined as a state of inadequate or mistimed sleep, is a growing and underappreciated determinant of health status. Sleep deprivation contributes to a number of molecular, immune, and neural changes that play a role in disease development, independent of primary sleep disorders. These changes in biological processes in response to chronic sleep deficiency may serve as etiological factors for the development and exacerbation of cardiovascular and metabolic diseases and, ultimately, a shortened lifespan. Sleep deprivation also results in significant impairments in cognitive and motor performance which increase the risk of motor vehicle crashes and work-related injuries and fatal accidents. The American Academy of Sleep Medicine and the Sleep Research Society have developed this statement to communicate to national health stakeholders the current knowledge which ties sufficient sleep and circadian alignment in adults to health.

  18. 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

  19. [Effect of unusual regimens of daily activity and sleep deprivation on the human functional state and work capacity].

    PubMed

    Litsov, A N; Saraev, I F

    1980-01-01

    Physiological functions, work capacity and sleep characteristics of six healthy test subjects were studied for 30 days. The test subjects adhered to one of the three different regimens (1--sleep from 2.00 a.m. to 10.00 a.m., 2--sleep from 6.00 p.m. to 2.00 a.m., and 3--sleep from 10.00 a.m. to 6.00 p.m.) which were aggravated by 64 hr or 72 hr vigilance during the experiment. The studies demonstrated general and specific changes in physiological functions, work capacity and sleep closely associated with the fact how far work-rest cycles were shifted and how long they were applied. Prolonged vigilance caused similar changes in physiological functions, work capacity and sleep. The test subjects showed very poor tolerance to an alteration in the work-rest cycle combined with sleep deprivation.

  20. Homeostatic response to sleep/rest deprivation by constant water flow in larval zebrafish in both dark and light conditions.

    PubMed

    Aho, Vilma; Vainikka, Maija; Puttonen, Henri A J; Ikonen, Heidi M K; Salminen, Tiia; Panula, Pertti; Porkka-Heiskanen, Tarja; Wigren, Henna-Kaisa

    2017-03-02

    Sleep-or sleep-like states-have been reported in adult and larval zebrafish using behavioural criteria. These reversible quiescent periods, displaying circadian rhythmicity, have been used in pharmacological, genetic and neuroanatomical studies of sleep-wake regulation. However, one of the important criteria for sleep, namely sleep homeostasis, has not been demonstrated unequivocally. To study rest homeostasis in zebrafish larvae, we rest-deprived 1-week-old larvae with a novel, ecologically relevant method: flow of water. Stereotyped startle responses to sensory stimuli were recorded after the rest deprivation to study arousal threshold using a high-speed camera, providing an appropriate time resolution to detect species-specific behavioural responses occurring in a millisecond time-scale. Rest-deprived larvae exhibited fewer startle responses than control larvae during the remaining dark phase and the beginning of the light phase, which can be interpreted as a sign of rest homeostasis-often used as equivalent of sleep homeostasis. To address sleep homeostasis further, we probed the adenosinergic system, which in mammals regulates sleep homeostasis. The adenosine A1 receptor agonist, cyclohexyladenosine, administered during the light period, decreased startle responses and increased immobility bouts, while the adenosine antagonist, caffeine, administered during the dark period, decreased immobility bouts. These results suggest that the regulation of sleep homeostasis in zebrafish larvae consists of the same elements as that of other species.

  1. Effects of sleep deprivation on cardiorespiratory functions of the runners and volleyball players during rest and exercise.

    PubMed

    Azboy, O; Kaygisiz, Z

    2009-03-01

    The effect of sleep deprivation on male runners (age 18.1 +/- 0.35) and volleyball players (age 17.8 +/- 0.36) has not been investigated. Therefore, we studied the possible effect of sleep deprivation in the sportsmen. The athletes performed spirometric tests at rest and then incremental exercise test on ergometer following one night sleep and one night (25-30 h) sleeplessness. Several standard measurements of spirometric function showed no significant change following sleep loss. Sleep loss raised resting oxygen uptake (VO2) in the runners and resting carbon dioxide production (VCO2) in both the runners and the volleyball players (p < 0.05). However, it left heart rate (HR), respiratory quotient (R), minute ventilation (VE) and arterial oxygen saturation (SaO2) unchanged at rest in both groups. Sleep loss decreased time to exhaustion in the volleyball players (p < 0.01). In the runners and the volleyball players, sleep loss did not alter exercise values of HR, VO2, VCO2, R and SaO2, but it reduced exercise VE (p < 0.05). We suggest that one night sleep deprivation may reduce exercise performance by decreasing exercise VE and time to exhaustion. We also indicate that sleep loss may decrease more the performance of volleyball players than that of runners.

  2. 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.

  3. 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.

  4. Effect of total sleep deprivation on postprandial metabolic and insulin responses in shift workers and non-shift workers.

    PubMed

    Wehrens, Sophie M T; Hampton, Shelagh M; Finn, Rebecca E; Skene, Debra J

    2010-08-01

    Epidemiological studies have shown that shift workers are at a greater risk of developing cardiovascular disease which may, in part, be related to metabolic and hormonal changes. Partial sleep deprivation, a common consequence of rotating shift work, has been shown to affect glucose tolerance and insulin sensitivity. The current study investigated the effects of one night of total sleep deprivation, as a proxy for the first night shift, on postprandial glucose, insulin and lipid (triacylglycerols (TAGs) and non-esterified fatty acids (NEFAs)) responses under controlled laboratory conditions in shift workers and non-shift workers. Eleven experienced shift workers (35.7+/-7.2 years, mean+/-s.d.) who had worked in shifts for 8.7+/-5.25 years were matched with 13 non-shift workers who had worked for 32.8+/-6.4 years. After an adaptation night and a baseline sleep night, volunteers were kept awake for 30.5 h, followed by a nap (4 h) and recovery sleep. Blood samples were taken prior to and after a standard breakfast following baseline sleep, total sleep deprivation and recovery sleep. Basal TAG levels prior to the standard breakfast were significantly lower after sleep deprivation, indicating higher energy expenditure. Basal NEFA levels were significantly lower after recovery sleep. Postprandial insulin and TAG responses were significantly increased, and the NEFA response was decreased after recovery sleep, suggestive of insulin insensitivity. Although there were no overall significant differences between non-shift workers and shift workers, non-shift workers showed significantly higher basal insulin levels, lower basal NEFA levels, and an increased postprandial insulin and a decreased NEFA response after recovery sleep. In future, the reasons for these inter-group differences are to be investigated.

  5. Homeostatic Changes in GABA and Glutamate Receptors on Excitatory Cortical Neurons during Sleep Deprivation and Recovery

    PubMed Central

    del Cid-Pellitero, Esther; Plavski, Anton; Mainville, Lynda; Jones, Barbara E.

    2017-01-01

    Neuronal activity is regulated in a homeostatic manner through changes in inhibitory GABA and excitatory glutamate (Glu) AMPA (A) receptors (GluARs). Using immunofluorescent staining, we examined whether calcium/calmodulin-dependent protein kinase IIα (CaMKIIα)-labeled (+) excitatory neurons in the barrel cortex undergo such homeostatic regulation following enforced waking with associated cortical activation during the day when mice normally sleep the majority of the time. Sleep deprived mice were prevented from falling asleep by unilateral whisker stimulation and sleep recovery (SR) mice allowed to sleep freely following deprivation. In parallel with changes in c-Fos reflecting changes in activity, (β2-3 subunits of) GABAA Rs were increased on the membrane of CaMKIIα+ neurons with enforced waking and returned to baseline levels with SR in barrel cortex on sides both contra- and ipsilateral to the whisker stimulation. The GABAAR increase was correlated with increased gamma electroencephalographic (EEG) activity across conditions. On the other hand, (GluA1 subunits of) AMPA Rs were progressively removed from the membrane of CaMKIIα+ neurons by (Rab5+) early endosomes during enforced waking and returned to the membrane by (Rab11+) recycling endosomes during SR. The internalization of the GluA1Rs paralleled the expression of Arc, which mediates homeostatic regulation of AMPA receptors through an endocytic pathway. The reciprocal changes in GluA1Rs relative to GABAARs suggest homeostatic down-scaling during enforced waking and sensory stimulation and restorative up-scaling during recovery sleep. Such homeostatic changes with sleep-wake states and their associated cortical activities could stabilize excitability and activity in excitatory cortical neurons.

  6. Sleep deprivation disrupts the contribution of the hippocampus to the formation of novel lexical associations.

    PubMed

    Sterpenich, Virginie; Ceravolo, Leonardo; Schwartz, Sophie

    2017-04-01

    Sleep is involved in the mechanisms underlying memory consolidation and brain plasticity. Consolidation refers to a process through which labile memories are reorganized into more stable ones. An intriguing but often neglected question concerns how pre-existing knowledge is modified when new information enters memory, and whether sleep can influence this process. We investigated how nonword learning may modify the neural representations of closely-related existing words. We also tested whether sleep contributes to any such effect by comparing a group of participants who slept during the night following a first encoding session to a sleep deprived group. Thirty participants were first intensively trained at writing nonwords on Day 1 (remote nonwords) and Day 4 (recent nonwords), following which they underwent functional MRI. This session consisted of a word lexical decision task including words orthographically-close to the trained nonwords, followed by an incidental memory task on the nonwords. Participants who slept detected real words related to remote nonwords faster than those related to recent nonwords, and showed better explicit memory for the remote nonwords. Although the full interaction comparing both groups for these effects was not significant, we found that participants from the sleep-deprivation group did not display such differences between remote and recent conditions. Imaging results revealed that the functional interplay between hippocampus and frontal regions critically mediated these behavioral effects. This study demonstrates that sleep may not only strengthen memory for recently learned items but also promotes a constant reorganization of existing networks of word representations, allowing facilitated access to orthographically-close words.

  7. Aerobic and anaerobic contributions to exhaustive high-intensity exercise after sleep deprivation.

    PubMed

    Hill, D W; Borden, D O; Darnaby, K M; Hendricks, D N

    1994-10-01

    The purpose of this study was to determine the effect of one night's sleep loss on the performance of high-intensity exercise and on the contribution of anaerobic and aerobic energy systems to the exercise. Seven males and seven females performed an all-out cycling exercise test during baseline testing and then on three consecutive days after a sleepless night. The work rates were 5.0 W kg-1 for the females and 6.0 W kg-1 for the males. The aerobic contribution was determined based on measured VO2 and the anaerobic contribution was determined by subtraction of the aerobic contribution from the total amount of work performed. The results of baseline tests and of tests performed following sleep loss were compared for evidence of an effect of sleep deprivation. The 25-30 h of sleep deprivation did not affect total work, the anaerobic contribution or the aerobic contribution (all P > 0.1), although there was a tendency (P = 0.13) for mean VO2 to decrease after the sleepless night. There were no interaction effects involving sex on total work, the anaerobic contribution or the aerobic contribution (all P > 0.1). The mean (+/- S.E.M.) values for total work (kJ) performed were: baseline, 21.9 +/- 2.7; after sleep loss, 21.1 +/- 2.5 (day 1), 21.7 +/- 2.5 (day 2), and 21.9 +/- 2.7 (day 3). It is concluded that, in both males and females, there are no changes in the contributions of the aerobic and anaerobic energy systems to high-intensity exercise performed following the loss of one night's sleep.

  8. 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.

  9. Behavioral and genetic effects promoted by sleep deprivation in rats submitted to pilocarpine-induced status epilepticus.

    PubMed

    Matos, Gabriela; Ribeiro, Daniel A; Alvarenga, Tathiana A; Hirotsu, Camila; Scorza, Fulvio A; Le Sueur-Maluf, Luciana; Noguti, Juliana; Cavalheiro, Esper A; Tufik, Sergio; Andersen, Monica L

    2012-05-02

    The interaction between sleep deprivation and epilepsy has been well described in electrophysiological studies, but the mechanisms underlying this association remain unclear. The present study evaluated the effects of sleep deprivation on locomotor activity and genetic damage in the brains of rats treated with saline or pilocarpine-induced status epilepticus (SE). After 50 days of pilocarpine or saline treatment, both groups were assigned randomly to total sleep deprivation (TSD) for 6 h, paradoxical sleep deprivation (PSD) for 24 h, or be kept in their home cages. Locomotor activity was assessed with the open field test followed by resection of brain for quantification of genetic damage by the single cell gel electrophoresis (comet) assay. Status epilepticus induced significant hyperactivity in the open field test and caused genetic damage in the brain. Sleep deprivation procedures (TSD and PSD) did not affect locomotor activity in epileptic or healthy rats, but resulted in significant DNA damage in brain cells. Although PSD had this effect in both vehicle and epileptic groups, TSD caused DNA damage only in epileptic rats. In conclusion, our results revealed that, despite a lack of behavioral effects of sleep deprivation, TSD and PSD induced genetic damage in rats submitted to pilocarpine-induced SE.

  10. Investigating the effect of acute sleep deprivation on hypothalamic-pituitary-adrenal-axis response to a psychosocial stressor.

    PubMed

    Vargas, Ivan; Lopez-Duran, Nestor

    2017-05-01

    The hypothalamic-pituitary-adrenal (HPA) axis has been previously identified as one potential mechanism that may explain the link between sleep deprivation and negative health outcomes. However, few studies have examined the direct association between sleep deprivation and HPA-axis functioning, particularly in the context of stress. Therefore, the aim of the current study was to investigate the relationship between acute sleep deprivation and HPA-axis reactivity to a psychosocial stressor. Participants included 40 healthy, young adults between the ages of 18-29. The current protocol included spending two nights in the laboratory. After an adaptation night (night 1), participants were randomized into either a sleep deprivation condition (29 consecutive hours awake) or a control condition (night 2). Following the second night, all participants completed the Trier Social Stress Test (TSST). Salivary cortisol was collected before, during, and after the TSST. Results indicated that there were significant group differences in cortisol stress reactivity. Specifically, compared to participants in the control condition, participants in the sleep deprivation condition had greater baseline (i.e., pre-stress) cortisol, yet a blunted cortisol response to the TSST. Taken together, a combination of elevated baseline cortisol (and its subsequent effect on HPA-axis regulatory processes) and a relative 'ceiling' on the amount of cortisol a laboratory stressor can produce may explain why participants in the sleep deprivation condition demonstrated blunted cortisol responses.

  11. Remediation of sleep-deprivation-induced working memory impairment with fMRI-guided transcranial magnetic stimulation.

    PubMed

    Luber, B; Stanford, A D; Bulow, P; Nguyen, T; Rakitin, B C; Habeck, C; Basner, R; Stern, Y; Lisanby, S H

    2008-09-01

    Repetitive transcranial magnetic stimulation (rTMS) was applied to test the role of selected cortical regions in remediating sleep-deprivation-induced deficits in visual working memory (WM) performance. Three rTMS targets were chosen using a functional magnetic resonance imaging (fMRI)-identified network associated with sleep-deprivation-induced WM performance impairment: 2 regions from the network (upper left middle occipital gyrus and midline parietal cortex) and 1 nonnetwork region (lower left middle occipital gyrus). Fifteen participants underwent total sleep deprivation for 48 h. rTMS was applied at 5 Hz during a WM task in a within-subject sham-controlled design. The rTMS to the upper-middle occipital site resulted in a reduction of the sleep-induced reaction time deficit without a corresponding decrease in accuracy, whereas stimulation at the other sites did not. Each subject had undergone fMRI scanning while performing the task both pre- and postsleep deprivation, and the degree to which each individual activated the fMRI network was measured. The degree of performance enhancement with upper-middle occipital rTMS correlated with the degree to which each individual failed to sustain network activation. No effects were found in a subset of participants who performed the same rTMS procedure after recovering from sleep deprivation, suggesting that the performance enhancements seen following sleep deprivation were state dependent.

  12. Imbalance between TNFα and progranulin contributes to memory impairment and anxiety in sleep-deprived mice

    PubMed Central

    Zhang, Kun; Li, Yu-jiao; Feng, Dan; Zhang, Peng; Wang, Ya-tao; Li, Xiang; Liu, Shui-bing; Wu, Yu-mei; Zhao, Ming-gao

    2017-01-01

    Sleep disorder is becoming a widespread problem in current society, and is associated with impaired cognition and emotional disorders. Progranulin (PGRN), also known as granulin epithelin precursor, promotes neurite outgrowth and cell survival, and is encoded by the GRN gene. It is a tumor necrosis factor α receptor (TNFR) ligand which is implicated in many central nervous system diseases. However, the role PGRN in sleep disorder remains unclear. In the present study, we found that sleep deprivation (S-DEP) impaired the memory and produced thigmotaxis/anxiety-like behaviors in mice. S-DEP increased the levels of TNFα but decreased PGRN levels in the hippocampus. The intracerebroventricular (ICV) injection of PGRN or intraperitoneal injection of TNFα synthesis blocker thalidomide (25 mg/kg), prevented the memory impairment and anxiety behaviors induced by S-DEP. PGRN treatment also restored dendritic spine density in the hippocampus CA1 region and neurogenesis in hippocampus dentate gyrus (DG). These results indicate that an imbalance between TNFα and PGRN contributes to memory impairment and thigmotaxis/anxiety caused by sleep deprivation. PMID:28300056

  13. Imbalance between TNFα and progranulin contributes to memory impairment and anxiety in sleep-deprived mice.

    PubMed

    Zhang, Kun; Li, Yu-Jiao; Feng, Dan; Zhang, Peng; Wang, Ya-Tao; Li, Xiang; Liu, Shui-Bing; Wu, Yu-Mei; Zhao, Ming-Gao

    2017-03-16

    Sleep disorder is becoming a widespread problem in current society, and is associated with impaired cognition and emotional disorders. Progranulin (PGRN), also known as granulin epithelin precursor, promotes neurite outgrowth and cell survival, and is encoded by the GRN gene. It is a tumor necrosis factor α receptor (TNFR) ligand which is implicated in many central nervous system diseases. However, the role PGRN in sleep disorder remains unclear. In the present study, we found that sleep deprivation (S-DEP) impaired the memory and produced thigmotaxis/anxiety-like behaviors in mice. S-DEP increased the levels of TNFα but decreased PGRN levels in the hippocampus. The intracerebroventricular (ICV) injection of PGRN or intraperitoneal injection of TNFα synthesis blocker thalidomide (25 mg/kg), prevented the memory impairment and anxiety behaviors induced by S-DEP. PGRN treatment also restored dendritic spine density in the hippocampus CA1 region and neurogenesis in hippocampus dentate gyrus (DG). These results indicate that an imbalance between TNFα and PGRN contributes to memory impairment and thigmotaxis/anxiety caused by sleep deprivation.

  14. Maternal sleep deprivation inhibits hippocampal neurogenesis associated with inflammatory response in young offspring rats.

    PubMed

    Zhao, Qiuying; Peng, Cheng; Wu, Xiaohui; Chen, Yubo; Wang, Cheng; You, Zili

    2014-08-01

    Although sleep complaints are very common among pregnant women, the potential adverse effects of sleep disturbance on the offspring are not well studied. Growing evidence suggests that maternal stress can induce an inflammatory environment on the fetal development. But people are not sure about the consequences of prenatal stress such as the inflammatory responses induced by maternal sleep deprivation (MSD). In the present study, we investigated the effects of MSD on long-term behavioral and cognitive consequences in offspring and its underlying inflammatory response pathway. The pregnant Wistar rats received prolonged sleep deprivation (72h) on gestational day (GD) 4, 9, and 18, respectively. The post-natal day (PND) 21 offspring showed impaired hippocampus-dependent spatial learning and memory in the Morris Water Maze task and anhedonia in sucrose preference experiment. Quantification of BrdU(+) and DCX(+) cells revealed a significant decrease in hippocampus neurogenesis in prepuberty offspring, especially for the late MSD (GD 18) group. Real-time RT-PCR showed that after MSD, the expression of pro-inflammatory cytokines (IL-1β, IL-6 and TNFα) increased in the hippocampus of offspring on PND 1, 7, 14 and 21, whereas anti-inflammatory cytokine IL-10 reduced at the same time. Immunofluorescence found that the cells of activated microglia were higher in the brains of MSD offspring. Taken together, these results suggested that the MSD-induced inflammatory response is an important factor for neurogenesis impairment and neurobehavioral outcomes in prepuberty offspring.

  15. Sleep deprivation reduces proliferation of cells in the dentate gyrus of the hippocampus in rats

    PubMed Central

    guzmán-marín, Ruben; Suntsova, Natalia; Stewart, Darya R; Gong, Hui; Szymusiak, Ronald; McGinty, Dennis

    2003-01-01

    The dentate gyrus (DG) of the adult hippocampus gives rise to progenitor cells, which have the potential to differentiate into neurons. To date it is not known whether sleep or sleep loss has any effect on proliferation of cells in the DG. Male rats were implanted for polysomnographic recording, and divided into treadmill sleep-deprived (SD), treadmill control (TC) and cage control (CC) groups. SD and TC rats were kept for 96 h on a treadmill that moved either for 3 s on/12 s off (SD group) or for 15 min on/60 min off (TC group) to equate total movement but permit sustained rest periods in TC animals. To label proliferating cells the thymidine analogue 5-bromo-2′-deoxyuridine (BrdU) was injected after the first 48 h of the experimental procedure in all groups (50 mg kg−1, i.p.). The percentage of time awake per day was 93.2 % in the SD group vs. 59.6 % in the TC group and 49.9 % in the CC group (P < 0.001). Stereological analysis showed that the number of BrdU-positive cells in the DG of the dorsal hippocampus was reduced by 54 % in the SD group in comparison with the TC and by 68 % in comparison with the CC group. These results suggest that sleep deprivation reduces proliferation of cells in the DG of the dorsal hippocampus. PMID:12679377

  16. 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

  17. 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

  18. 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.

  19. Sleep apnoea.

    PubMed

    Jun, Jonathan C; Chopra, Swati; Schwartz, Alan R

    2016-03-01

    Sleep apnoea is a disorder characterised by repetitive pauses in breathing during sleep caused by airway occlusion (obstructive sleep apnoea) or altered control of breathing (central sleep apnoea). In this Clinical Year in Review, we summarise high-impact research from the past year pertaining to management, diagnosis and cardio-metabolic consequences of sleep apnoea.

  20. 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

  1. Methylphenidate and Pemoline: Effects on Sleepiness and Mood during Sleep Deprivation

    DTIC Science & Technology

    1991-03-04

    characteristics of these effects. However, pemoline differs from both the amphetamines and methylphenidate in that it is not addictive, not a drug of abuse . As...AD-A234 659 METHYLPHENIDATE AND PEMOLINE: EFFECTS ON SLEEPINESS AND MOOD DURING SLEEP DEPRIVATION L.T. MATTESON DTIC T.L. KELLY ELECTE H. BABKOFF MAY...CALIFORNIA 92186-5122 NAVAL MEDICAL RESEARCH AND DEVELOPMENT COMMAND BETHESDA, MARYLAND 91 5 01 022 METHYLPHENIDATE AND PENOLINE: EFFECTS ON

  2. Innate immunity modulation in the duodenal mucosa induced by REM sleep deprivation during infection with Trichinella spirallis

    PubMed Central

    Ibarra-Coronado, Elizabeth G.; Pérez-Torres, Armando; Pantaleón-Martínez, Ana M.; Velazquéz-Moctezuma, Javier; Rodriguez-Mata, Veronica; Morales-Montor, Jorge

    2017-01-01

    Sleep is considered to be an important predictor of the immunity, since the absence of sleep can affect the development of the immune response, and consequently increase the susceptibility to contract an infection. The aim of the present study was to investigate if sleep deprivation and stress induce dysregulation of the duodenal mucous membrane during the acute infection with Trichinella spiralis. Our results shows that, in the intestinal mucous membrane, stress and sleep deprivation, produces different effect in the cells, and this effect depends on the studied duodenal compartment, glands or villi. The sleep deprivation affect mast cells mainly, and the stress response is more heterogeneous. Interestingly, in the duodenal mucous membrane, none population of cells in the infected groups responded equally to both conditions. These findings suggest that the response of the intestinal mucous membrane during the infection caused for T. spiralis turns out to be affected in the sleep-deprived rats, therefore, the results of the present study sustain the theory that sleep is a fundamental process that is capable of modulating the immune response of mucous membranes, particularly the one generated against the parasite Trichinella spiralis. PMID:28374797

  3. Innate immunity modulation in the duodenal mucosa induced by REM sleep deprivation during infection with Trichinella spirallis.

    PubMed

    Ibarra-Coronado, Elizabeth G; Pérez-Torres, Armando; Pantaleón-Martínez, Ana M; Velazquéz-Moctezuma, Javier; Rodriguez-Mata, Veronica; Morales-Montor, Jorge

    2017-04-04

    Sleep is considered to be an important predictor of the immunity, since the absence of sleep can affect the development of the immune response, and consequently increase the susceptibility to contract an infection. The aim of the present study was to investigate if sleep deprivation and stress induce dysregulation of the duodenal mucous membrane during the acute infection with Trichinella spiralis. Our results shows that, in the intestinal mucous membrane, stress and sleep deprivation, produces different effect in the cells, and this effect depends on the studied duodenal compartment, glands or villi. The sleep deprivation affect mast cells mainly, and the stress response is more heterogeneous. Interestingly, in the duodenal mucous membrane, none population of cells in the infected groups responded equally to both conditions. These findings suggest that the response of the intestinal mucous membrane during the infection caused for T. spiralis turns out to be affected in the sleep-deprived rats, therefore, the results of the present study sustain the theory that sleep is a fundamental process that is capable of modulating the immune response of mucous membranes, particularly the one generated against the parasite Trichinella spiralis.

  4. 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

    2013-09-05

    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.

  5. 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

  6. 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

  7. Module number of default mode network: inter-subject variability and effects of sleep deprivation.

    PubMed

    Wang, Yulin; Liu, Huan; Hitchman, Glenn; Lei, Xu

    2015-01-30

    Sleep deprivation have shown its great influence on the default mode network (DMN). The DMN is a core system in resting state brain activity. Recent studies have focused on its subsystems and multiple functions. However, the individual specific organization of the DMN is rarely investigated. As the effects of sleep deprivation (SD) on mood are well documented, a more interesting question is whether changes in the processing of emotional information due to sleep deprivation are related to any specific topological properties of the DMN. In this study, we proposed an index, module number of DMN (mnDMN), to measure the specific modular structure of the DMN for each individual. Our results showed that the DMN was generally split into two modules after SD, and the decreased functional connectivity between the two modules was related to a worsening of the participants׳ self-reported emotional state. Furthermore, the mnDMN was correlated with participants' rating scores of high valence pictures in the SD session, indicating that the mnDMN might reflect mood valuation in the human brain. Overall, our research reveals the diversity of the DMN, and may contribute towards a better understanding of the properties and functions of the DMN.

  8. 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

  9. 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

  10. Effects of sleep deprivation on Color-Word, Emotional, and Specific Stroop interference and on self-reported anxiety.

    PubMed

    Sagaspe, Patricia; Sanchez-Ortuno, Montserrat; Charles, André; Taillard, Jacques; Valtat, Cédric; Bioulac, Bernard; Philip, Pierre

    2006-02-01

    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. Twelve healthy young subjects were tested at four-hourly intervals through a 36-h period of wakefulness under a constant routine protocol. Analyses of variance for repeated measurements revealed that self-assessment of sleepiness on a visual analogue scale as well as mean reaction time performance on the sustained attention task, both for the first minute and for 10 min of testing, were worsened by sleep deprivation. Analyses revealed an increase in self-reported anxiety scores on the STAI questionnaire but did not reveal any significant effect after sleep deprivation either on indexes of interference or on accuracy in Stroop tasks. However, analyses showed sensitivity to circadian effect on verbal reaction times in the threat-related (Emotional) and sleep-related (Specific) Stroop tasks. We concluded that 36 h of prolonged wakefulness affect self-reported anxiety and Emotional Stroop task resulting in a cognitive slowing. Moreover, total sleep deprivation does not affect interference control in any of the three short Stroop tasks.

  11. 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.

  12. Effects Of Moderate Sleep Deprivation and Low-Dose Alcohol On Driving Simulator Performance and Perception In Young Men

    PubMed Central

    Vakulin, A.; Baulk, S.D.; Catcheside, P.G.; Anderson, R.; van den Heuvel, C.J.; Banks, S.; McEvoy, R.D.

    2007-01-01

    Study Objectives: To determine the combined effects of sleep restriction and low-dose alcohol on driving simulator performance, EEG, and subjective levels of sleepiness and performance in the mid-afternoon. Design: Repeated measures with 4 experimental conditions. Normal sleep without alcohol, sleep restriction alone (4 hours) and sleep restriction in combination with 2 different low blood alcohol concentrations (0.025 g/dL and 0.035 g/dL). Setting: Sleep Laboratory, Adelaide Institute for Sleep Health. Participants: Twenty-one healthy young men, aged 18–30 years, mean (±SD) = 22.5(±3.7) years, BMI = 25(±6.7) kg/m2; all had normal sleep patterns and were free of sleep disorders. Measurements: Participants completed a 70-minute simulated driving session, commencing at 14:00. Driving parameters included steering deviation, braking reaction time, and number of collisions. Alpha and theta EEG activity and subjective driving performance and sleepiness were also measured throughout the driving task. Results: All measures were significantly affected by time. Steering deviation increased significantly when sleep restriction was combined with the higher dose alcohol. This combination also resulted in a significant increase in alpha/theta EEG activity throughout the drive, as well as greater subjective sleepiness and negative driving performance ratings compared to control or sleep restriction alone. Discussion: These data indicate that combining low-dose alcohol with moderate sleep restriction results in significant decrements to subjective alertness and performance as well as to some driving performance and EEG parameters. This highlights the potential risks of driving after consumption of low and legal doses of alcohol when also sleep restricted. Citation: Vakulin A; Baulk SD; Catcheside PG; Anderson R; van den Heuvel CJ; Banks S; McEvoy RD. Effects of moderate sleep deprivation and low-dose alcohol on driving simulator performance and perception in young men. SLEEP

  13. Leucine supplementation is anti-atrophic during paradoxical sleep deprivation in rats.

    PubMed

    de Sá Souza, Helton; Antunes, Hanna Karen Moreira; Dáttilo, Murilo; Lee, Kil Sun; Mônico-Neto, Marcos; de Campos Giampa, Sara Quaglia; Phillips, Stuart M; Tufik, Sergio; de Mello, Marco Túlio

    2016-04-01

    The purpose of this study was to identify sleep deprivation-induced atrophy and the muscle-specific fiber types affected and to determine the effects of leucine supplementation on atrophy and pertinent portions of the pathways of muscle protein synthesis and degradation in rats. A total of 46 Wistar rats were distributed in four groups: control (CTL), leucine supplementation (LEU), sleep deprivation (SD), and leucine supplementation + sleep deprivation (LEU + SD). Leucine supplementation was by gavage (1.35 g/kg/daily), and the animals were subjected to SD for 96 h. Testosterone and corticosterone concentrations, along with proteins involved in protein synthesis and degradation and proteasome activity levels, were measured in the gastrocnemius (GA) muscle. Myosin ATPase staining was used to evaluate the different muscle fibers. After sleep deprivation, GA muscle and body masses decreased in the SD group compared to the CTL, LEU, and LEU + SD groups. There was no difference between groups in type I fiber cross-sectional area (CSA). The CSAs for type IIa fibers were lower in the SD and LEU + SD groups vs. the CTL and LEU groups, while the IIb fiber CSA was lower in the SD group vs. the CSAs in all other groups. The phospho (p)-Akt levels were lower in the SD and LEU + SD groups vs. the CTL and LEU groups. The p-mTORC1 levels were higher in the LEU, SD, and LEU + SD groups vs. the CTL group. The p-p70S6k levels were higher in the LEU and LEU + SD groups; the 4E-BP1 levels were higher in the SD and LEU + SD groups compared to those in the CTL and LEU groups, and the p-4E-BP1 levels were higher in the LEU and SD groups compared to those in the CTL group and even higher in the LEU + SD group compared to those in the LEU and SD groups. Ubiquitinated proteins, LC3, and p62/SQSTM, and proteasome activity levels were higher in the SD and LEU + SD groups vs. the LEU and CTL groups. Sleep deprivation led to the atrophy of IIa and IIb muscle fibers; however, leucine

  14. The effect of venlafaxine on behaviour, body weight and striatal monoamine levels on sleep-deprived female rats.

    PubMed

    de Oliveira, Ricardo A; Cunha, Geanne M A; Borges, Karla Daisy M; de Bruin, Gabriela S; dos Santos-Filho, Emídio A; Viana, Glauce S B; de Bruin, Veralice M S

    2004-11-01

    Partial sleep deprivation is clinically associated with fatigue, depressive symptoms and reduced memory. Previously, it has been demonstrated that venlafaxine, an atypical antidepressant, increases the levels of noradrenaline and serotonin in rat hippocampus. The aim of this study was to evaluate the effects of venlafaxine on depression, anxiety, locomotor activity and memory in a model of REM sleep (REMs) deprivation in rats. We have also studied the influence of venlafaxine on monoamine levels in the striatum. Six groups of animals (N=20 each) were treated with saline or venlafaxine (1 or 10 mg/kg) during 10 days, submitted or not to REMs deprivation and studied with the forced swimming test of Porsolt (STP), plus-maze, passive avoidance and open-field tests right after sleep deprivation. Animals were also studied for passive avoidance 24 h later (rebound period). Brain samples for monoamine measurements were collected either immediately after REMs deprivation or after 24 h. Both REMs deprivation and venlafaxine showed an antidepressant effect. An anxiolytic effect was also observed after REMs deprivation. Previous treatment with venlafaxine blocked the antidepressant and anxiolytic effects of REMs deprivation. REMs deprivation alone and treatment with venlafaxine 10 mg/kg increased locomotor activity, and this effect was inhibited by venlafaxine in REMs deprived rats. Both venlafaxine treatment and REMs deprivation induced weight loss. Venlafaxine treatment, but not REMs deprivation, induced an increase in striatal dopamine (DA) levels. The combination of REMs deprivation and venlafaxine treatment was associated with an increase in serotonin turnover 24 h after rebound sleep. In this study, venlafaxine treatment hindered most behavioral effects of REMs deprivation and was associated with an interference on dopamine and serotonin systems in the striatum.

  15. 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

  16. Nitric oxide modulates the hyperalgesic response to mechanical noxious stimuli in sleep-deprived rats

    PubMed Central

    2013-01-01

    Background Sleep restriction alters pain perception in animals and humans, and many studies have indicated that paradoxical sleep deprivation (PSD) promotes hyperalgesia. The hyperalgesia observed after mechanical nociceptive stimulus is reversed through nitric oxide synthase (NOS) inhibition. Both nitric oxide (NO) and the dorsolateral periaqueductal gray matter (dlPAG) area of the brainstem are involved in hyperalgesia. Thus, in this work, we investigated the pain-related behavior response after mechanical noxious stimuli (electronic von Frey test), and the activity of nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), an indicator of NOS activity, within the dlPAG of paradoxical sleep-deprived rats. We also evaluated the effects of pre-treatment with L-NAME on these parameters. Results These data revealed that PSD reduced the hindpaw withdrawal threshold (−47%, p < 0.0001) confirming the hyperalgesic effect of this condition. In addition, there were more NADPH-d positive cells in dlPAG after PSD than in control rats (+ 59%, p < 0.0001). L-NAME treatment prevented the reduction in the hindpaw withdrawal threshold (+ 93%, p < 0.0001) and the increase in the NADPH-d positive cells number in the dlPAG of PSD-treated rats (−36%, p < 0.0001). Conclusion These data suggest that the hyperalgesic response to mechanical noxious stimuli in paradoxical sleep-deprived rats is associated with increased NOS activity in the dlPAG, which presumably influences the descending antinociceptive pathway. PMID:23987566

  17. Cholinergic Oculomotor Nucleus Activity Is Induced by REM Sleep Deprivation Negatively Impacting on Cognition.

    PubMed

    Santos, Patrícia Dos; Targa, Adriano D S; Noseda, Ana Carolina D; Rodrigues, Lais S; Fagotti, Juliane; Lima, Marcelo M S

    2016-09-22

    Several efforts have been made to understand the involvement of rapid eye movement (REM) sleep for cognitive processes. Consolidation or retention of recognition memories is severely disrupted by REM sleep deprivation (REMSD). In this regard, pedunculopontine tegmental nucleus (PPT) and other brainstem nuclei, such as pontine nucleus (Pn) and oculomotor nucleus (OCM), appear to be candidates to take part in this REM sleep circuitry with potential involvement in cognition. Therefore, the objective of this study was to investigate a possible association between the performance of Wistar rats in a declarative memory and PPT, Pn, and OCM activities after different periods of REMSD. We examined c-Fos and choline acetyltransferase (ChaT) expressions as indicators of neuronal activity as well as a familiarity-based memory test. The animals were distributed in groups: control, REMSD, and sleep rebound (REB). At the end of the different REMSD (24, 48, 72, and 96 h) and REB (24 h) time points, the rats were immediately tested in the object recognition test and then the brains were collected. Results indicated that OCM neurons presented an increased activity, due to ChaT-labeling associated with REMSD that negatively correlated (r = -0.32) with the cognitive performance. This suggests the existence of a cholinergic compensatory mechanism within the OCM during REMSD. We also showed that 24 h of REMSD impacted similarly in memory, compared to longer periods of REMSD. These data extend the notion that REM sleep is influenced by areas other than PPT, i.e., Pn and OCM, which could be key players in both sleep processes and cognition.

  18. 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.

  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. Hypothalamic L-Histidine Decarboxylase Is Up-Regulated During Chronic REM Sleep Deprivation of Rats

    PubMed Central

    Hoffman, Gloria E.; Koban, Michael

    2016-01-01

    A competition of neurobehavioral drives of sleep and wakefulness occurs during sleep deprivation. When enforced chronically, subjects must remain awake. This study examines histaminergic neurons of the tuberomammillary nucleus of the posterior hypothalamus in response to enforced wakefulness in rats. We tested the hypothesis that the rate-limiting enzyme for histamine biosynthesis, L-histidine decarboxylase (HDC), would be up-regulated during chronic rapid eye movement sleep deprivation (REM-SD) because histamine plays a major role in maintaining wakefulness. Archived brain tissues of male Sprague Dawley rats from a previous study were used. Rats had been subjected to REM-SD by the flowerpot paradigm for 5, 10, or 15 days. For immunocytochemistry, rats were transcardially perfused with acrolein-paraformaldehyde for immunodetection of L-HDC; separate controls used carbodiimide-paraformaldehyde for immunodetection of histamine. Immunolocalization of histamine within the tuberomammillary nucleus was validated using carbodiimide. Because HDC antiserum has cross-reactivity with other decarboxylases at high antibody concentrations, titrations localized L-HDC to only tuberomammillary nucleus at a dilution of ≥ 1:300,000. REM-SD increased immunoreactive HDC by day 5 and it remained elevated in both dorsal and ventral aspects of the tuberomammillary complex. Our results suggest that up-regulation of L-HDC within the tuberomammillary complex during chronic REM-SD may be responsible for maintaining wakefulness. PMID:27997552

  1. Hypothalamic L-Histidine Decarboxylase Is Up-Regulated During Chronic REM Sleep Deprivation of Rats.

    PubMed

    Hoffman, Gloria E; Koban, Michael

    2016-01-01

    A competition of neurobehavioral drives of sleep and wakefulness occurs during sleep deprivation. When enforced chronically, subjects must remain awake. This study examines histaminergic neurons of the tuberomammillary nucleus of the posterior hypothalamus in response to enforced wakefulness in rats. We tested the hypothesis that the rate-limiting enzyme for histamine biosynthesis, L-histidine decarboxylase (HDC), would be up-regulated during chronic rapid eye movement sleep deprivation (REM-SD) because histamine plays a major role in maintaining wakefulness. Archived brain tissues of male Sprague Dawley rats from a previous study were used. Rats had been subjected to REM-SD by the flowerpot paradigm for 5, 10, or 15 days. For immunocytochemistry, rats were transcardially perfused with acrolein-paraformaldehyde for immunodetection of L-HDC; separate controls used carbodiimide-paraformaldehyde for immunodetection of histamine. Immunolocalization of histamine within the tuberomammillary nucleus was validated using carbodiimide. Because HDC antiserum has cross-reactivity with other decarboxylases at high antibody concentrations, titrations localized L-HDC to only tuberomammillary nucleus at a dilution of ≥ 1:300,000. REM-SD increased immunoreactive HDC by day 5 and it remained elevated in both dorsal and ventral aspects of the tuberomammillary complex. Our results suggest that up-regulation of L-HDC within the tuberomammillary complex during chronic REM-SD may be responsible for maintaining wakefulness.

  2. 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…

  3. The Neuroprotective Aspects of Sleep.

    PubMed

    Eugene, Andy R; Masiak, Jolanta

    2015-03-01

    Sleep is an important component of human life, yet many people do not understand the relationship between the brain and the process of sleeping. Sleep has been proven to improve memory recall, regulate metabolism, and reduce mental fatigue. A minimum of 7 hours of daily sleep seems to be necessary for proper cognitive and behavioral function. The emotional and mental handicaps associated with chronic sleep loss as well as the highly hazardous situations which can be contributed to the lack of sleep is a serious concern that people need to be aware of. When one sleeps, the brain reorganizes and recharges itself, and removes toxic waste byproducts which have accumulated throughout the day. This evidence demonstrates that sleeping can clear the brain and help maintain its normal functioning. Multiple studies have been done to determine the effects of total sleep deprivation; more recently some have been conducted to show the effects of sleep restriction, which is a much more common occurrence, have the same effects as total sleep deprivation. Each phase of the sleep cycle restores and rejuvenates the brain for optimal function. When sleep is deprived, the active process of the glymphatic system does not have time to perform that function, so toxins can build up, and the effects will become apparent in cognitive abilities, behavior, and judgment. As a background for this paper we have reviewed literature and research of sleep phases, effects of sleep deprivation, and the glymphatic system of the brain and its restorative effect during the sleep cycle.

  4. 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

  5. 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

  6. Twenty-four hours, or five days, of continuous sleep deprivation or experimental sleep fragmentation do not alter thirst or motivation for water reward in rats.

    PubMed

    Christie, Michael A; McCarley, Robert W; Strecker, Robert E

    2010-12-25

    Sleep disruption results in an increased demand for energy, which typically causes hyperphagia in an attempt to redress the energy metabolism imbalance. Therefore, experiments combining food reward and sleep disruption may underestimate the effect of sleep disruption due to their contradictory influences on behavior (for example on operant measures of attention). In contrast, water is not a central component of energy metabolism and thus thirst may not be affected by sleep disruption. However, little work has been done examining the effect of sleep disruption on thirst and motivation for water. The effect of total sleep deprivation (SD) and experimental sleep fragmentation (SF) on thirst and motivation for water was assessed. In experiment 1 (using 22 month old male Fisher-Norway rats) the amount of water consumed during a 15 min period immediately following a period of 24h SD or SF (in which water was not available) was measured, and, in a separate session, the amount of water consumed during the 24h of SD or SF was measured. Thereafter, the effect of 5 days SD or SF on motivation for water was assessed with the progressive ratio task (using water reward), which is widely used to assess motivation. Experiment 2 (using 6 month, and 22 month, old male Sprague- Dawley rats) followed an identical design except that the SF condition was dropped (due to a lack of any difference between the SD and SF conditions in experiment 1), and only the 6 month old rats experienced the full 5 day SD condition. Daily measurements of body weight and food consumption were recorded in experiment 2 in order to confirm previously published findings that food consumption goes up and body weight declines in sleep deprived rats. In both experiments the quantity of water rats consumed during a 15 min period immediately following the 24h period of sleep disruption, or consumed during the 24h period of SD or SF, did not change compared to control rats. Furthermore, 5 days of SD or SF had no

  7. Sleep deprivation impairs spontaneous object-place but not novel-object recognition in rats.

    PubMed

    Ishikawa, Hiroko; Yamada, Kazuo; Pavlides, Constantine; Ichitani, Yukio

    2014-09-19

    Effects of sleep deprivation (SD) on one-trial recognition memory were investigated in rats using either a spontaneous novel-object or object-place recognition test. Rats were allowed to explore a field in which two identical objects were presented. After a delay period, they were placed again in the same field in which either: (1) one of the two objects was replaced by another object (novel-object recognition); or (2) one of the sample objects was moved to a different place (object-place recognition), and their exploration behavior to these objects was analyzed. Four hours SD immediately after the sample phase (early SD group) disrupted object-place recognition but not novel-object recognition, while SD 4-8h after the sample phase (delayed SD group) did not affect either paradigm. The results suggest that sleep selectively promotes the consolidation of hippocampal dependent memory, and that this effect is limited to within 4h after learning.

  8. Effect of paradoxical sleep deprivation and stress on passive avoidance behavior.

    PubMed

    Wang, Jian Hong; van den Buuse, Maarten; Tian, Shao Wen; Ma, Yuan Ye

    2003-09-01

    Previous studies have shown that several types of stress can induce memory impairment. However, the memory effects of paradoxical sleep deprivation (PSD), a stressor in itself, are unclear. We therefore compared passive avoidance behavior of rats undergoing PSD and PSD stress yoked-control (PSC) using the "reversed flowerpot method." When rats were kept isolated on a PSC platform for 24 h immediately after criterion training, retention trials showed impaired aversive memory storage. When delayed for 24 h after criterion training, PSC stress did not disrupt retention performance. In rats subjected to PSD, either immediately or 24 h after criterion training, there was no disruption of aversive memory consolidation. These results suggest that, during stress, paradoxical sleep plays a role in erasing aversive memory traces, in line with the theory that we "dream in order to forget."

  9. The trait of Introversion-Extraversion predicts vulnerability to sleep deprivation.

    PubMed

    Killgore, William D S; Richards, Jessica M; Killgore, Desiree B; Kamimori, Gary H; Balkin, Thomas J

    2007-12-01

    According to Eysenck's theory of Introversion-Extroversion (I-E), introverts demonstrate higher levels of basal activity within the reticular-thalamic-cortical loop, yielding higher tonic cortical arousal than Extraverts, who are described conversely as chronically under-aroused and easily bored. We hypothesized that higher scores on the trait of Extraversion would be associated with greater declines in psychomotor vigilance performance during prolonged wakefulness. We evaluated the relationship between I-E and overnight psychomotor vigilance performance during 77 h of continuous sleep deprivation in a sample of 23 healthy adult military personnel (19 men; four women), ranging in age from 20 to 35 years. At baseline, volunteers completed the Revised NEO Personality Inventory (NEO PI-R) and completed psychomotor vigilance testing at approximately 10-min intervals from 00:15 to 08:50 hours over three nights of continuous sleep deprivation. In addition, 12 participants received four repeated administrations of caffeine (200 mg) every 2 h each night. Analysis of covariance and stepwise multiple regression analyses showed that, above and beyond the effects of caffeine, higher Extraversion was significantly related to more extensive declines in speed of responding and more frequent attentional lapses, but only for the first overnight testing session. Sub-factors of Extraversion, including Gregariousness and higher Activity level were most predictive of these changes following sleep loss. These findings are consistent with Eysenck's cortico-reticular activation theory of I-E and suggest that individual differences in the trait of Extraversion confer some vulnerability/resistance to the adverse effects of sleep loss on attention and vigilance.

  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. Inhibition of hippocampal neurogenesis by sleep deprivation is independent of circadian disruption and melatonin suppression.

    PubMed

    Mueller, A D; Mear, R J; Mistlberger, R E

    2011-10-13

    Procedures that restrict or fragment sleep can inhibit neurogenesis in the hippocampus of adult rodents, although the underlying mechanism is unknown. We showed that rapid-eye-movement (REM) sleep deprivation (RSD) by the platform-over-water method inhibits hippocampal cell proliferation in adrenalectomized rats with low-dose corticosterone clamp. This procedure also greatly disrupts daily behavioral rhythms. Given recent evidence for circadian clock regulation of cell proliferation, we asked whether disruption of circadian rhythms might play a role in the anti-neurogenic effects of sleep loss. Male Sprague-Dawley rats were subjected to a 4-day RSD procedure or were exposed to constant bright light (LL) for 4 days or 10 weeks, a non-invasive procedure for eliminating circadian rhythms of behavior and physiology in this species. Proliferating cells in the granule cell layer of the dentate gyrus were identified by immunolabeling for the thymidine analogue 5-bromo-2-deoxyuridine. Consistent with our previous results, the RSD procedure suppressed cell proliferation by ∼50%. By contrast, although LL attenuated or eliminated daily rhythms of activity and sleep-wake without affecting daily amounts of REM sleep, cell proliferation was not affected. Melatonin, a nocturnally secreted neurohormone that is inhibited by light, has been shown to promote survival of new neurons. We found that 3-weeks of LL eliminated daily rhythms and decreased plasma melatonin by 88% but did not significantly affect either total cell survival or survival of new neurons (doublecortin+). Finally, we measured cell proliferation rates at the beginning and near the end of the daily light period in rats entrained to a 12:12 light/lark (LD) cycle, but did not detect a daily rhythm. These results indicate that the antineurogenic effect of RSD is not secondary to disruption of circadian rhythms, and provide no evidence that hippocampal cell proliferation and survival are regulated by the circadian

  12. Sleep in postmenopausal women.

    PubMed

    Vigeta, Sônia Maria Garcia; Hachul, Helena; Tufik, Sergio; de Oliveira, Eleonora Menicucci

    2012-04-01

    The aim of this study was to identify factors that most influence the perception of sleep quality in postmenopausal women. We used the methodological strategy of the Collective Subject Discourse (CSD), which is based on a theoretical framework of social representations theory. We obtained the data by interviewing 22 postmenopausal Brazilian women who were experiencing insomnia. The women gave accounts of their difficulties with sleep; a variety of dimensions were identified within the data. The onset of sleep disorders might have occurred during childhood or in situations considered to be stressful, and were not necessarily associated with menopause. We found that hormonal alterations occurring during menopause, psychosocial factors, and sleep-breathing disorders triggered occasional sleep disturbances during this time of life. Participants were aware of the consequences of sleep deprivation. In addition, inadequate sleep hygiene habits figured prominently as determinants in the persistence of sleep disturbances.

  13. Sleep deprivation in the dark period does not impair memory in OF1 mice.

    PubMed

    Palchykova, Svitlana; Winsky-Sommerer, Raphaëlle; Tobler, Irene

    2009-05-01

    There is increasing evidence that sleep facilitates memory acquisition and consolidation. Moreover, the sleep-wake history preceding memory acquisition and retention as well as circadian timing may be important. We showed previously that sleep deprivation (SD) following learning in OF1 mice impaired their performance on an object recognition task. The learning task was scheduled at the end of the 12 h dark period and the test 24 h later. To investigate the influence of the prominent circadian sleep-wake distribution typical for rodents, we now scheduled the learning task at the beginning of the dark period. Wakefulness following immediately after the learning task was attained either by gentle interference (SD; n = 20) or by spontaneous wheel running (RW; n = 20). Two control groups were used: one had no RW throughout the experiment (n = 23), while the other group's wheel was blocked immediately after acquisition (n = 16), thereby preventing its use until testing. Recognition memory, defined as the difference in exploration of a novel and of familiar objects, was assessed 24 h later during the test phase. Motor activity and RW use were continuously recorded. Remarkably, performance on the object recognition task was not influenced by the protocols; the waking period following acquisition did not impair memory, independent of the method inducing wakefulness (i.e., sleep deprivation or spontaneous running). Thus, all groups explored the novel object significantly longer than the familiar ones during the test phase. Interestingly, neither the amount of rest lost during the SD interventions nor the amount of rest preceding acquisition influenced performance. However, the total amount of rest obtained by the control and SD mice subjected to acquisition at "dark offset" correlated positively (r = 0.66) with memory at test, while no such relationship occurred in the corresponding groups tested at dark onset. Neither the amount of running nor intermediate rest correlated

  14. 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

  15. Sleep deprivation has a neuroprotective role in a traumatic brain injury of the rat.

    PubMed

    Martinez-Vargas, Marina; Estrada Rojo, Francisco; Tabla-Ramon, Erika; Navarro-Argüelles, Hilda; Ortiz-Lailzon, Nathan; Hernández-Chávez, Alejandro; Solis, Barbara; Martínez Tapia, Ricardo; Perez Arredondo, Adan; Morales-Gomez, Julio; Gonzalez-Rivera, Ruben; Nava-Talavera, Karen; Navarro, Luz

    2012-11-07

    During the process of a brain injury, responses to produce damage and cell death are activated, but self-protective responses that attempt to maintain the integrity and functionality of the brain are also activated. We have previously reported that the recovery from a traumatic brain injury (TBI) is better in rats if it occurs during the dark phase of the diurnal cycle when rats are in the waking period. This suggests that wakefulness causes a neuroprotective role in this type of injury. Here we report that 24h of total sleep deprivation after a TBI reduces the morphological damage and enhances the recovery of the rats, as seen on a neurobiological scale.

  16. [Effect of sleep deprivation on visual evoked potentials and brain stem auditory evoked potentials in epileptics].

    PubMed

    Urumova, L T; Kovalenko, G A; Tsunikov, A I; Sumskiĭ, L I

    1984-01-01

    The article reports on the first study of the evoked activity of the brain in epileptic patients (n = 20) following sleep deprivation. An analysis of the data obtained has revealed a tendency to the shortening of the peak latent intervals of visual evoked potentials in the range of 100-200 mu sec and the V component and the interpeak interval III-V of evoked auditory trunk potentials in patients with temporal epilepsy. The phenomenon may indicate the elimination of stabilizing control involving the specific conductive pathways and, possibly, an accelerated conduction of a specific sensor signal.

  17. 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).

  18. 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

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

    PubMed

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

    2016-04-14

    Sleep deprivation (SD) has adverse effects on mental and physical health, affecting the cognitive abilities and emotional states. Specifically, cognitive functions and alertness are known to decrease after SD. The aim of this work was to identify the directional information transfer after SD on scalp EEG signals using transfer entropy (TE). Using a robust methodology based on EEG recordings of 18 volunteers deprived from sleep for 36 h, TE and spectral analysis were performed to characterize EEG data acquired every 2 h. Correlation between connectivity measures and subjective somnolence was assessed. In general, TE showed medium- and long-range significant decreases originated at the occipital areas and directed towards different regions, which could be interpreted as the transfer of predictive information from parieto-occipital activity to the rest of the head. Simultaneously, short-range increases were obtained for the frontal areas, following a consistent and robust time course with significant maps after 20 h of sleep deprivation. Changes during sleep deprivation in brain network were measured effectively by TE, which showed increased local connectivity and diminished global integration. TE is an objective measure that could be used as a potential measure of sleep pressure and somnolence with the additional property of directed relationships.

  20. Food restriction or sleep deprivation: which exerts a greater influence on the sexual behaviour of male rats?

    PubMed

    Alvarenga, Tathiana A; Andersen, Monica L; Velázquez-Moctezuma, Javier; Tufik, Sergio

    2009-09-14

    The purpose of this study was to determine the effects of food restriction (FR) and paradoxical sleep deprivation (PSD), either alone or in combination, on sexual behaviours (mount, intromission and ejaculation) in adult male rats. Diet restriction began at weaning with 6g/day of food, and the amount of food was increased by 1g/week until it reached 15g/day amount (in adulthood). During adulthood, rats under FR and those fed ad libitum were either subjected to PSD for 96h or maintained in home-cage groups. The results indicated that both FR and ad libitum sleep-deprived groups showed a significant decrease in performance and motivation to initiate sexual behaviour, reflected by the increase in mount and intromission latencies and decreased copulatory rate. FR associated with PSD reversed the adverse effects of sleep deprivation on the number of ejaculations and inter-copulatory interval. Testosterone concentrations decreased after sleep deprivation, regardless of food availability; while progesterone was significantly higher in the FR-PSD group only. In light of the limited understanding of the link between secretion patterns and neural-hormonal control of food availability related to sexual behaviour, our data indicate that sleep loss affects sexual responses, and FR was able to restore some of the sexual parameters investigated.

  1. 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

  2. Effects of methylphenidate on the impairment of spontaneous alternation behavior in mice intermittently deprived of REM sleep.

    PubMed

    Niijima-Yaoita, Fukie; Nagasawa, Yuka; Tsuchiya, Masahiro; Arai, Yuichiro; Tadano, Takeshi; Tan-No, Koichi

    2016-11-01

    Attention deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by inattention, hyperactivity, and impulsivity. We have previously shown that abnormal behaviors elicited by intermittent rapid eye movement (REM) sleep deprivation stress may fulfill the profile of a model of ADHD. It is well known that the impairment of spontaneous alternation behavior (SAB) in the Y-maze indicates inattentive features of ADHD model animals. On the other hand, it has been reported that nitric oxide (NO) in the hippocampus is required for SAB. In this study, using mice, we investigated whether intermittent REM sleep deprivation stress causes changes in SAB and the expression of NO synthase (NOS) mRNA and in the levels of NO metabolites in the hippocampus. Mice were deprived of REM sleep intermittently by the small-platform method (20 h/day) for 3 days. The SAB, the level of nitrite and expression of endothelial NOS (eNOS) and inducible NOS (iNOS) mRNA in the hippocampus, but not neuronal NOS (nNOS), were significantly decreased by intermittent REM sleep deprivation stress. The decreased levels of SAB, nitrite and iNOS mRNA were significantly increased by methylphenidate treatment, which is used clinically to treat ADHD symptoms. Moreover, these improvement effects of methylphenidate on SAB and the nitrite level were decreased by the administration of selective iNOS and eNOS inhibitors. However, the eNOS inhibitor decreased both nitrate and total NOx levels of the hippocampus in saline treated intermittent REM sleep-deprived mice. These results suggest that the impairment of SAB induced by intermittent REM sleep deprivation stress may serve as a model of the inattention symptom in ADHD. Further, the ameliorating effects of methylphenidate on the impairment of SAB may be mediated through NO production mainly by iNOS in the hippocampus of mice.

  3. 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

  4. Metabolic consequences of sleep and sleep loss.

    PubMed

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

    2008-09-01

    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.

  5. 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

  6. [Fenibut and its citrate prevent psychoneurological disorders caused by chronic stress (paradoxical sleep deprivation)].

    PubMed

    Tiurenkov, I N; Bagmetova, V V; Borodkina, L E; Berestovitskaia, V M; Vasil'eva, O S

    2012-01-01

    The antistress protective action of two structural analogs of GABA, fenibut and its salt with citric acid (fenibut citrate, citrocard, RGPU-147), has been studied using a model of chronic stress caused by seven-fold 24-h deprivation of paradoxical sleep phase at an interval of 24 h between the deprivations. It is established that fenibut and fenibut citrate produce a protective action by (i) reducing the intensity of emotional disorders in the open-field test and elevated plus maze test, (ii) decreasing cognitive disorders in the tests for conditioned avoidance response and extrapolatory deliverance; and (iii) limiting stress reaction due to a decrease in the intensity of adrenal hypertrophy, thymus involution, and stomach mucous membrane ulceration. Fenibut citrate surpasses fenibut in the intensity of antistress protective action.

  7. 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.

  8. 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

    2011-12-02

    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.

  9. 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.

  10. Sleep Deprivation Impairs and Caffeine Enhances My Performance, but Not Always Our Performance.

    PubMed

    Faber, Nadira S; Häusser, Jan A; Kerr, Norbert L

    2017-02-01

    What effects do factors that impair or enhance performance in individuals have when these individuals act in groups? We provide a framework, called the GIE ("Effects of Grouping on Impairments and Enhancements") framework, for investigating this question. As prominent examples for individual-level impairments and enhancements, we discuss sleep deprivation and caffeine. Based on previous research, we derive hypotheses on how they influence performance in groups, specifically process gains and losses in motivation, individual capability, and coordination. We conclude that the effect an impairment or enhancement has on individual-level performance is not necessarily mirrored in group performance: grouping can help or hurt. We provide recommendations on how to estimate empirically the effects individual-level performance impairments and enhancements have in groups. By comparing sleep deprivation to stress and caffeine to pharmacological cognitive enhancement, we illustrate that we cannot readily generalize from group results on one impairment or enhancement to another, even if they have similar effects on individual-level performance.

  11. Sleep Deprivation Impairs and Caffeine Enhances My Performance, but Not Always Our Performance

    PubMed Central

    Faber, Nadira S.; Häusser, Jan A.; Kerr, Norbert L.

    2016-01-01

    What effects do factors that impair or enhance performance in individuals have when these individuals act in groups? We provide a framework, called the GIE ("Effects of Grouping on Impairments and Enhancements”) framework, for investigating this question. As prominent examples for individual-level impairments and enhancements, we discuss sleep deprivation and caffeine. Based on previous research, we derive hypotheses on how they influence performance in groups, specifically process gains and losses in motivation, individual capability, and coordination. We conclude that the effect an impairment or enhancement has on individual-level performance is not necessarily mirrored in group performance: grouping can help or hurt. We provide recommendations on how to estimate empirically the effects individual-level performance impairments and enhancements have in groups. By comparing sleep deprivation to stress and caffeine to pharmacological cognitive enhancement, we illustrate that we cannot readily generalize from group results on one impairment or enhancement to another, even if they have similar effects on individual-level performance. PMID:26468077

  12. Sleep-deprivation regulates α-2 adrenergic responses of rat hypocretin/orexin neurons.

    PubMed

    Uschakov, Aaron; Grivel, Jeremy; Cvetkovic-Lopes, Vesna; Bayer, Laurence; Bernheim, Laurent; Jones, Barbara E; Mühlethaler, Michel; Serafin, Mauro

    2011-02-08

    We recently demonstrated, in rat brain slices, that the usual excitation by noradrenaline (NA) of hypocretin/orexin (hcrt/orx) neurons was changed to an inhibition following sleep deprivation (SD). Here we describe that in control condition (CC), i.e. following 2 hours of natural sleep in the morning, the α(2)-adrenergic receptor (α(2)-AR) agonist, clonidine, had no effect on hcrt/orx neurons, whereas following 2 hours of SD (SDC), it hyperpolarized the neurons by activating G-protein-gated inwardly rectifying potassium (GIRK) channels. Since concentrations of clonidine up to a thousand times (100 µM) higher than those effective in SDC (100 nM), were completely ineffective in CC, a change in the availability of G-proteins is unlikely to explain the difference between the two conditions. To test whether the absence of effect of clonidine in CC could be due to a down-regulation of GIRK channels, we applied baclofen, a GABA(B) agonist known to also activate GIRK channels, and found that it hyperpolarized hcrt/orx neurons in that condition. Moreover, baclofen occluded the response to clonidine in SDC, indicating that absence of effect of clonidine in CC could not be attributed to down-regulation of GIRK channels. We finally tested whether α(2)-ARs were still available at the membrane in CC and found that clonidine could reduce calcium currents, indicating that α(2)-ARs associated with calcium channels remain available in that condition. Taken together, these results suggest that a pool of α(2)-ARs associated with GIRK channels is normally down-regulated (or desensitized) in hcrt/orx neurons to only become available for their inhibition following sleep deprivation.

  13. REM sleep deprivation reverses neurochemical and other depressive-like alterations induced by olfactory bulbectomy.

    PubMed

    Maturana, Maira J; Pudell, Cláudia; Targa, Adriano D S; Rodrigues, Laís S; Noseda, Ana Carolina D; Fortes, Mariana H; Dos Santos, Patrícia; Da Cunha, Cláudio; Zanata, Sílvio M; Ferraz, Anete C; Lima, Marcelo M S

    2015-02-01

    There is compelling evidence that sleep deprivation (SD) is an effective strategy in promoting antidepressant effects in humans, whereas few studies were performed in relevant animal models of depression. Acute administration of antidepressants in humans and rats generates a quite similar effect, i.e., suppression of rapid eye movement (REM) sleep. Then, we decided to investigate the neurochemical alterations generated by a protocol of rapid eye movement sleep deprivation (REMSD) in the notably known animal model of depression induced by the bilateral olfactory bulbectomy (OBX). REMSD triggered antidepressant mechanisms such as the increment of brain-derived neurotrophic factor (BDNF) levels, within the substantia nigra pars compacta (SNpc), which were strongly correlated to the swimming time (r = 0.83; P < 0.0001) and hippocampal serotonin (5-HT) content (r = 0.66; P = 0.004). Moreover, there was a strong correlation between swimming time and hippocampal 5-HT levels (r = 0.70; P = 0.003), strengthen the notion of an antidepressant effect associated to REMSD in the OBX rats. In addition, REMSD robustly attenuated the hippocampal 5-HT deficiency produced by the OBX procedure. Regarding the rebound (REB) period, we observed the occurrence of a sustained antidepressant effect, indicated mainly by the swimming and climbing times which could be explained by the maintenance of the increased nigral BDNF expression. Hence, hippocampal 5-HT levels remained enhanced in the OBX group after this period. We suggested that the neurochemical complexity inflicted by the OBX model, counteracted by REMSD, is directly correlated to the nigral BDNF expression and hippocampal 5-HT levels. The present findings provide new information regarding the antidepressant mechanisms triggered by REMSD.

  14. Sleep deprivation impairs performance in the 5-choice continuous performance test: similarities between humans and mice.

    PubMed

    van Enkhuizen, Jordy; Acheson, Dean; Risbrough, Victoria; Drummond, Sean; Geyer, Mark A; Young, Jared W

    2014-03-15

    Several groups undergo extended periods without sleep due to working conditions or mental illness. Such sleep deprivation (SD) can deleteriously affect attentional processes and disrupt work and family functioning. Understanding the biological underpinnings of SD effects may assist in developing sleep therapies and cognitive enhancers. Utilizing cross-species tests of attentional processing in humans and rodents would aid in mechanistic studies examining SD-induced inattention. We assessed the effects of 36h of: (1) Total SD (TSD) in healthy male and female humans (n=50); and (2) REM SD (RSD) in male C57BL/6 mice (n=26) on performance in the cross-species 5-choice continuous performance test (5C-CPT). The 5C-CPT includes target trials on which subjects were required to respond and non-target trials on which subjects were required to inhibit from responding. TSD-induced effects on human psychomotor vigilance test (PVT) were also examined. Effects of SD were also examined on mice split into good and poor performance groups based on pre-deprivation scores. In the human 5C-CPT, TSD decreased hit rate and vigilance with trend-level effects on accuracy. In the PVT, TSD slowed response times and increased lapses. In the mouse 5C-CPT, RSD reduced accuracy and hit rate with trend-level effects on vigilance, primarily in good performers. In conclusion, SD induced impaired 5C-CPT performance in both humans and mice and validates the 5C-CPT as a cross-species translational task. The 5C-CPT can be used to examine mechanisms underlying SD-induced deficits in vigilance and assist in testing putative cognitive enhancers.

  15. Sleep Talking (Somniloquy)

    MedlinePlus

    ... Overview & Facts Symptoms & Risk Factors Diagnosis & Treatment Sleep Hallucinations Overview & Facts Symptoms & Risk Factors Diagnosis & Treatment Exploding ... Sleep Behavior Disorder Sleep Paralysis Nightmares Bedwetting Sleep Hallucinations Exploding Head Syndrome Sleep Talking Sleep Talking – Overview ...

  16. Nocturnal sustained attention during sleep deprivation can be predicted by specific periods of subjective daytime alertness in normal young humans.

    PubMed

    Taillard, Jacques; Moore, Nicholas; Claustrat, Bruno; Coste, Olivier; Bioulac, Bernard; Philip, Pierre

    2006-03-01

    In our 24-h society, nocturnal sleep-related accidents are common. Because all individuals are not equal in their responses to sleep loss, it is very important to identify predictors of vulnerability to sleep deprivation in normal subjects. We investigated the performance of a cognitive test of sustained attention, electroencephalogram theta/alpha power, subjective sleepiness, and two circadian markers (core temperature and melatonin) in 18 healthy men (nine morning types and nine evening types, 21.4 +/- 1.9 years) during a 36-h sleep deprivation in a constant routine protocol. Sleep need (self-reported) and baseline sleep structure were also investigated. Nighttime performance impairment was defined as the difference between the mean nocturnal number of lapses (00:00-07:30 [corrected] hours) and the mean diurnal number of lapses (07:30-20:30 hours) expressed as a percentage. Feeling fully alert in the morning just after awakening and/or sleepy in early afternoon were the only two factors (Multiple R > 0.80, > 60% of explained variance) which better predicted the decrease in performances of nocturnal operational tasks requiring sustained attention.

  17. Effects of one night of partial sleep deprivation upon diurnal rhythms of accuracy and consistency in throwing darts.

    PubMed

    Edwards, Benjamin J; Waterhouse, Jim

    2009-05-01

    Sixty subjects were tested five times per waking day on two occasions for accuracy and reliability in throwing 20 darts at a target. Two experimental conditions were investigated: following a normal nocturnal sleep (7-8 h sleep, normal) and after having retired to bed 4 h later than normal the previous night but rising at the normal time (3-4 h sleep, sleep deprivation). Sublingual (core) temperature and subjective estimates of alertness and fatigue were measured in all sessions. Performance at throwing darts was assessed by three methods: mean distance of the dart from the bulls-eye; number of times the target was missed; and variability of the scores from the darts thrown. There was no evidence that performance was affected by physical fatigue arising during the course of throwing the 20 darts. All variables showed significant diurnal rhythms, those of alertness and performance being phased over 1 h earlier than core temperature, and that of fatigue over 1 h earlier than the inverse of temperature. Core temperature was not affected by sleep deprivation, but all other variables showed significant changes, indicative of mood and performance decrement. Increasing time awake was associated with decreased alertness and increased fatigue, as well as slight negative effects upon performance. We conclude that the simple task of throwing darts at a target provides information about chronobiological changes in circumstances where time awake and sleep loss might affect psychomotor performance.

  18. Sleep disturbances in Parkinsonism.

    PubMed

    Askenasy, J J M

    2003-02-01

    The present article is meant to suggest an approach to the guidelines for the therapy of sleep disturbances in Parkinson's Disease (PD) patients.The factors affecting the quality of life in PD patients are depression, sleep disturbances and dependence. A large review of the literature on sleep disturbances in PD patients, provided the basis for the following classification of the sleep-arousal disturbances in PD patients. We suggest a model based on 3 steps in the treatment of sleep disturbances in PD patients. This model allowing the patient, the spouse or the caregiver a quiet sleep at night, may postpone the retirement and the institutionalization of the PD patient. I. Correct diagnosis of sleep disorders based on detailed anamnesis of the patient and of the spouse or of the caregiver. One week recording on a symptom diary (log) by the patient or the caregiver. Correct diagnosis of sleep disorders co morbidities. Selection of the most appropriate sleep test among: polysomnography (PSG), multiple sleep latency test (MSLT), multiple wake latency test (MWLT), Epworth Sleepiness Scale, actigraphy or video-PSG. II. The nonspecific therapeutic approach consists in: a) Checking the sleep effect on motor performance, is it beneficial, worse or neutral. b) Psycho-physical assistance. c) Dopaminergic adjustment is necessary owing to the progression of the nigrostriatal degeneration and the increased sensitivity of the terminals, which alter the normal modulator mechanisms of the motor centers in PD patients. Among the many neurotransmitters of the nigro-striatal pathway one can distinguish two with a major influence on REM and NonREM sleep. REM sleep corresponds to an increased cholinergic receptor activity and a decreased dopaminergic activity. This is the reason why REM sleep deprivation by suppressing cholinergic receptor activity ameliorates PD motor symptoms. L-Dopa and its agonists by suppressing cholinergic receptors suppress REM sleep. The permanent adjustment

  19. Sleep deprivation in parents caring for children with complex needs at home: a mixed methods systematic review.

    PubMed

    McCann, Damhnat; Bull, Rosalind; Winzenberg, Tania

    2015-02-01

    A significant number of children with a range of complex conditions and health care needs are being cared for by parents in the home environment. This mixed methods systematic review aimed to determine the amount of sleep obtained by these parents and the extent to which the child-related overnight health or care needs affected parental sleep experience and daily functioning. Summary statistics were not able to be determined due to the heterogeneity of included studies, but the common themes that emerged are that parents of children with complex needs experience sleep deprivation that can be both relentless and draining and affects the parents themselves and their relationships. The degree of sleep deprivation varies by diagnosis, but a key contributing factor is the need for parents to be vigilant at night. Of particular importance to health care professionals is the inadequate overnight support provided to parents of children with complex needs, potentially placing these parents at risk of poorer health outcomes associated with sleep deprivation and disturbance. This needs to be addressed to enable parents to remain well and continue to provide the care that their child and family require.

  20. Paradoxical (REM) sleep deprivation in mice using the small-platforms-over-water method: polysomnographic analyses and melanin-concentrating hormone and hypocretin/orexin neuronal activation before, during and after deprivation.

    PubMed

    Arthaud, Sebastien; Varin, Christophe; Gay, Nadine; Libourel, Paul-Antoine; Chauveau, Frederic; Fort, Patrice; Luppi, Pierre-Herve; Peyron, Christelle

    2015-06-01

    Studying paradoxical sleep homeostasis requires the specific and efficient deprivation of paradoxical sleep and the evaluation of the subsequent recovery period. With this aim, the small-platforms-over-water technique has been used extensively in rats, but only rare studies were conducted in mice, with no sleep data reported during deprivation. Mice are used increasingly with the emergence of transgenic mice and technologies such as optogenetics, raising the need for a reliable method to manipulate paradoxical sleep. To fulfil this need, we refined this deprivation method and analysed vigilance states thoroughly during the entire protocol. We also studied activation of hypocretin/orexin and melanin-concentrating hormone neurones using Fos immunohistochemistry to verify whether mechanisms regulating paradoxical sleep in mice are similar to those in rats. We showed that 48 h of deprivation was highly efficient, with a residual amount of paradoxical sleep of only 2.2%. Slow wave sleep and wake quantities were similar to baseline, except during the first 4 h of deprivation, where slow wave sleep was strongly reduced. After deprivation, we observed a 124% increase in paradoxical sleep quantities during the first hour of rebound. In addition, 34% of hypocretin/orexin neurones were activated during deprivation, whereas melanin-concentrated hormone neurones were activated only during paradoxical sleep rebound. Corticosterone level showed a twofold increase after deprivation and returned to baseline level after 4 h of recovery. In summary, a fairly selective deprivation and a significant rebound of paradoxical sleep can be obtained in mice using the small-platforms-over-water method. As in rats, rebound is accompanied by a selective activation of melanin-concentrating hormone neurones.

  1. A test of the effects of acute sleep deprivation on general and specific self-reported anxiety and depressive symptoms: an experimental extension.

    PubMed

    Babson, Kimberly A; Trainor, Casey D; Feldner, Matthew T; Blumenthal, Heidemarie

    2010-09-01

    Evidence indicates acute sleep deprivation affects negative mood states. The present study experimentally tested the effects of acute sleep deprivation on self-reported symptoms of state anxiety and depression as well as general distress among 88 physically and psychologically healthy adults. As hypothesized, the effects of acute sleep deprivation increased state anxiety and depression, as well as general distress, relative to a normal night of sleep control condition. Based on the tripartite model of anxiety and depression, these findings replicate and extend prior research by suggesting sleep deprivation among individuals without current Axis I disorders increases both state symptoms of anxiety and depression specifically, and general distress more broadly. Extending this work to clinical samples and prospectively testing mechanisms underlying these effects are important future directions in this area of research.

  2. Sleep Disturbances

    MedlinePlus

    ... middle of the night. Sleep in a cool dark place and use the bed only for sleeping ... in Parkinson's Navigating Employment, Insurance, Financial and Legal Matters PD Take Three: Tips from the Health Care ...

  3. Sleep Apnea

    MedlinePlus

    Sleep apnea is a common disorder that causes your breathing to stop or get very shallow. Breathing ... an hour. The most common type is obstructive sleep apnea. It causes your airway to collapse or ...

  4. Sleeping sickness

    MedlinePlus

    ... this page: //medlineplus.gov/ency/article/001362.htm Sleeping sickness To use the sharing features on this page, please enable JavaScript. Sleeping sickness is an infection caused by germs carried ...

  5. Sleep Deprivation Alters Rat Ventral Prostate Morphology, Leading to Glandular Atrophy: A Microscopic Study Contrasted with the Hormonal Assays

    PubMed Central

    Venâncio, Daniel P.; Andersen, Monica L.; Vilamaior, Patricia S. L.; Santos, Fernanda C.; Zager, Adriano; Tufik, Sérgio; Taboga, Sebastião R.; De Mello, Marco T.

    2012-01-01

    We investigated the effect of 96 h paradoxical sleep deprivation (PSD) and 21-day sleep restriction (SR) on prostate morphology using stereological assays in male rats. After euthanasia, the rat ventral prostate was removed, weighed, and prepared for conventional light microscopy. Microscopic analysis of the prostate reveals that morphology of this gland was altered after 96 h of PSD and 21 days of SR, with the most important alterations occurring in the epithelium and stroma in the course of both procedures compared with the control group. Both 96 h PSD and 21-day SR rats showed lower serum testosterone and higher corticosterone levels than control rats. The significance of our result referring to the sleep deprivation was responsible for deep morphological alterations in ventral prostate tissue, like to castration microscopic modifications. This result is due to the marked alterations in hormonal status caused by PSD and SR. PMID:22927719

  6. One Night of Sleep Deprivation Affects Reaction Time, but Not Interference or Facilitation in a Stroop Task

    ERIC Educational Resources Information Center

    Cain, Sean W.; Silva, Edward J.; Chang, Anne-Marie; Ronda, Joseph M.; Duffy, Jeanne F.

    2011-01-01

    The Stroop color-naming task is one of the most widely studied tasks involving the inhibition of a prepotent response, regarded as an executive function. Several studies have examined performance on versions of the Stroop task under conditions of acute sleep deprivation. Though these studies revealed effects on Stroop performance, the results…

  7. Effect of sleep deprivation on the growth hormone response to the alpha-3 adrenergic receptor agonist, c