SEARCH · PubMed Health

Results for “SLEEP DEPRIVATION”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources

PubMed1982

[Differentiation of 2 paroxysmal reaction types in the EEG after sleep deprivation].

In the EEG after sleep deprivation paroxysms with spikes and spike wave-complexes as well as paroxysms with slow waves can be seen. The paroxysms occur either spontaneously (it means at any time during the record) or at moments of shifting vigilance. These moments are characterized by sudden changes of the EEG frequency for instance by transition from one sleep stage to another. Paroxysms with spikes or spike wave-complexes occur mainly at the transition from lower to higher levels of vigilance and are accompanied by abnormal K-complexes and abnormal photosensibility. Paroxysms of slow waves occur mainly at the transition from higher to lower levels of vigilance, abnormal K-complexes and abnormal photosensitivity are lacking but in some cases the before diffuse abnormal EEG is improved after sleep deprivation. It assumed that we are dealing with two different types of reaction.

Arousal↗

PubMed1995

Atropine increases pilocarpine-induced yawning behavior in paradoxical sleep deprived rats.

Paradoxical sleep (PS) deprivation has been suggested to induce supersensitivity of postsynaptic dopamine (DA) receptors and subsensitivity of acetylcholine (ACh) receptors. Yawning behavior is reduced after PS deprivation and is believed to result from an interaction between ACh and DA systems. Concomitant treatment of PS deprived animals with DA agonists reverses PS deprivation effects on stereotypy and aggressiveness. To examine this possibility on yawning behavior, rats were treated, during the deprivation period, with atropine, methamphetamine, haloperidol or distilled water. Following PS deprivation, rats were injected with apomorphine or pilocarpine and number of yawns was recorded. Atropine increased yawning of PS deprived rats induced by pilocarpine, but not by apomorphine. Treatment with methamphetamine and haloperidol did not change PS deprivation effect on pilocarpine- and apomorphine-induced yawning. The data suggest that reversal of PS deprivation-induced yawning inhibition is mediated distinctly by both acetylcholine and dopamine systems.

Animals↗

PubMed2001

Effect of sleep deprivation on motor performance in patients with Parkinson's disease.

Animal research provides evidence that sleep deprivation influences the dopamine system. Knowledge about the effect of sleep deprivation on motor performance in patients with Parkinsons disease is scarce. This study examines the influence of total and partial sleep deprivation compared to normal sleep on motor state and performance in Parkinson's disease. Fifteen nondepressed patients with Parkinson's disease underwent one night of total sleep deprivation (TSD), one night of partial sleep deprivation (PSD) after 3 a.m., and one control night of normal sleep (S), performed in a random, nonconsecutive order. Over a period of 3 hours the following morning, motor evaluations (United Parkinson's Disease Rating Scale, [UPDRS] and tapping rate) were performed before and every 30 minutes after intake of the usual morning dopaminergic drug dose. All patients underwent polysomnography apart from the sleep deprivation protocol. Mean UPDRS motor scores and tapping velocities did not differ significantly after each of the schedules, but a subgroup of four patients improved their motor score after partial sleep deprivation. These data do not confirm previous findings of an overall positive influence of sleep deprivation on motor function in Parkinson's disease. However, the results indicate that different response types to sleep deprivation may exist and that a subgroup of patients could benefit from partial sleep deprivation.

Aged↗

PubMed1990

Effect of total sleep deprivation on 5'-deiodinase activity of rat brown adipose tissue.

Prolonged sleep deprivation of the rat produces a progressive increase in energy expenditure and an eventual decrease in body temperature, which suggests a profound derangement in thermoregulation. Because increased thermogenic activity in brown adipose tissue (BAT) is a likely mechanism mediating the observed increase in energy expenditure, we focused our attention on the effect of total sleep deprivation on BAT type II 5'-deiodinase (5'D-II), since its activation indicates BAT stimulation and is essential for full BAT thermogenic response. Five euthyroid rats were subjected to total (92%) sleep deprivation (euD-rats). Sharing the sleep deprivation apparatus, yoked control rats (euC-rats) received the same degree of physical stimulation as the D-rats, but were only partially (25%) sleep deprived. Additional cage controls (euCC-rats) were housed in the same room. Since during sleep deprivation the animals undergo a reduction in plasma T4 concentration and inability to maintain body temperature heralds death, an identical study was performed in five trios of hyperthyroid rats (hyperD-, hyperC-, and hyper CC-rats) given daily ip injections of 15 micrograms T4/100 g BW, 10 days before and throughout the deprivation period. Experiments were carried out at an ambient temperature of 29 C, close to thermoneutrality for rats. Sleep deprivation in hyperD-rats was maintained until death seemed imminent (9-14 days), and in euD-rats for 12-15 days. Sleep deprivation induced a significant increase in BAT 5'D-II activity in both hyperD- and euD-rats compared with that in euCC-rats (P less than 0.01). BAT 5'D-II in euC-rats was also significantly higher than that in euCC-rats (P less than 0.05), probably because they were partially sleep deprived. BAT 5'D-II activity in hyperD-rats was increased compared to that in both hyperC- and hyperCC-rats (P less than 0.05), in which the activity was slightly but not significantly lower than that in euCC-rats. No significant differences were observed in liver and kidney type I 5'-D (5'D-I) and in pituitary 5'D-II among euD-rats, euC-rats, and euCC-rats. As expected, the hyperthyroid groups (hyperD-rats, hyperC-rats, and hyperCC-rats) had significantly higher kidney 5'D-I and lower pituitary 5'D-II than the euCC-rats. Liver 5'D-I was also significantly increased in the hyperC-rats and hyperCC-rats, but not in the hyperD-rats. These observations indicate that total sleep deprivation is associated with a marked increase in BAT 5'D-II activity in both euthyroid and hyperthyroid rats.(ABSTRACT TRUNCATED AT 400 WORDS)

Acclimatization↗

PubMed1999

Effects of 48 hours sleep deprivation on human immune profile.

It is a common belief that sleep deprivation increases the susceptibility to diseases. In order to evaluate the effects of sleep deprivation on immune profile in humans, peripheral venous blood was obtained from sixteen healthy young male volunteers. Ten of the volunteers underwent 48 hours of sleep deprivation and the other six maintained their regular sleep schedule and acted as controls. The first blood samples were taken at the end of the first polysomnographic recording at 8:00 a.m. After this sampling, ten subjects were sleep deprived for 48 hours in sedentary conditions. The second and third blood samples were taken at the 24th and 48th hours. The subjects were recorded again to verify rebound effects of sleep deprivation after the third blood sampling. In this second polysomnographic recording, all sleep-deprived subjects showed slow wave and REM sleep rebound. The last blood samples were taken at the 72nd hour of study at 8:00 a.m. CD4, CD8, CD5, CD16, CD19 surface antigen positive lymphocyte subsets, serum IgG, IgM, and cortisol levels were assessed in all samples. Our results showed that the proportion of NK cells were decreased during sleep deprivation and returned to normal values after recovery sleep. In the control group, we did not observe any changes in the same direction as the sleep-deprived group.

Adult↗

PubMed2001

The effect of total sleep deprivation on cognitive functions in normal adult male subjects.

This study was conducted to evaluate the effect of acute sleep deprivation on cognitive functions. A total of 18 healthy right handed males were deprived of sleep for 24 hours. Luria-Nebraska Neuropsychological Battery and calculation & digit-span subtest of K-WAIS were administered before and after sleep deprivation in order to examine the changes of cognitive functions. There were no differences in freedom from distractibility, tacile function, visual function, reading, writing, arithmetic and intellectual process function. However, the cognitive functions such as motor, rhythm, receptive & expressive speech, memory and complex verbal arithmetic function were decreased after sleep deprivation. All of these functions are known to be related to the right anterior hemisphere. For localization scales, the scores of right frontal and right temporal dysfunction scale were increased after sleep deprivation. These results indicate that sleep deprivation has a negative effect on cognitive functions, especially those associated with right anterior hemisphere or subcortical areas.

Adult↗

PubMed1998

Heterogeneous effects of rapid eye movement sleep deprivation on binding to alpha- and beta-adrenergic receptor subtypes in rat brain.

Quantitative receptor autoradiography was used to map alterations in binding to alpha1-, alpha2-, beta1- and beta2-adrenergic receptors throughout the brain of rats deprived of rapid eye movement sleep for 96 h. Binding of [3H]prazosin to alpha1 sites, while not significantly different in any of 46 brain regions examined, showed a clear overall tendency towards decreased values after sleep deprivation. [3H]UK-14,314-labeled alpha2 binding sites were not significantly affected by sleep deprivation in any of 91 brain regions analysed, despite a trend towards increased values. In contrast, beta-adrenergic binding was significantly reduced throughout the brain. Binding to beta1 sites labeled by [125I]iodopindolol in the presence of ICI-11855 was significantly reduced in 13 of 69 brain areas examined; binding to beta2 sites labeled by [125I]iodopindolol in the presence of CGP-20712A was likewise reduced throughout the brain and significantly so in 25 of the 72 brain areas analysed. Rank ordering of the binding changes indicated that reductions in beta1 vs beta2 binding were maximal in different brain areas. This pattern of results may reflect a particular configuration of effects specifically associated with sleep loss stress. The results are consistent with evidence of persisting noradrenergic cell activity during sleep deprivation. The observed heterogeneity of effects suggests that not all norepinephrine receptors are equally affected by rapid eye movement sleep deprivation.

Animals↗

PubMed2005

Sleep deprivation and daily torpor impair object recognition in Djungarian hamsters.

Sleep has been shown to play a facilitating role in memory consolidation, whereas sleep deprivation leads to performance impairment both in humans and rodents. The effects of 4-h sleep deprivation on recognition memory were investigated in the Djungarian hamster (Phodopus sungorus). Because sleep during the first hours after daily torpor has many similarities to recovery from sleep deprivation, the effects of spontaneous torpor on object recognition were also assessed. A 4-h sleep deprivation, starting immediately after an object learning task, diminished the ability of the hamsters to: (1) discriminate between an already encountered object (target) and a novel object presented in a novel context, (2) retrieve a target within a complex spatial scene, and (3) detect a spatial rearrangement of familiar objects in a familiar context. Plasma stress hormone levels were similar in sleep-deprived and control hamsters. The occurrence of a daily torpor episode during retention was associated with impaired old-new object discrimination performance in the more effortful complex spatial scene task only, and in a two-object choice situation in a novel context no torpor-induced deficit was found. Our results show that post learning sleep deprivation and daily torpor induce a deficit in familiar object retrieval performance in a complex spatial scene, while sparing familiarity-based recognition and novelty processing. Sleep deprivation during the first 4 h of memory consolidation hampered also recency memory for discrete objects. Stress was not a factor contributing to the sleep deprivation-induced impairment.

Adaptation, Physiological↗

PubMed2006

Effects of sleep deprivation on the development of autoimmune disease in an experimental model of systemic lupus erythematosus.

Sleep is hypothesized to play a restorative role on immune system. In addition, disturbed sleep is thought to impair host defense mechanisms. Chronic sleep deprivation is a common occurrence in modern society and has been observed in a number of chronic inflammatory conditions, such as systemic lupus erythematosus (SLE). New Zealand Black/New Zealand White (NZB/NZW) F1 mice develop an autoimmune disease that strongly resembles SLE in humans, exhibiting high titers of antinuclear antibodies associated with the development of rapidly progressive and lethal glomerulonephritis. On the basis of this evidence, the present study examined the onset and progress of lupus in as-yet healthy female mice submitted to sleep deprivation. Sleep deprivation was accomplished by two 96-h periods in the multiple-platform method when mice were 10 wk old, and they were observed until 28 wk of age. Blood samples were collected from the orbital plexus fortnightly to evaluate serum antinuclear antibodies and anti-double-stranded DNA. Proteinuria and longevity as well as body weight were also assessed. The results indicated that mice submitted to sleep deprivation exhibited an earlier onset of the disease, as reflected by the increased number of antinuclear antibodies. However, no statistical difference was found in the other parameters analyzed. According to these results, sleep deprivation could be considered as a risk factor for the onset but not for the evolution of the disease.

Animals↗

PubMed1983

The diagnostic value of the sleep EEG with and without sleep deprivation in patients with atypical absences.

Hitherto it has not been known whether or not the sleep EEG after sleep deprivation is more effective than the simple or drug-induced sleep EEG. To investigate this, we recorded for 32 patients both sleep EEGs without sleep deprivation and, on the following day, sleep EEGs after 24 h of sleep deprivation. All the patients had atypical absences which were almost exclusively combined with generalized seizures or some other seizure types. All patients were receiving antiepileptic therapy. Sleep without sleep deprivation was induced by oral administration of 2 mg/kg body weight Protactyl (promazine hydrochloride). In patients showing no epileptic activity in the routine EEG, epileptic discharges could be provoked in 78% without sleep deprivation and in 72% after sleep deprivation. Epileptic activity was already seen in 28.1% of the cases in the awake EEG without sleep deprivation, recorded immediately before the sleep EEG, and in 50% of the cases in the awake EEG after sleep deprivation. It is unlikely that promazine hydrochloride in the dose used here has an additional inherent provocative effect. Generalized spike-and-wave complexes or sharp slow wave complexes which were combined twice with foci and runs of rapid spikes were recorded. In the sleep EEG without sleep deprivation, epileptic discharges were seen in the somewhat shallower stages (C leads to A leads to B leads to D) and, in the sleep EEG after sleep deprivation, in the somewhat deeper stages (D leads to C leads to B leads to A). Fewer epileptic discharges were elicited in patients who were older at the time of their first seizure. The illness was mild in patients whose sleep EEGs showed no epileptic activity. It is concluded that, as a rule, it is not necessary to record an EEG after sleep deprivation in patients with atypical absences whose routine EEGs show no epileptic activity; the drug-induced sleep EEG shows the same provocative effect.

Adolescent↗

PubMed2006

Glucocorticoid receptor-dependent desensitization of 5-HT1A autoreceptors by sleep deprivation: studies in GR-i transgenic mice.

UNLABELLED: Sleep deprivation for one night induces mood improvement in depressed patients, an action that probably involves the serotonergic (5-HT) system. In animals, sleep deprivation and pharmacologic treatment with antidepressants exert similar effects on 5-HT neurotransmission, notably functional desensitization of 5-HT1A autoreceptors located on 5-HT neurons in the dorsal raphe nucleus (DRN). However, in stressful conditions, corticosterone can also induce a desensitization of these autoreceptors. STUDY OBJECTIVES: To investigate the mechanisms of this adaptation during sleep deprivation and the possible involvement of corticosterone, we studied the effects of an 18-hour sleep deprivation, by forced locomotion, on 5-HT1A receptor-mediated firing response of DRN 5-HT neurons in transgenic mice with impaired glucocorticoid-receptor expression (GR-i) and in wild-type animals. We also examined the effects of chronic treatment with the antidepressant drug fluoxetine in the same paradigm. MEASUREMENTS AND RESULTS: In both wild-type and GR-i mice, the 18-hour sleep deprivation or fluoxetine treatment had no effect on the spontaneous firing of 5-HT neurons recorded under anesthesia. However, sleep deprivation decreased the potency of the 5-HT1A agonist 8-OH-DPAT to inhibit 5-HT neuronal firing in wild-type mice, whereas it had no effect in GR-i animals. Conversely, after chronic fluoxetine treatment, the induced reduction of this 5-HT1A autoreceptor-driven response was of larger amplitude in GR-i than in wild-type mice. CONCLUSIONS: These data suggest that glucocorticoid-receptor activation by corticosterone participates in the antidepressant-like adaptive changes in 5-HT1A autoreceptors in sleep-deprived mice. On the other hand, GR-i animals exhibited enhanced 5-HT1A autoreceptor desensitization induced by fluoxetine, in line with data in other animal models of depression.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1997

Effects of alcohol on sleep parameters of sleep-deprived healthy volunteers.

Both partial and total sleep deprivation frequently result in a rebound of paradoxical sleep (PS), as well as of slow-wave or delta sleep. Acute administration of ethanol inhibits PS in normal volunteers. This effect is dose-dependent and consists of increased latency to and reduced duration of paradoxical sleep. It has also been shown that PS rebound may occur on the same night, as blood alcohol concentration (BAC) declines. The present study examined the effects of sleep deprivation prior to ethanol administration on nocturnal-sleep parameters in healthy male volunteers. Polysomnograms were performed with a randomized, crossover design on baseline, placebo, post-placebo, ethanol (0.9 g/kg), and post-ethanol recovery nights. Subjects were submitted to partial (PSD) (n = 6) or total (TSD) (n = 6) sleep deprivation for 40 hours before placebo or ethanol conditions. Results evidenced a PS inhibition after ethanol treatment in both deprivation groups, despite their sleep debt (PSD, placebo = 103.7 minutes and ethanol = 72.7 minutes; TSD, placebo = 111.8 minutes and ethanol = 76.6 minutes). This inhibition was BAC-dependent and specific to PS, since delta sleep remained unaltered. These effects could be due to the reduction of cholinergic release and/or glutamatergic inhibition, both of which modulate acetylcholine release.

Adult↗

PubMed1991

General considerations of sleep and sleep deprivation.

The state of affairs in the field of sleep deprivation has been discussed in this chapter. Special emphasis was placed on total sleep deprivation, a domain in which the most important work has been done since the dawning of this century, and especially during the 'golden years' between 1955 and 1975. After a discussion of the biorhythmical aspects, the general condition of sleep deprived subjects was pointed out. Psychological-psychiatric changes and impairment of performance were further topics of discussion, followed by sections on EEG, neurological, autonomic and metabolic changes. The relationship of SD to epileptic phenomena and endogenous depression has been considered. The characteristics of recovery sleep have also been presented. Most of the author's impressions are based on personal data, and especially on 2 subjects who underwent most elaborate testing. A discussion of partial sleep deprivation and selective sleep deprivation is also included.

Brain↗

PubMedDate not supplied

Differential behavioural effects of two instrumental paradoxical sleep deprivation techniques in rats.

Behavioural consequences of deprivation of paradoxical sleep were studied by placing rats in a light-dark preference box following 0, 24, 48, and 72 h of treatment and after 96 h, following a 24 h recovery period. Paradoxical sleep deprivation was induced either by the platform or pendulum technique, and three control groups were tested on the same regime. The number of crossings between parts of the box was taken as an estimation of locomotor activity, while time spent in the various compartments of the preference box was also measured. Surprisingly, behavioural consequences were found to be dependent on the technique employed. An increase of ambulation and decrease of dark preference were obtained when paradoxical sleep was deprived by the platform technique, but no changes were noticed following exposure to the pendulum procedure. It is suggested that non-specific effects rather than PS deprivation per se are responsible for the behavioural changes found after platform deprivation.

Animals↗

PubMed2005

Decreased cortical response to verbal working memory following sleep deprivation.

STUDY OBJECTIVE: To investigate the cerebral hemodynamic response to verbal working memory following sleep deprivation. DESIGN: Subjects were scheduled for 3 functional magnetic resonance imaging scanning visits: an initial screening day (screening state), after a normal night of sleep (rested state), and after 30 hours of sleep deprivation (sleep-deprivation state). Subjects performed the Sternberg working memory task alternated with a control task during an approximate 13-minute functional magnetic resonance imaging scan. SETTING: Inpatient General Clinical Research Center and outpatient functional magnetic resonance imaging center. PATIENTS OR PARTICIPANTS: Results from 33 men (mean age, 28.6 +/- 6.6 years) were included in the final analyses. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: Subjects performed the same Sternberg working memory task at the 3 states within the magnetic resonance imaging scanner. Neuroimaging data revealed that, in the screening and rested states, the brain regions activated by the Sternberg working memory task were found in the left dorsolateral prefrontal cortex, Broca's area, supplementary motor area, right ventrolateral prefrontal cortex, and the bilateral posterior parietal cortexes. After 30 hours of sleep deprivation, the activations in these brain regions significantly decreased, especially in the bilateral posterior parietal cortices. Task performance also decreased. A repeated-measures analysis of variance revealed that subjects at the screening and rested states had similar activation patterns, with each having significantly more activation than during the sleep-deprivation state. CONCLUSIONS: These results suggest that human sleep-deprivation deficits are not caused solely or even predominantly by prefrontal cortex dysfunction and that the paretal cortex, in particular, and other brain regions involved in verbal working memory exhibit significant sleep-deprivation vulnerability.

Adolescent↗

PubMed1993

Nutritional and metabolic adaptations to prolonged sleep deprivation in the rat.

To understand how and why sleep deprivation is physically harmful, we explored the possible causal relationship between its two main effects, 1) negative energy balance and 2) a composite of symptoms that resemble protein malnutrition, both of which occur despite increased food consumption. We provided balanced diets augmented with either protein or calories (by increased fat content) to freely moving rats. Interactions between sleep deprivation symptoms and energy and protein supplies were assessed from measurements of body weight regulation, consumption of macronutrients, clinical chemistry and hematology profiles, and physical appearance. The results indicate that sleep deprivation causes malnutrition, which is secondary to increased energy expenditure. Even though food consumption remained normal in sleep-deprived rats fed a diet of high protein-to-calorie ratio, body weight loss was more than 16% of baseline, development of skin lesions was hastened, and longevity was shortened by 40% compared with sleep-deprived rats fed the calorie-augmented diet. Food consumption of the calorie-fed rats was lower during baseline than that of the protein-fed group but during sleep deprivation increased to amounts 250% of normal without net body weight gain. Despite a fat-laden diet the calorie-fed hyperphagic group did not have abnormal levels of plasma cholesterol, triglycerides, or glucose, indicating accelerated turnover of nutrients. As would be consistent with calorie malnutrition, pronounced clinical chemistry or hematological abnormalities were not found in any group. Beneficial effects of the calorie-augmented diet are attributed to 1) caloric density of fat, 2) induction of hyperphagia, and 3) efficiency of utilization of fat. We conclude that diet composition interacts strongly with sleep deprivation, affecting the time course and development of pathologies, whereas it exerted negligible influence on body weight regulation under normal conditions.

Adaptation, Physiological↗

PubMed2006

Total sleep deprivation can increase vestibulo-ocular responses.

The effect of sleep deprivation on the vestibular function is largely unknown. Some studies have found that postural balance or vestibular reflexes are decreased in sleep-deprived subjects while others found no change. The aim of this study was to evaluate the effect of sleep deprivation on the vestibulo-ocular reflex (VOR). Horizontal eye movements were recorded in healthy subjects during earth vertical axis rotation in darkness once after an ordinary night sleep and once after 26-29 h of sleep deprivation. In the first experiment (n = 8), for which rotation was a 60 degrees s(-1) velocity step, sleep deprivation induced a significant increase in VOR gain. In the second experiment (n = 12), for which rotation was sinusoidal (0.2 Hz +/- 25 degrees s(-1)), sleep deprivation induced no significant modification in VOR gain. The difference between the two studies was the abrupt onset of the step stimulation in comparison with the sinusoidal rotation. Because of its unexpected onset and the potential threat to postural balance, the step stimulation may activate the system specialized in reorienting attention towards salient or behaviourally relevant events. This system includes the right temporoparietal cortex, an area also involved in VOR control. A number of studies have found that sleep deprivation alters the activity of this cortical area during attentional tasks. It is therefore our hypothesis that the difference between the effects of these two vestibular stimulations results from a sleep deprivation-induced modulation of the right temporoparietal cortex.

Adult↗

PubMed1997

Rapid eye movement (REM) sleep deprivation reduces rat frontal cortex acetylcholinesterase (EC 3.1.1.7) activity.

Rapid eye movement (REM) sleep deprivation induces several behavioral changes. Among these, a decrease in yawning behavior produced by low doses of cholinergic agonists is observed which indicates a change in brain cholinergic neurotransmission after REM sleep deprivation. Acetylcholinesterase (Achase) controls acetylcholine (Ach) availability in the synaptic cleft. Therefore, altered Achase activity may lead to a change in Ach availability at the receptor level which, in turn, may result in modification of cholinergic neurotransmission. To determine if REM sleep deprivation would change the activity of Achase, male Wistar rats, 3 months old, weighing 250-300 g, were deprived of REM sleep for 96 h by the flower-pot technique (N = 12). Two additional groups, a home-cage control (N = 6) and a large platform control (N = 6), were also used. Achase was measured in the frontal cortex using two different methods to obtain the enzyme activity. One method consisted of the obtention of total (900 g supernatant), membrane-bound (100,000 g pellet) and soluble (100,000 g supernatant) Achase, and the other method consisted of the obtention of a fraction (40,000 g pellet) enriched in synaptic membrane-bound enzyme. In both preparations, REM sleep deprivation induced a significant decrease in rat frontal cortex Achase activity when compared to both home-cage and large platform controls. REM sleep deprivation induced a significant decrease of 16% in the membrane-bound Achase activity (nmol thiocholine formed min-1 mg protein-1) in the 100,000 g pellet enzyme preparation (home-cage group 152.1 +/- 5.7, large platform group 152.7 +/- 24.9 and REM sleep-deprived group 127.9 +/- 13.8). There was no difference in the soluble enzyme activity. REM sleep deprivation also induced a significant decrease of 20% in the enriched synaptic membrane-bound Achase activity (home-cage group 126.4 +/- 21.5, large platform group 127.8 +/- 20.4, REM sleep-deprived group 102.8 +/- 14.2). Our results suggest that REM sleep deprivation changes Ach availability at the level of its receptors through a decrease in Achase activity.

Acetylcholine↗