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PubMed2003

Differential increase in the expression of heat shock protein family members during sleep deprivation and during sleep.

Although sleep is thought to be restorative from prior wakeful activities, it is not clear what is being restored. To determine whether the synthesis of macromolecules is increased in the cerebral cortex during sleep, we subjected C57BL/6 mice to 6 hours of sleep deprivation and then screened the expression of 1176 genes of known function by using cDNA arrays. The expression of the heat shock proteins (HSP), endoplasmic reticulum protein (ERp72) and glucose-regulated protein (GRp78), was among the genes whose expression was significantly elevated in the cortex during sleep deprivation, whereas GRp78 and GRp94 mRNAs were elevated in the cortex during recovery sleep after sleep deprivation, as confirmed by conventional and quantitative real-time polymerase chain reaction and/or Northern analyses. A systematic evaluation of the expression of six heat shock protein family members (ERP72, GRp78, GRp94, HSP27, HSP70-1, and HSP84) in seven brain regions revealed increased mRNA levels in cortex, basal forebrain, hypothalamus, cerebellum and medulla during sleep deprivation, whereas increased mRNA levels during recovery sleep were limited to the cortex and medulla. Immunohistochemical studies identified increased numbers of GRp78-, GRp94-, and ERp72-immunoreactive cells in the dorsal and lateral cortex during sleep deprivation but, during recovery sleep, elevated numbers of these cells were found only in the lateral cortex. In the medulla, increased numbers of GRp94-immunoreactive cells were observed in nucleus tractus solitarius, dorsal motor nucleus of the vagus and the rostroventrolateral medulla during recovery sleep. The widespread increase of heat shock protein family mRNAs in brain during sleep deprivation may be a neuroprotective response to prolonged wakefulness. In contrast, the relatively limited heat shock protein family mRNA expression during recovery sleep may be related to the role of heat shock proteins in protein biogenesis and thus to the restorative function of sleep.

Animals↗
PubMed2000

Vascular resistance in the rat during baseline, chronic total sleep deprivation, and recovery from total sleep deprivation.

Rats subjected to total sleep deprivation (TSD) by the disk-over-water method exhibit an elevated temperature set point, increased energy expenditure (EE), and increased circulating norepinephrine--all of which should militate for an increase in body temperature. Instead, after a small rise early in TSD, intraperitoneal temperature (T(ip)) fell progressively, indicating a reduced ability to retain body heat. To evaluate whether vasoconstrictor defenses against heat loss in the regions of major heat dissipation in the rat (hindpaws and tail) were impaired, peripheral vascular resistance (PVR) was calculated from aortic blood pressure (BP) and blood flow (BF) (BP and BF were continuously recorded at the aortic-iliac junction). TSD rats and their yoked control (TSC) rats were subjected to TSD for 10 to 22 days. As in earlier studies, TSD rats showed excessive heat loss indicated by a falling T(ip) (after an initial rise) while EE was elevated. Temperature set point was presumably raised throughout deprivation as shown previously. Although a small decline in PVR early in deprivation could have increased heat loss, there was no evidence of a massive vasodilation in the region examined which could, in itself, account for the progressive inability to retain heat over the course of TSD. In fact, PVR was near baseline levels during the latter half of TSD. Nevertheless, there was evidence of impaired vasoconstrictive defenses in TSD rats inasmuch as they showed significantly lower PVR than TSC rats during most of the deprivation period in spite of indications that they were farther below set point. It is not yet clear whether this impairment was a major determinant of the heat loss in TSD rats. A rapid PVR rebound during recovery suggested a release from a TSD-linked blockage of vasomotor compensation for excessive heat loss.

Animals↗
PubMed1994

Effects of sleep deprivation on performance of Naval seamen: I. Total sleep deprivation on performance.

Sleep deprivation leads to impairment in performance, loss of efficiency and deterioration in mood states such as tension, depression, aggression, fatigue, confusion and vigour. These can be detrimental to combat readiness and could contribute to "battle stress". In the present study, a homogeneous group of 20 seamen under total sleep deprivation was rated 6 hourly with the Stanford Sleepiness Scale (SSS), Profile of Mood States (POMS) and a battery of performance tests including the trail making, grooved peg board, digit span, digit symbol, sea-shore rhythm, flicker fusion, dynamometer and naval tasks. With the exception of the trail making test and naval tasks, the test performance was observed to correlate significantly (P < 0.05) with the SSS. A higher sleepiness score was associated with a poorer performance in test scores. On the time trends of sleep deprivation on the performance tests measured, a dip in performance was observed in all the tests at 42 hours of sleep deprivation and continuous deterioration of performance was observed after 72 hours of sleep deprivation. The cognitive, vigilance, mood and sleepiness tests were substantially affected by sleep deprivation. Greater effect was observed in tests that involved cognition, speed and precision and smaller effect was observed in routine tasks that involved gross manual movement. The decrease in performance observed at 42 hours of sleep deprivation was 5.9 standard deviation from initial values for SSS; 3.9 for sea-shore rhythm, 3.0 for grooved peg board; 2.6 for dynamometer; 2.4 for mood; 1.8 for digit span; 1.6 for trail making and digit symbol; 1.0 for naval tasks and addition; and 0.9 for flicker fusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1982

Comparative evaluation of sleep deprivation and sedated sleep EEGs as diagnostic aids in epilepsy.

The comparative value of sedated sleep and sleep deprivation EEGs was investigated in a consecutive series of 43 patients who had received both types of activation study for diagnostic purposes. Patients were referred because of persisting doubt concerning either the diagnosis of epilepsy, or the type of epilepsy present in those with definite seizures. Forty-one had had routine waking EEGs, all of which were normal or only mildly abnormal. EEGs were rated without access to previous reports or clinical data, and epileptiform discharges (ED) were semiquantified during wakefulness and sleep. De novo precipitation of ED, increase in abundance of ED and discovery of a new independent focus or a new type of ED were taken as the yield of useful information. 44% of sleep deprivation records provided useful information compared to 14% of sedated sleep recordings (P less than 0.005). In addition, sleep deprivation was significantly superior to sedated sleep in differentiating those with a final clinical diagnosis of epilepsy from those with doubtful or no epilepsy (P less than 0.001). It is suggested that the usefulness of the interictal EEG in patients with uncertain epilepsy or epilepsy of unknown type is increased by performance of a diagnostic series to include routine waking, sedated sleep and sleep deprivation recordings.

Adolescent↗
PubMed1995

Noradrenergic activity in rat brain during rapid eye movement sleep deprivation and rebound sleep.

Noradrenergic locus ceruleus neurons are most active during waking and least active during rapid eye movement (REM) sleep. We expected REM sleep deprivation (REMSD) to increase norepinephrine utilization and activate the tyrosine hydroxylase (TH) gene critical for norepinephrine production. Male Wistar rats were deprived of REM sleep with the platform method. Rats were decapitated after 8, 24, or 72 h on small (REMSD) or large (control) platforms or after 8 or 24 h of rebound sleep after 72 h of the platform treatment. During the first 24 h, norepinephrine concentration, measured by high-performance liquid chromatography/electrochemical detection, was lower in the neocortex, hippocampus, and posterior hypothalamus in REMSD rats than in large-platform controls. After 72 h of REMSD, TH mRNA, measured by in situ hybridization, was increased in the locus ceruleus and norepinephrine concentrations were increased. Polygraphy showed that small-platform treatment caused effective and selective REMSD. Serum corticosterone measurement by radioimmunoassay indicated that the differences found in norepinephrine and TH mRNA were not due to differences in stress between the treatments. The novel finding of sleep deprivation-specific increase in TH gene expression indicates an important mechanism of adjusting to sleep deprivation.

Animals↗
PubMed1999

Poor recovery sleep after sleep deprivation in delayed sleep phase syndrome.

To clarify disturbances in sleep regulation in patients with delayed sleep phase syndrome (DSPS), we studied three patients with DSPS and seven healthy controls. Sleep propensity and melatonin rhythms after 24-h sleep deprivation were investigated under dim light condition by using the ultra-short sleep-wake schedule. The sleep propensity curves displayed clear differences between DSPS patients and the controls. During the subjective day when melatonin was not produced, recovery sleep after the sleep deprivation did not occur in DSPS patients, while recovery sleep occurred during the subjective day in controls. This suggests that DSPS may involve problems related to the homeostatic regulation of sleep after sleep deprivation.

Adult↗
PubMed1983

The effect of sleep deprivation and recovery sleep on plasma corticosterone in the rat.

The effect of 24-h sleep deprivation by forced locomotion on plasma corticosterone was investigated in the rat. Corticosterone was slightly elevated after 21.5 h sleep deprivation, but did not differ from controls after a 2.5-h recovery period. An acute 20-min forced locomotion period caused a marked rise in plasma corticosterone. It is concluded that stress is not a major factor contributing to the massive effects of sleep deprivation on sleep parameters.

Animals↗
PubMedDate not supplied

Effects of a 25-h sleep deprivation on daytime sleep in the middle-aged.

Our understanding of the mechanisms by which sleep deteriorates with age almost exclusively stems from comparisons of young and elderly subjects. The present study investigated the different effects of a 25-h sleep deprivation on the recovery sleep initiated in the morning (when circadian sleep propensity decreases) of young (20-39 y) and middle-aged subjects (40-60 y). Middle-aged subjects showed a steeper increase in the duration of wakefulness during daytime recovery sleep than the young subjects. Slow-wave sleep (SWS) and EEG slow-wave activity (SWA: spectral power between 0.5-4.5 Hz) were potentiated in both groups following sleep deprivation. However, the rebound of SWS and SWA was significantly less pronounced in the middle-aged than in the young. This reduction in homeostatic recuperative drive in middle-aged subjects might account for the decrease in their ability to maintain sleep when they have to recuperate at an abnormal circadian phase. These results helps to understand the increase in complaints related to shift work and jet lag in the middle years of life.

Adult↗
PubMed1994

[Sleep deprivation and continuous sleep treatment for depression].

We explained about sleep deprivation (SD) and continuous sleep treatment (CST) such as nonpharmacological approaches for depression. Total sleep deprivation (TSD) showed dramatic, but transient, improvement in severe depression following one or more nights of SD. We reported the effects of TSD on 8 depressives. Consequently, after the TSD, the patients were divided into the groups of 3 responders and 5 non-responders in the score of on the basis of a 50% reduction in the score of Hamilton Rating Scale. The minimum rectal temperature (RT) of the non-responders was significant higher on the TSD night compared to the baseline night, but no significant change was observed in the responders. In addition, the minimum nocturnal RT of the responders before TSD tended to be higher. Nowadays, it is not so popular to use CST for depression because the technique is difficult.

Circadian Rhythm↗
PubMed2000

Brain site-specificity of extracellular adenosine concentration changes during sleep deprivation and spontaneous sleep: an in vivo microdialysis study.

Previous data suggested that increases in extracellular adenosine in the basal forebrain mediated the sleep-inducing effects of prolonged wakefulness. The present study sought to determine if the state-related changes found in basal forebrain adenosine levels occurred uniformly throughout the brain. In vivo microdialysis sample collection coupled to microbore high-performance liquid chromatography measured extracellular adenosine levels in six brain regions of the cat: basal forebrain, cerebral cortex, thalamus, preoptic area of hypothalamus, dorsal raphe nucleus and pedunculopontine tegmental nucleus. In all these brain regions extracellular adenosine levels showed a similar decline of 15 to 20% during episodes of spontaneous sleep relative to wakefulness. Adenosine levels during non-rapid eye movement sleep did not differ from rapid eye movement sleep. In the course of 6h of sleep deprivation, adenosine levels increased significantly in the cholinergic region of the basal forebrain (to 140% of baseline) and, to a lesser extent in the cortex, but not in the other regions. Following sleep deprivation, basal forebrain adenosine levels declined very slowly, remaining significantly elevated throughout a 3-h period of recovery sleep, but elsewhere levels were either similar to, or lower than, baseline. The site-specific accumulation of adenosine during sleep deprivation suggests a differential regulation of adenosine levels by as yet unidentified mechanisms. Moreover, the unique pattern of sleep-related changes in basal forebrain adenosine level lends strong support to the hypothesis that the sleep-promoting effects of adenosine, as well as the sleepiness associated with prolonged wakefulness, are both mediated by adenosinergic inhibition of a cortically projecting basal forebrain arousal system.

Adenosine↗
PubMed1989

Sleep deprivation in the rat: IV. Paradoxical sleep deprivation.

Twelve rats were subjected to paradoxical sleep deprivation (PSD) by the disk apparatus. All PSD rats died or were sacrificed when death seemed imminent within 16-54 days. No anatomical cause of death was identified. All PSD rats showed a debilitated appearance, lesions on their tails and paws, and weight loss in spite of increased food intake. Their yoked control (PSC) rats remained healthy. Since dehydration was ruled out and several measures indicated normal or accelerated use of nutrients, the food-weight changes in PSD rats were attributed to increased energy expenditure (EE). The measurement of EE, based upon caloric value of food, weight, and wastes, indicated that all PSD rats increased EE, with mean levels reaching more than twice baseline values. All of these changes had been observed in rats deprived totally of sleep; the major difference was that they developed more slowly in PSD rats.

Animals↗
PubMedDate not supplied

Alterations of blood platelet MAO-B activity and LSD-binding in humans after sleep deprivation and recovery sleep.

Sleep deprivation (SD) is an effective, however short-lived, method of treatment of depression. Preliminary findings suggest that the antidepressive effect of sleep deprivation is mediated by serotoninergic (5-HT) mechanisms. We therefore assessed serotoninergic activity before and after total SD (TSD) as well as after the following night sleep by investigating platelet LSD-binding, MAO B-activity, and 5-HT-content as well as plasma norepinephnne (NE) in 10 healthy men (age: 27.4 +/- 2.8 years). Blood samples were drawn on three consecutive days at 0700, 1300 and 1900 h, respectively. After TSD, a significant increase of LSD-binding KD and Bmax as well as of MAO-B KM and plasma NE could be observed, which, however, vanished after consecutive night sleep. Our findings favour an increased serotoninergic transmission after TSD and thus support the hypothesis, that sleep deprivation exerts its antidepressant effects by pro-serotoninergic mechanisms.

Adult↗
PubMed2002

Effect of sleep deprivation on NREM sleep ERPs and related activity at sleep onset.

This research assessed the impact of one night of sleep deprivation on the amplitudes of NREM-sleep event-related potentials (NREM ERPs) and on the frequency of occurrence of related electroencephalogram activity including sleep spindles, arousals, K-complexes, and vertex sharp waves (VSWs). The NREM ERPs identified included P220, N350, P450, N550 and P900. During a pre-deprivation night, ten subjects took two 20-min naps separated by a 20-min break at their normal bedtime. Brief tones were presented at three intensity levels (60, 75 and 90 dB) with a 5-s interstimulus interval. Following these naps, subjects were kept awake until their normal bedtime the following day. At that time, they repeated the two-nap procedure. The ERPs obtained for each tone and wake/sleep state for pre- and post-deprivation conditions were analyzed using repeated measures statistical procedures. As anticipated, NREM ERP amplitudes recorded both pre- and post-deprivation increased with tone intensity and with approaching sleep. Also, sleep deprivation was associated with more rapid sleep onset, reduced arousability, and greater spindle production. While sleep deprivation had no effect on the amplitude of P220. Post-deprivation amplitudes of N350, N550 and P900 were greater, especially following the 90-dB tone. There was a corresponding increase in VSWs and K-complexes. These findings are inconsistent with the view that NREM ERPs reflect arousal. The underlying mechanism(s) may facilitate initiation and maintenance of sleep.

Adult↗
PubMed1994

Cortisol and beta-endorphin responses to sleep deprivation in major depression--the hyperarousal theories of sleep deprivation.

To test theories that response to sleep deprivation in depression is the result of either stress reactions or down-regulation of hyperarousal, the early morning cortisol and beta-endorphin levels of depressed sleep deprivation responders and nonresponders before and after sleep deprivation were compared (areas under the curve of 8 blood samples between 7:30 and 10 a.m.). The beta-endorphin response was significantly different in responders and nonresponders, whereas all other comparisons remained nonsignificant. The results do not support theories that sleep deprivation acts as a stressor, but are not contradictory to the hyperarousal hypothesis of sleep deprivation.

Adult↗
PubMed1989

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

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.

Adrenal Glands↗
PubMed2003

Does sleep deprivation worsen mild obstructive sleep apnea?

STUDY OBJECTIVES: Sleep deprivation is believed to worsen obstructive sleep apnea (OSA). We assessed the effect of acute sleep deprivation on polysomnography in a cohort of subjects with mild OSA and a cohort of subjects without OSA. DESIGN: Crossover study in which subjects initially had polysomnography after a normal night's sleep or after 36 hours of sleep deprivation, followed by a 2- to 4-week interval, after which subjects were restudied under the alternate testing condition. SETTING AND PARTICIPANTS: 13 subjects with mild OSA and 16 subjects without OSA were studied in a university teaching hospital sleep laboratory. INTERVENTIONS: 36 hours of supervised sleep deprivation. MEASUREMENTS: Subjects' age, body mass index, neck circumference and Epworth Sleepiness Scale scores were measured; actigraphy and sleep diaries were used to estimate prior sleep debt before each sleep study. RESULTS: Sleep deprivation was found to significantly increase total sleep time, sleep efficiency, and rapid eye movement and slow-wave sleep time. Subjects with OSA showed a lower minimum oxygen saturation after sleep deprivation. However, subjects did not show a significantly different respiratory disturbance index, arousal index, or length of the longest apnea after sleep deprivation. CONCLUSIONS: Acute sleep deprivation did not worsen most OSA parameters as measured by polysomnography. A lower minimum oxygen saturation in mild OSA subjects after sleep deprivation may be important in patients with significant cardiorespiratory disease. More research is needed to assess whether daytime performance and function (eg, driving, sleepiness) is more greatly impaired in OSA subjects who are sleep deprived, compared to normal subjects who are sleep deprived.

Acute Disease↗