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PubMed2003

Changes in brain glycogen after sleep deprivation vary with genotype.

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.

Anesthesia↗
PubMed1991

Enforced 24-hour recovery following sleep deprivation.

The pattern of recovery sleep after sleep deprivation was investigated in healthy young adults. Six subjects experienced three experimental conditions (0, 24, and 48 hr sleep deprivation) in a Latin Square design. The recovery period consisted of a 24-hr enforced time in bed during which subjects were polysomnographically recorded beginning at 0800. To assess the differential effects of the deprivation conditions, the total sleep time on the 24-hr recordings was submitted to a six (4-hr block) by three (deprivation condition) multivariate analysis of variance. Subjects slept more following the 24- and 48-hr conditions when compared to the 0-hr condition. Across conditions, subjects slept more during the first 4 hr when compared to the remaining five blocks. Importantly, there was a significant interaction of sleep deprivation by 4-hr block. In block 1 sleep was differentially recovered between each condition with more sleep being recorded following longer hours of deprivation. In block 2 subjects in the 24- and 48-hr conditions slept comparable amounts and significantly more than those in the 0-hr condition. In blocks 3 and 4 only the 48-hr condition exhibited significantly more sleep than the 0-hr condition. However, significantly less sleep was found in block 6 following the 48-hr condition. Overall, subjects recovered 72% and 42% of the total amount of sleep lost during the 24- and 48-hr conditions, respectively.

Adult↗
PubMed2001

Extracellular serotonin levels in the medullary reticular formation during normal sleep and after REM sleep deprivation.

Rapid eye movement (REM) sleep is hypothesized to result from the activity of REM sleep-generating and REM sleep-inhibiting neurons. The serotoninergic (5-HT) neurons of the dorsal raphe nucleus (DRN) represents one such population of REM-sleep inhibiting neurons since they are silent during REM sleep. Consistent with the decrease in activity of 5-HT neurons, the brain extracellular levels of 5-HT are lower during REM sleep compared to wakefulness. It is not known whether serotonin release is also reduced as a consequence of REM sleep rebound. Using microdialysis sampling coupled to HPLC-ECD, we measured the extracellular levels of 5-HT and its metabolite (5-HIAA) in the medial medullary reticular formation (mMRF) of freely behaving rats during normal sleep, REM sleep deprivation as well as during REM sleep rebound. We found that the levels 5-HT and 5-HIAA were significantly decreased by REM sleep deprivation. The reduction of 5-HT release was maintained during REM sleep rebound but the extracellular level of its main metabolite was increased. In addition, even during REM sleep rebound, 5-HT release during sleep was low compared to wakefulness. Taken together these data support the permissive role of 5-HT neurotransmission for REM sleep expression.

Animals↗
PubMed2003

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

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.

Adult↗
PubMed1997

Operant control of ambient temperature during sleep deprivation.

Rats subjected to total sleep deprivation (TSD) by the disk-over-water method were provided with a continuously available operant by which they could increase ambient temperature (T(amb)). TSD rats progressively increased operant responses for heat to 700% of baseline levels. During the last quarter of sleep deprivation, they maintained mean T(amb) at 9 degrees C above baseline and held T(amb) over 40 degrees C for 35% of the day. In contrast, yoked control rats (TSC) did not change mean T(amb). Although both TSD and TSC rats showed a progressive decline in intraperitoneal temperature (T(ip)), TSD rats maintained an elevated T(amb) even during periods when T(ip) and brain temperatures (T(br)) were above baseline levels. Thus these results confirm and extend earlier findings that rats subjected to TSD show an increase in temperature set point (T(set)). The earlier studies, which utilized short daily trials in a thermal gradient, demonstrated an increase in T(set) early in the deprivation period. The present study, which obtained more extensive data on thermal preference at a range of body temperatures demonstrated an increasing T(amb) for almost all T(ip) and T(br) values, suggesting a progressive increase in T(set) over the course of sleep deprivation. Surprisingly, survival time was shorter than in previous TSD studies. Reduced survival could not be attributed to differences in T(br), T(ip), energy expenditure, or sleep loss from previous studies.

Animals↗
PubMed1982

Sleep regulation after reduction of brain serotonin: effect of p-chlorophenylalanine combined with sleep deprivation in the rat.

Sleep was recorded in the rat after combined treatment with p-chlorophenylalanine (PCPA; 300 mg/kg) and 24-h sleep deprivation (SD) and then compared with sleep recorded after either treatment alone. PCPA alone reduced total sleep (TS), rapid eye movement sleep (REMS) per TS, as well as the power density of the EEG delta band (1.25-4.00 Hz) of non-REM sleep (NREMS). SD enhanced these sleep parameters and reduced the frequency of wake episodes. The combined treatment with PCPA and SD reduced TS and REMS/TS to a level similar to that induced by PCPA alone, and it increased delta activity to a level similar to that induced by SD alone. The frequency of wake episodes was reduced. It is concluded that essential aspects of sleep regulation are still functional during PCPA-induced insomnia. The sleep-inhibiting action of PCPA may be related to the hyperresponsiveness to stimuli rather than to the impairment of sleep regulation itself.

Animals↗
PubMed1993

Sustained sleep deprivation impairs host defense.

Prolonged sleep deprivation in rats causes an unexplained hypercatabolic state, secondary malnutrition symptoms, and mortality. The nature of the vital impairment has long been a mystery. Its determination would help to elucidate the type of organic dysfunction that sleep prevents. There are no gross detectable disturbances in intermediary metabolism, clinical chemistry, or hematological indexes that provide substantial clues to the mediation of sleep-deprivation effects. Furthermore, postmortem examinations reveal no systematic morphological or histopathological findings. Taken together, the cachexia and the absence of evidence of structural damage or organ dysfunction pointed to involvement of a regulatory system that was diffuse, possibly the immune system. Blood cultures revealed invasion by opportunistic microbes to which there was no febrile response. These results suggest that the life-threatening condition of prolonged sleep deprivation is a breakdown of host defense against indigenous and pathogenic microorganisms.

Animals↗
PubMed1994

Leukocytosis and natural killer cell function parallel neurobehavioral fatigue induced by 64 hours of sleep deprivation.

The hypothesis that sleep deprivation depresses immune function was tested in 20 adults, selected on the basis of their normal blood chemistry, monitored in a laboratory for 7 d, and kept awake for 64 h. At 2200 h each day measurements were taken of total leukocytes (WBC), monocytes, granulocytes, lymphocytes, eosinophils, erythrocytes (RBC), B and T lymphocyte subsets, activated T cells, and natural killer (NK) subpopulations (CD56/CD8 dual-positive cells, CD16-positive cells, CD57-positive cells). Functional tests included NK cytotoxicity, lymphocyte stimulation with mitogens, and DNA analysis of cell cycle. Sleep loss was associated with leukocytosis and increased NK cell activity. At the maximum sleep deprivation, increases were observed in counts of WBC, granulocytes, monocytes, NK activity, and the proportion of lymphocytes in the S phase of the cell cycle. Changes in monocyte counts correlated with changes in other immune parameters. Counts of CD4, CD16, CD56, and CD57 lymphocytes declined after one night without sleep, whereas CD56 and CD57 counts increased after two nights. No changes were observed in other lymphocyte counts, in proliferative responses to mitogens, or in plasma levels of cortisol or adrenocorticotropin hormone. The physiologic leukocytosis and NK activity increases during deprivation were eliminated by recovery sleep in a manner parallel to neurobehavioral function, suggesting that the immune alterations may be associated with biological pressure for sleep.

Adult↗
PubMed1980

Improvement of depression by REM sleep deprivation. New findings and a theory.

We compared sleep variables in 14 drug-free endogenous depressives and in 14 age- and insomnia-matched, nondepressed controls before and after brief rapid eye movement (REM) sleep deprivation by awakenings. Before REM sleep deprivation, compared with controls, depressives had lower REM latency, higher REM frequency, and--a new finding--an abnormal temporal distribution of REM sleep. Depression improvement by REM sleep deprivation correlated with the ameliorative effect of brief REM sleep deprivation on on indicator of the abnormal temporal distribution of REM sleep. Several findings suggest that the depressive abnormalities represent a "damaged," weakened sleep cycle "oscillator" and its correlate, a circadian rhythm disturbance, and that REM sleep deprivation improved depression to the extent that it stimulated the oscillator and corrected one manifestation of the circadian rhythm disturbance.

Adult↗
PubMed2004

Age, performance and sleep deprivation.

Young subjects are frequently involved in sleep-related accidents. They could be more affected than older drivers by sleep loss and therefore worsen their driving skills quicker, or have a different perception of their level of impairment. To test these hypotheses we studied variations of reaction time (RT), a fundamental prerequisite for safe performing, as measured by lapses, i.e. responses > or = 500 ms and self-assessment of performance and sleepiness after a night awake and after a night asleep in a balanced crossover design in young versus older healthy subjects. Ten young (20-25 years old) and 10 older volunteers (52-63 years old) were tested with and without 24 h of sleep deprivation. Without sleep deprivation, RTs were slower in older subjects than in the younger ones. However, after sleep deprivation, the RTs of young subjects increased while that of the older subjects remained almost unaffected. Sleepiness and self-perception of performance were equally affected in both age groups showing different perception of performance in the age groups. Our findings are discussed in terms of vulnerability to sleep-related accidents.

Accidents, Traffic↗
PubMed2004

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

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.

Animals↗
PubMed1977

Homovanillic acid and 5-hydroxyindoleacetic acid in lumbar cerebrospinal fluid after total and REM sleep deprivation in humans.

Lumbar CSF HVA and 5-HIAA levels were assayed in 3 groups each of 10 subjects, which were respectively deprived of sleep for 30 h, deprived of REM sleep and disturbed with several awakenings during SW sleep for two consecutive nights. HVA levels after total sleep (39 +/- 20 ng/ml) or REM (35 +/- 11 ng/ml) deprivation as well as after SW sleep awakenings (32 +/- 26 ng/ml) were not different from controls (42 +/- 14 ng/ml). 5-HIAA levels after REM deprivation (32 +/- 15 ng/ml) appeared increased when compared with controls (21 +/- 7 ng/ml), total sleep-deprived subjects (21 +/- 10 ng/ml) or subjects with SW sleep awakenings (27 +/- 13 ng/ml). Possible increase in 5-HT turnover after REM deprivation and possible 5-HT role in REM sleep regulation in humans are discussed.

Adult↗
PubMed2001

Decrease in motor cortical excitability in human subjects after sleep deprivation.

The effect of sleep deprivation on human motor cortical excitability was investigated by evaluating the changes in motor evoked potentials from the thenar eminence muscles of the right hand in seven subjects. Motor threshold, motor evoked potential amplitude, silent period, intracortical inhibition, intracortical facilitation and F wave were studied. Recordings were performed every 6 h during the day-time (from 09.00 to 21.00 h) and every 3 h during the night-time (from 21.00 to 09.00 h). Significant increases in motor threshold, intracortical inhibition and silent period were noted in the recordings during the night associated with a return to baseline values in the morning. No significant changes were observed in any of the other parameters. Enhancement of intracortical motor inhibition is suggested to explain the effect of sleep deprivation.

Adult↗
PubMed2002

Circadian rhythm of rectal temperature during sleep deprivation with modafinil.

BACKGROUND: Sleep deprivation (SD) induces many adverse psychological and physiological effects, particularly on vigilance and the thermoregulatory system. The drug modafinil appears to suppress or diminish the harmful effects on vigilance. However, the effects of modafinil combined with SD on the circadian rhythm of core temperature are not well established. HYPOTHESIS: We studied the circadian rhythm of rectal temperature (CRTre) during 62 h of SD alone or with three dosage levels of modafinil. METHODS: Six men underwent repeated SD experiments lasting 7 d each, including a 24-h control period, 62 h of SD, and a 24-h recovery period. Experiments were repeated four times in mixed order for placebo and three levels of modafinil (50, 150, or 300 mg x 24 h(-1)). The Tre was recorded each minute throughout the experiment and the CRTre was studied by the single cosinor method. RESULTS: Independent of modafinil, SD increased the mesor (p < 0.05) and reduced the amplitude (p < 0.01) of the CRTre without changing the acrophase. During the recovery period, a rebound increase was seen in the amplitude of the CRTre (p < 0.01). The 50 mg x 24 h(-1) dose of modafinil, but not the higher doses, induced a lower mesor (p < 0.01) independent of SD. CONCLUSIONS: The observed changes may reflect a threshold for the central action of modafinil on core temperature. The hyperthermic effect reported in the literature for SD with modafinil may actually result from the sleep deprivation alone.

Adult↗
PubMed2003

No Influence of a functional polymorphism within the serotonin transporter gene on partial sleep deprivation in major depression.

Sleep deprivation exerts transient antidepressant efficacy. As a potential mechanism of action an enhancement of serotonergic and dopaminergic neurotransmission within the CNS is discussed. Because genetic variations influencing neurotransmission could have an impact on therapeutic outcome and stability of improvement, we investigated the functional polymorphism of the serotonin transporter (5-HTT) gene, the 5-HTT-linked polymorphic region (5-HTTLPR), to examine the serotonergic pathway. We included 56 patients with major depression (DSM-IV). Psychiatric ratings including the HAM-D21 and HAM-D6 scale were assessed on the day prior to partial sleep deprivation (PSD) and on day 1 and 2 after PSD and related to the different genotypes. The 5-HTTLPR variants were determined following PCR amplification using genomic DNA. 58.1% of the patients were responders to PSD. A significant overall reduction in depression scores could be observed on day 1. Subdivision according 5-HTTLPR gene variants showed no differences in clinical outcome on day 1. As expected the therapeutical effect of PSD was only transient and most patients experienced an exacerbation of depressive symptoms on day 2. 5-HTTLPR variants had no influence on reduction of depressive symptoms on day 2 or relapse on day 3. Thus, the previously reported influence of the serotonin transporter gene on PSD outcome in bipolar depression could not be confirmed in unipolar depressed patients.

Adult↗
PubMed1992

Unihemispheric sleep deprivation in bottlenose dolphins.

Unihemispheric and bihemispheric sleep deprivation were performed in bottlenose dolphins. One brain hemisphere was capable of being deprived of delta (0.5-3.0 Hz) sleep in the former condition. Here, an increase in sleep pressure was observed during sleep deprivation in the deprived hemisphere. In the recovery sleep, following unihemispheric sleep deprivation, there was a rebound of delta sleep only in the deprived hemisphere. Following bihemispheric sleep deprivation the animals exhibited an increase in delta sleep in both hemispheres.

Journal Article↗
PubMed2000

Circadian clock resetting by sleep deprivation without exercise in the Syrian hamster.

Circadian rhythms in several species can be phase-shifted by procedures that stimulate locomotor activity ("exercise") during the usual sleep period. The role of arousal or sleep loss, independent of activity, in this effect has not been adequately resolved. We show here, using the sleep deprivation procedure of gentle handling, that comparably large phase shifts (up to 240 min advances) of the rest-activity cycle can be induced in Syrian hamsters by 3 hr of behavioral arousal, with minimal locomotion, beginning 6 hr before the usual active period. Horizontal distance traveled during the deprivation procedure averaged approximately 0.08 km, compared to 2. 5 km typical in exercise studies. Hamsters requiring fewer interventions exhibited larger shifts, suggesting that the level or continuity of spontaneous arousal determines shift size. The circadian rhythm of light-induced c-fos expression in the suprachiasmatic nucleus (SCN) was used as a phase marker to further demonstrate that the clock is reset within 1 hr after a 3 hr deprivation. Sleep deprivation mimicked the effects of exercise on basal c-fos expression in two components of the circadian system, suppressing basal Fos immunoreactivity in the SCN, and increasing Fos in the intergeniculate leaflet. Sleep deprivation without exercise in hamsters can rapidly reset the circadian clock and alter gene expression within the circadian system.

Animals↗