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PubMed1998

Neurobiological similarities in antidepressant sleep deprivation and psychostimulant use: a psychostimulant theory of antidepressant sleep deprivation.

This paper attempts to summarize the evidence for the hypothesis that psychostimulant-like neurotransmitter processes within certain regions of the limbic system induce the positive effects of antidepressant sleep deprivation (SD). Preclinical and human studies indicate similar neurobiological effects of psychostimulants such as amphetamines, cocaine and SD. In clinical use, SD and psychostimulants have similar characteristics and behavioral effects. Furthermore, acute psychostimulant challenge decreases limbic metabolism in imaging studies, and SD decreases elevated limbic metabolism in SD responders, indicating that psychostimulant-like neurotransmitter release could decrease limbic metabolism in SD responders. Most antidepressant pharmacotherapies change the reactivity of the dopamine system, and a decrease of presynaptic dopamine or postsynaptic availability can induce depression. Sleep is accompanied by a reduction of catecholamine release and those processes which are increased by psychostimulants. It is concluded that a proposed regional postsynaptic deficit in catecholaminergic neurotransmission can be overcome either acutely by enhanced release during SD or psychostimulant use, or chronically by changes in receptor sensitivity or gene expression due to antidepressant therapies. A postsynaptic deficit in these areas becomes evident if presynaptic release is reduced in conditions such as sleep. Therefore, sleep is depressiogenic for predisposed individuals and the reduction of sleep avoids understimulation of subsensitive postsynaptic processes, which are enhanced by psychostimulants.

Animals↗
PubMed1984

Increased brain serotonin metabolism during rebound sleep in sleep-deprived rats.

Adult male Wistar rats were almost totally deprived of sleep by handling for 24 hr. 5-Hydroxyindolacetic acid concentrations in the dorsal raphe nucleus area and thalamus increased by 140-180%, immediately after sleep deprivation and when the rats had a 3- or 30-min rebound sleep. The higher levels of 5-hydroxyindolacetic acid were still observed after the rats were awakening from a 4-hr sleep. The concentrations of 5-hydroxytryptamine (serotonin) decreased after sleep deprivation and increased during and after sleep, but the differences were not significant. Tryptophan accumulated in the dorsal raphe area and thalamus after sleep deprivation, and an elevated level did not return to baseline concentrations until the rats were awakening. Tryptophan hydroxylase activity did not change in the dorsal raphe area during and after sleep deprivation. These results suggest that the release and synthesis of 5-hydroxytryptamine in the dorsal raphe area and thalamus increased when the rats had a sleep pressure or a rebound sleep after total sleep deprivation. An increased transport of tryptophan into the brain may be closely involved in sleep-inducing mechanisms.

Animals↗
PubMed1999

No evidence of brain cell degeneration after long-term sleep deprivation in rats.

Sleep deprivation leads to cognitive impairments in humans and, if sustained for 2-3 weeks in rats, it is invariably fatal. It has been suggested that neural activity associated with waking, if it is not interrupted by periods of sleep, may damage brain cells through excitotoxic or oxidative mechanisms and eventually lead to cell death. To determine whether sustained waking causes brain cell degeneration, three parallel strategies were used. The presence and extent of DNA fragmentation was analyzed with the TUNEL technique on brain sections from rats sleep deprived for various periods of time (from 8 h to 14 days) and from their respective controls. Adjacent sections from the same animals were stained with a newly developed fluorochrome (Fluoro-Jade) specific for degenerating neurons. Finally, total RNA from the cerebral cortex of the same animals was used to determine whether the expression of several stress response genes and apoptosis-related genes is modified after sustained waking. In most long-term sleep deprived rats only a few scattered TUNEL positive nuclei (1-3) were found in any given brain section. The overall number, distribution, and morphology of TUNEL positive cells in long-term sleep deprived rats did not differ significantly from yoked controls, short-term sleep deprived rats, and sleep controls. No evidence of degenerating neurons as detected by Fluoro-Jade was found in any experimental group. mRNA levels of all the stress response genes and apoptosis-related genes tested did not differ between long-term sleep deprived rats and their yoked controls. These results argue against the hypothesis that sustained waking can significantly damage brain cells through excitotoxic or oxidative mechanisms and that massive cell death may explain the fatal consequences of sleep deprivation.

Animals↗
PubMed1989

Sleep deprivation in the rat: VIII. High EEG amplitude sleep deprivation.

The disk apparatus was used to deprive six rats of the portion of non-rapid eye movement (NREM) sleep with high electroencephalogram (EEG) amplitude (HS2). All HS2 deprived (HS2D) rats died or were sacrificed when death seemed imminent within 23 to 66 days. No anatomical cause of death was identified. All deprived rats showed a debilitated appearance, lesions on their tails and paws, and weight loss in spite of increased food intake. Energy expenditure (calculated from the caloric value of food, weight change, and wastes) increased to more than twice baseline values. With one exception, yoked control rats remained generally healthy. It was not clear whether the changes in HS2D rats resulted from the loss of HS2 or the general disruption of NREM sleep that accompanied this loss. Also, it was not possible to produce major HS2 loss without incurring some loss of paradoxical sleep (PS). Control studies indicated that the partial PS loss in HS2D rats could not, in and of itself, account for all the pathological effects. However, an interaction of HS2D and partial PS loss in producing pathological effects cannot be ruled out.

Animals↗
PubMed1989

Effects of sleep deprivation on respiratory events during sleep in healthy infants.

This study was designed to determine the effects of sleep deprivation on respiratory events during sleep in healthy infants. Ten unsedated full-term infants (1-6 mo) were monitored polygraphically during "afternoon naps" on a control day and on the day after sleep deprivation. Respiratory events, i.e., central apnea, obstructive apnea and hypopnea, and periodic breathing were tabulated. Results for respiratory events were expressed as 1) indexes of the total number of respiratory events and of specific respiratory events per hour of total sleep (TST), "quiet" sleep (QS) and "active" sleep (AS) times; 2) total duration of total and specific respiratory events, expressed as a percentage of TST, QS, and AS times. After sleep deprivation, significant increases were observed for 1) respiratory event (P less than 0.001), central apnea (P less than 0.05), and obstructive respiratory event (P less than 0.01) indexes; 2) respiratory event time as a percentage of TST (P less than 0.002) and as a percentage of AS time (P less than 0.001); 3) obstructive respiratory event time as a percentage of TST (P less than 0.01), QS (P less than 0.05), and AS times (P less than 0.002). The present study shows that short-term sleep deprivation in healthy infants increases the number and timing of respiratory events, especially obstructive events in AS.

Female↗
PubMed1995

Some measures to reduce effects of prolonged sleep deprivation.

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.

Amphetamines↗
PubMed1999

Dopamine receptor D4 is not associated with antidepressant activity of sleep deprivation.

Total sleep deprivation (TSD) is an effective treatment for mood disorders which is thought to act through an enhancement in several neurotransmitter pathways including dopaminergic transmission. However, not all patients respond to TSD and genetic factors are likely to play a major role in determining TSD response. The aim of this study is to investigate the influence of dopamine receptor D4 exon 3 (DRD4) variants on TSD antidepressant efficacy in bipolar disorder. One hundred and twenty-four depressed inpatients affected by bipolar disorder (DSM-IV) were treated with repeated cycles of TSD and were typed for DRD4 variants at the third exon using polymerase chain reaction (PCR) techniques. DRD4 variants were not associated with TSD outcome. Consideration of possible stratification effects such as gender, age at onset and duration of illness did not reveal any association either. DRD4 exon 3 variants are not a main factor influencing TSD outcome in bipolar disorder.

Alleles↗
PubMed1992

Sleep deprivation in human males and its effect on SCE rates in chromosomes--a preliminary study.

The present preliminary study on 5 healthy volunteers deprived of sleep for a day showed a considerable increase in sister-chromatid exchange (SCE) rate in the chromosomes after sleep deprivation. Although the rate of increase varied between the studied subjects, interestingly the 5% plasma from a volunteer with a statistically significant increase after sleep deprivation, when supplemented to cell cultures from an age-matched normal subject, induced high SCEs. This suggests the presence/absence of some factor(s) in plasma samples of subjects showing high SCEs after sleep deprivation, playing a role in the induction of high SCEs in normal cells exposed to the samples in vitro. The present study also suggests that there could be categories which may or may not respond to sleep deprivation with high SCE induction and their plasma supplemented to normal cell culture in turn may or may not induce high SCEs. Nevertheless, the pathophysiological role of high SCEs induced by sleep deprivation in some cases remains intriguing and unresolved and needs further extensive study.

Adult↗
PubMed1994

Effect of sleep deprivation on responses to airway obstruction in the sleeping dog.

The effect of sleep deprivation on sleep architecture and respiratory responses to repetitive airway obstruction during sleep was investigated in four chronically instrumented tracheostomized dogs during 12-h nocturnal experiments. A 24-h period of prior sleep deprivation increased (P < 0.05) the rate at which airway obstruction could be induced from 20 +/- 3 (SE) to 37 +/- 10 times/h compared with non-sleep-deprived dogs. During non-rapid-eye-movement sleep the duration of obstruction, minimum arterial hemoglobin saturation, and peak negative inspiratory effort at arousal were 20.5 +/- 1.0 s, 91.7 +/- 0.5%, and 28.4 +/- 1.8 mmHg, respectively, in non-sleep-deprived dogs. Sleep deprivation increased (P < 0.01) the duration of obstruction to 28.0 +/- 0.9 s, worsened (P < 0.05) the minimal arterial hemoglobin desaturation to 85.4 + 3.1%, and increased (P < 0.025) the peak negative inspiratory effort at arousal to 36.1 +/- 1.6 mmHg. Sleep deprivation also caused increases (P < 0.025) in total sleep time, rapid-eye-movement (REM) sleep time, and percentage of time in REM sleep in a 2-h recovery period without airway obstruction at the end of the study. We conclude that airway obstruction in the sleeping dog can reproduce the disturbances in sleep architecture and respiration that occur in obstructive sleep apnea and that prior sleep deprivation will increase apnea severity, degree of somnolence, and REM sleep rebound independent of change in upper airway collapsibility.

Airway Obstruction↗
PubMed2003

Effect of total sleep deprivation on the landmarks of stage 2 sleep.

OBJECTIVE: To assess the effects of total sleep deprivation on sleep spindle and K-complex (KC) density. METHODS: Eight healthy male subjects (mean age=23.4 years) participated in the experiment: they slept in the laboratory for 3 nights (one adaptation, one baseline, one recovery); baseline and recovery night were separated by a period of 40 h of continuous wake. RESULTS: One night of total sleep deprivation caused a doubling of slow-wave sleep (SWS) amount, an increase of sleep efficiency and a reduction of the latencies of non-rapid eye movement (NREM) sleep stages during the recovery night. These effects were accompanied by a significant reduction in spindle density in the first sleep cycle of the recovery night. Mean KC density did not change as a result of total sleep deprivation, while KC density and inter-KC intervals showed linear trends across the first 4 sleep cycles, respectively decreasing and increasing. Finally, a clear evidence of an antagonist relationship between spindle and KC changes across sleep cycles was provided. CONCLUSIONS: The present study further supports the existence of a reciprocal relationship between SWS and sleep spindles, but fails to show an increase of KC density after total sleep deprivation. The opposite time courses of spindle and KC density across sleep cycles points to an antagonist relation between the two main phasic events of NREM sleep. The latter result, together with the increase of inter-KC distance and the decrease of KC density across subsequent sleep cycles, is consistent with the hypothesis of a role of the spontaneous KC as the "forerunner" of delta waves.

Adult↗
PubMed2002

Sleep deprivation as a probe of homeostatic sleep regulation in primary alcoholics.

BACKGROUND: Alcoholic patients show prominent disturbances of sleep electroencephalograms (EEGs) with a marked loss of slow wave sleep that is even more profound in African American alcoholics as compared to European Americans. Using partial sleep deprivation, this study examined the extent to which abnormal sleep is reversible in alcoholic subjects. METHODS: In a sample stratified on ethnicity, polysomnographic and spectral sleep EEG measures were compared in male primary alcoholic in patients (n=46) and age-matched comparison controls (n=32) at baseline-and recovery sleep following a night of partial sleep deprivation. RESULTS: As compared to controls, alcoholic patients showed a loss of slow wave sleep and more spectral power in beta frequencies. Following sleep deprivation, slow wave sleep and delta power differentially changed between the groups. European American controls showed increases of slow wave sleep that were more robust than responses found in African American controls, whereas both alcoholic groups failed to show increases of slow wave sleep from baseline to recovery. Spectral EEG analyses revealed similar results; sleep deprivation induced significant increases of delta power during NREM-1 in the controls, but not in the alcoholics. CONCLUSIONS: Alcohol dependence compromises the augmentation of slow wave sleep and delta power seen in healthy adults following sleep deprivation. The differential effect of alcoholism on sleep stage physiology suggests a defect in the regulation or plasticity of slow wave sleep with implications for theories linking sleep depth to morbidity and outcome in alcoholics.

Adult↗
PubMed2003

Changes in the expression of steroid metabolism-related genes in rat adrenal glands during selective REM sleep deprivation.

Selective REM sleep deprivation was carried out under the conditions designed to minimize the adverse influence of environmental conditions and restricted movement, and the influence of REM sleep deprivation on adrenocortical steroid metabolism was investigated by measuring the steady-state levels of mRNAs encoding steroid metabolism-related genes, steroidogenic acute regulatory protein (StAR), cholesterol side-chain cleavage enzyme cytochrome P450 (P450scc) and steroid 5alpha-reductase (5alpha-R), in rat adrenal glands. Selective REM sleep deprivation caused a significant decrease in StAR mRNA and an increase in 5alpha-R mRNA levels without any notable change in P450scc mRNA levels in the adrenal gland. In contrast, non-selective sleep disturbance, resulting in the partial reductions of non-REM and REM sleep, tended to increase both StAR and P450scc mRNA levels without any statistical significance. These results indicate that REM sleep deprivation by itself may affect the expression of steroid metabolism-related genes in the adrenal gland, suggesting a possible relation between REM sleep and adrenocortical steroid metabolism.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1990

Neuroendocrinological investigations during sleep deprivation in depression. II. Longitudinal measurement of thyrotropin, TH, cortisol, prolactin, GH, and LH during sleep and sleep deprivation.

Thyrotropin (TSH), thyroxin (T4), triiodothyronine (T3), free T3 (fT3), cortisol, prolactin, and human growth hormone (HGH) were measured every 2 hr during a night of sleep, the following day, and a night of sleep deprivation (SD) in 14 patients with major depressive disorder. In subgroups fT4 (n = 5), reverse T3 (rT3), and luteinizing hormone (LH) (n = 6) were also investigated. Significant increases in TSH, T4, fT4, T3, fT3, rT3, and cortisol and decreases in prolactin levels occurred during the night of SD, compared to the pattern during the night of sleep. The pre-SD T4 and T3 levels of the responders to SD were already higher than in the nonresponders, and increased less during SD. The cortisol and HGH concentrations of the responders rose higher during SD than those of the nonresponders. Changes in TSH and prolactin were not correlated to clinical response. Analysis of possible neurochemical mechanisms underlying this "pattern" of changes in different endocrine profiles suggests that enhanced noradrenergic activity might play a role in the changes in TSH, cortisol, thyroid hormones, and possibly HGH secretion during SD, and increased dopaminergic tone probably induced the decline in prolactin levels. Additional effects of the serotonergic system cannot be excluded at present. In conclusion, the data suggest that enhanced noradrenergic activity of the locus coeruleus stimulates alpha and/or beta adrenergic receptors in depressed patients during SD. This mechanism could well be involved in the antidepressant effect of this therapy.

Adult↗
PubMed2006

Volumetric bone mineral density and bone size in sleep-deprived individuals.

INTRODUCTION: Chronic sleep deprivation, which is associated with several age-related pathologies and altered endocrine function, may adversely affect bone. Our a priori hypothesis was that bone mineral density was lower in sleep-deprived (<6.5 h/night) vs. sleep-adequate (>6.5-10 h/night) individuals. METHODS: Cross-sectional analysis of sleep and bone data on 1,146 individuals (652 women) was performed. Measurements were obtained at the distal radius by pQCT, and the spine and hip by DXA. Bone differences between sleep-deprived and sleep-adequate groups were compared after stratifying by sex and controlling for covariates. RESULTS: Overall, 19% of the population was sleep deprived. Sleep-deprived women had lower cortical volumetric BMD (1,208+/-4 vs. 1,219+/-2 mg/cm(3), P=0.03) than sleep-adequate women. Sleep-deprived men had lower pSSI, an estimate of torsional bending strength, than sleep-adequate men (358+/-10 vs. 382+/-5 mm(3), P=0.04), due to a slightly smaller periosteal circumference (43.9+/-0.4 vs. 44.8+/-0.2 mm, P=0.07) and cortical area (103+/-2 vs. 106+/-1+/-mm(2), P=0.06). CONCLUSION: Sleep deprivation is associated with some, but not all, bone outcomes. These findings may have important public health significance given the increasing prevalence of sleep deprivation.

Absorptiometry, Photon↗
PubMed1976

Effects of sleep deprivation on mood and central amine metabolism in depressed patients.

Nineteen patients, each hospitalized with a major depressive episode, were deprived of sleep for one night. Ten patients responded with clear improvement in depressive symptoms; the substantial clinical change was transient, usually lasting one day. Those who responded had significantly higher initial depression ratings (P less than .01) and tended to be older than nonresponders who experienced mild increases in irritability, fatigue, and discomfort following sleep deprivation. Amine metabolites, 5-hydroxyindoleacetic acid (5HIAA), and homovanillic acid (HVA) were not substantially affected by sleep deprivation, although there was a significant interaction of clinical response and direction of 3-methoxy-4-hydroxyphenylglycol (MHPG) change. Sleep deprivation thus produces acute, but only transient improvement in a selected group of severely depressed patients; it appears to be an important tool in the study of the affective disorders.

Adult↗
PubMed1998

Dissimilarity of slow-wave activity enhancement by torpor and sleep deprivation in a hibernator.

Sleep regulation processes have been hypothesized to be involved in function and timing of arousal episodes in hibernating ground squirrels. We investigated the importance of sleep regulation during arousal episodes by sleep deprivation experiments. After sleep deprivation of 4, 12, and 24 h, starting 4 h after onset of euthermy, a duration-dependent enhancement of slow-wave activity (SWA) of the cortical electroencephalogram during non-rapid eye movement sleep was found, as expected for normal sleep regulation. When sleep deprivation was applied during the initial phase of the arousal episode, in which effects of prior torpor were present in undisturbed recordings, no subsequent recurrence of SWA was found. In addition, prior torpor induced a reduction in the spectral activity of the sigma frequency range (7-14 Hz), which was not observed after sleep deprivation. The effects of torpor and sleep deprivation on subsequent SWA appear qualitatively different. This indicates that effects of deep torpor on sleep are dissimilar to normal sleep regulation.

Animals↗
PubMed1981

Sleep stage responses of older and younger subjects after sleep deprivation.

EEG sleep stage measures were obtained on younger subjects (18-22 years) and older subjects (40-50 years) at 9 a.m. after 2 nights of sleep loss. The first 200 min were compared. Both groups displayed sharply reduced latencies and increased stage 4 sleep. The proportionate distribution of stage amounts and numbers was not different. However, the younger group entered slow wave sleep more quickly.

Adolescent↗