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PubMed2001

Short-term REM sleep deprivation effect on temperature rhythm of rats.

Circadian rhythm of body temperature (CRT) is altered in endogenous depression and many psychiatric disorders. Even the sleep pattern is disrupted. Sleep deprivation alleviates symptoms in depression. The present study was conducted to find the role of noradrenergic innervation to the pineal gland in bringing about the effect of REM sleep deprivation (REMSD) on the CRT. Adult male Wistar rats (n = 12) divided into 2 groups were used for the study. The group I rats (n = 6) underwent superior cervical ganglionectomy and the group II rats (n = 6) were sham ganglionectomised. After recovery rats were given REMSD for 48 hours. The CRT was measured in three periods of the study i.e. basal, post operative and post REMSD. The results indicated REMSD increased the Amplitude and Mesor of the CRT in both the groups which was shortlasting and reversible thus suggesting non sympathetic mediation of the pineal in bringing about the circadian rhythm alteration due to REMSD.

Animals↗
PubMed2001

Hypothalamo-pituitary-adrenal axis activity is related to the level of central arousal: effect of sleep deprivation on the association of high-frequency waking electroencephalogram with cortisol release.

The temporal and quantitative interrelationships between the hypothalamo-pituitary-adrenal (HPA) axis activity and the level of central arousal were studied in 10 healthy young men during daytime wakefulness. Two experimental sessions were conducted randomly between 09.00 and 18.00 h, once after nocturnal sleep and once after a night of total sleep deprivation. Spectral analysis of serial waking electroencephalography (EEG) from a short target fixation task repeated every 10 min was undertaken, along with an estimation of cortisol secretory profiles by deconvolution of plasma radioimmunoassay measures obtained from continuous blood withdrawal with regular sampling at a 10-min interval. Following nocturnal sleep, a temporal association between the HPA axis activity and the waking EEG activity was found, cortisol secretory rate following changes in frontal gamma (20-45 Hz) band power by 10 min (average R = 0.458, p < 0.001). Although it remained significant (average R = 0.276, p < 0.05), the association strength decreased significantly following total sleep deprivation (p < 0.05, Wilcoxon test). Cortisol plasma level, secretory rate and pulse amplitude were increased as well as waking EEG power in the delta (0.5-5.5 Hz), theta (5.5-8.5 Hz) and gamma frequency bands (all p values <0.05, Student t tests). The sleep deprivation-related increases in cortisol secretory rate and waking EEG gamma activity were quantitatively associated (R = 0.504, p < 0.05). These results support the existence of a common ultradian regulatory mechanism, co-ordinating HPA axis activity to the level of central arousal in man, which seems involved in the sleep deprivation-induced hyper-arousal.

Adrenal Glands↗
PubMed2003

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

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

Animals↗
PubMed1977

Further studies of the aggressive behavior induced by delta9-tetrahydrocannabinol in REM sleep-deprived rats.

The aggressive behavior induced by delta9-tetrahydrocannabinol in pairs of REM sleep-deprived rats was studied in five experiments by measuring dominant and submissive behavioral patterns. When 2 REM-deprived rats received delta9-THC, one of the animals displayed very aggressive postures, while its partner assumed incomplete defensive postures. The intensity of these behavioral postures was dose-dependent. In pairs composed of one REM-deprived rat injected with delta9-THC and one normal or one REM-deprived partner injected with control solution the deprived/drugged rat showed an aggressive posture and catatonia, or a strikingly bizarre behavior, while the control partner displayed typical defensive postures. The behavioral alterations induced in REM-deprived rats by amphetamine, LSD-25, and pentobarbital failed to provoke defense postures in the normal rats paired with them; however, apomorphine partially mimicked the delta9-THC-effects. It is concluded that in REM-deprived rats delta9-THC not only provokes aggressive behavior but also impairs the defensive-submissive behavioral patterns.

Aggression↗
PubMed1999

Circadian timed wakefulness at dawn opposes compensatory sleep responses after sleep deprivation in Octodon degus.

The circadian timing system in mammals is thought to promote wakefulness and oppose sleep drive that accumulates across the activity phase in diurnal and nocturnal species. Whether the circadian system actively opposes compensatory sleep responses in mammals with episodes of alertness consolidated at dawn and dusk is unknown. In the present study, an interaction between circadian timed arousal at dawn and compensatory sleep responses after sleep deprivation (SD) was examined in Octodon degus, a hystricomorph rodent with crepuscular episodes of wakefulness. Recovery sleep was compared after 6 hours and 12 hours of SD ending at either CT 21 or 12, just before the dawn, and just after the dusk crepuscular episodes of consolidated wakefulness, respectively. Total sleep time and NREM sleep after SD increased proportionally to the amount of sleep loss; however, compensatory sleep responses after SD were attenuated at CT 23, a circadian time when a crepuscular event of wakefulness occurs in this species. EEG slow-wave activity (SWA) and body temperature levels in the first two hours after 6 and 12 hours of SD ending at CT 12 were similar. However, both were significantly higher than after 12 hours of SD ending at CT 21, suggesting factors other than the amount of prior wake duration can influence SWA levels. This study provides evidence that the circadian arousal system opposes compensatory sleep responses at dawn by actively promoting wakefulness in this species.

Animals↗
PubMed1991

Biperiden administration in normal sleep and after rapid eye movement sleep deprivation in healthy volunteers.

Twenty-six healthy volunteers were randomly assigned to one of four groups. Groups Bip-4 and Bip-6, each with six subjects, received 4 and 6 mg of biperiden, respectively, and were studied on acclimatization, baseline, biperiden, and follow-up nights. Group REM-P (n = 7) and Group REM-Bip (n = 7) were studied on acclimatization, baseline, six nights of REM sleep deprivation, and one recovery (treatment) night with either placebo (group REM-P) or biperiden (group REM-Bip), and one follow-up night. Biperiden 4 and 6 mg increased REM sleep latency and biperiden 6 mg reduced REM sleep time. On the recovery night following REM sleep deprivation Group REM-P and REM-Bip showed an increase in sleep continuity. REM sleep time in the REM-P group was increased during the recovery (treatment) night (REM sleep recovery), while the REM-Bip group did not show a significant REM sleep increase during recovery (treatment) night. It was not until the follow-up night that REM sleep increased in the REM-Bip group.

Adult↗
PubMed2000

Prepro-hypocretin (prepro-orexin) expression is unaffected by short-term sleep deprivation in rats and mice.

The hypocretin/orexin ligand-receptor system has recently been implicated in the sleep disorder narcolepsy. During the dark (active) period, null mutants of the prepro-orexin (prepro-hypocretin) gene have cataplectic attacks and increased levels of both rapid eye movement (REM) and non-REM (NREM) sleep. Intracerebroventricular injection of one of the encoded neuropeptides, orexin-A, early in the light period increases wakefulness and reduces REM sleep in the rat, suggesting that this system may be involved in the normal regulation of sleep and wakefulness. To further test this hypothesis, we measured hypocretin (hcrt) mRNA levels by both Northern hybridization and Taqman analysis in mouse and rat hypothalamus after short-term (6 h) sleep deprivation (SD) and 2-4 hours after recovery from SD. Although our SD procedures effectively induced a sleep debt and increased c-fos mRNA expression in the cortex and hypothalamus as described by other investigators, we found that hcrt mRNA levels were not significantly changed in either species either after SD or after recovery from SD. If the hcrt system is involved in normal regulation of sleep and wakefulness, longer periods of SD may be necessary to affect hcrt mRNA levels or changes may occur at the protein rather than mRNA level. Alternatively, this system may also be involved in another function that counterbalances any SD-induced changes in hcrt mRNA levels.

Animals↗
PubMed1992

The effects of biperiden on nap sleep after sleep deprivation in depressed patients.

Sixteen patients with a major depressive disorder were allowed to take a nap at 5 A.M. after a period of total sleep deprivation. The patients were randomly assigned to biperiden or placebo treatment prior to the nap to test the hypothesis that anticholinergic medication is capable of preventing a nap-related worsening of mood. Total sleep deprivation positively influenced mood for the whole group. Contrary to expectations, the rate of nap-related relapses of mood did not differ between placebo- and biperiden-treated individuals, and biperiden did not significantly suppress rapid eye movement (REM) sleep. There was only a tendency for lower REM time after administration of biperiden compared to placebo. This unexpected result may be due to a high cholinergic tone in the patient group investigated and a high REM propensity in the early morning hours. Studies with more selective M1/M2 receptor antagonists are necessary to clarify whether nap-related changes of mood can be prevented by anticholinergic blockade.

Affect↗
PubMed2005

The impact of sleep deprivation on product quality and procedure effectiveness in a laparoscopic physical simulator: a randomized controlled trial.

BACKGROUND: To compare the impact of sleep deprivation after 24-hour duty (post-call) with that of 8-hour work (post-work) on product quality (PQ) and procedure effectiveness (PE) in a laparoscopic physical simulator. METHODS: Voluntary surgeons and nurses were pretested with the Epworth Sleepiness Scale (ESS) and Minimally Invasive Surgical Trainer-Virtual Reality (MIST-VR). Surgical task was suturing perforated ulcer on a foam stomach in a physical simulator. PQ and PE were measured by accuracy error (AE), tissue damage (TD) leak rate (LR), goal- (GDA) non-goal-directed actions (NGDA), and operating time (OT), respectively. Construct validity was assessed comparing measures when surgeons and nurses performed the surgical task. Inter-rater reliability (IRR) was assessed by Kendall's tau b coefficient. An 80% power parallel block randomization design at alpha = .05 required 60 subjects. RESULTS: Thirty-two post-call surgeons and 32 post-work surgeons were well matched for age, gender, practice duration, and ESS and MIST-VR scores. The amount of time slept in the previous 24 hours was 1.5 versus 6.5 hours (P < .05). AE (1.0 mm vs. .5 mm), TD (2.18 mm vs. 2.18 mm), LR (56.2% vs. 65.6%), GDA (33.5 vs. 32.5), NGDA (.56 vs. .31), and OT (381.0 seconds vs. 364.5 seconds) were not significantly different when 32 surgeons in the post-call arm were compared with their 32 counterparts in the post-work arm, respectively. Construct validity was shown by significant improvement in 4 outcome measures (AE 1.0 mm vs. 2.0 mm, P = .00001; GDA 32.5 vs. 39.0, P = .07, NGDA .43 vs. .96, P = .045; and OT 377.5 vs. 557.0, P = .0005) when 64 surgeons performed the task as compared to 64 nurses. Tau b for IRR was 1.0 (P < .0001) for AE, TD, LR, and OT, .75 (P = .325) for GDA, and .77 (P = .305) for NGDA. CONCLUSIONS: Sleep deprivation had no impact on the studied outcome measures of a surgical task performed in a laparoscopic simulator.

Adult↗
PubMed1984

Sleep deprivation and the physiological response to exercise under steady-state conditions in untrained subjects.

Seven physically untrained subjects underwent 72 h total sleep deprivation, followed a baseline day. Daily, at 0400 and 1600 h, subjects pedalled on a bicycle ergometer under individually set work loads of 40, 60, and 80% VO2max. This was not a study oriented towards endurance but towards capacity, requiring steady-state measurement. From assessments of heart rate, VO2 and VCO2 were calculated: VO2max, gross mechanical efficiency, VO2 at a heart rate of 150, and respiratory quotient. To assess possible training effects, a control group underwent identical procedures except that they slept at night and had the morning measure delayed until 0830 h. A series of statistical models were applied to the data, which centered on quantifying the inherent underlying variability, to estimate the level any main effect had to reach to become significant. the analysis showed that the noise level was small enough for any real effect of importance to have been detected, with a reasonably large probability. No statistically significant effects were found for any of the parameters with respect to conditions, days, and time. The main significant outcome was with mechanical efficiency, which displayed greater variability during sleep deprivation. Both groups displayed similar trends in training effects. It was concluded that the physiological ability to do work of the type and duration used here was not adversely affected by 72 h of sleep loss.

Adult↗
PubMed1985

Paradoxical sleep deprivation and the immobility response in the rat: effects of desipramine and phentolamine.

A series of experiments was conducted on the presumption that instrumental deprivation of paradoxical sleep (PS) has an effect comparable with that of antidepressant drug treatment in a behavioral paradigm, Porsolt's forced swim test. After long-term PS deprivation, we studied the duration of immobility, which can be markedly reduced by antidepressant drugs, using both the platform and the pendulum technique. In addition to a small common effect for PS deprivation, differences confirming the platform-pendulum controversy were also detected. Nonspecific platform effects are considered to explain these differences. In a second experiment it was shown that the small PS deprivation effect can be enlarged by desipramine treatment, suggesting similarities in the underlying mechanisms. In the third experiment, just before the end of the deprivation, phentolamine, a drug that blocks the rebound of PS, was administered. It reduced the effect of pendulum PS deprivation, suggesting that PS propensity is an important factor in the reduction of duration of immobility.

Animals↗
PubMed1978

[EEG after sleep deprivation in patients with unequivocal and equivocal epileptic seizures, as well as no epileptic patients (author's transl)].

In 107 patients the EEG after sleep deprivation was performed. The patients have been divided in three groups: 1) with clinically unequivocal, 2) equivocal and 3) no epileptic seizures. All the patients where subdivided in those with and those without anticonvulsive medication. In patients with a previous normal EEG, sleep deprivation had the most activating effect regarding focal or generalized spikes or spike wave complexes in group one. However, patients without medication showed more often activation compared with untreated patients. In the second group the activation was less pronounced, again presenting the same relation between treated and untreated patients. Patients with no seizures as well as a control group of 20 volunteers had no activation at all.

Adolescent↗
PubMed1987

Rem sleep deprivation in an experimental model of Parkinson's disease.

Previous investigations have shown that REM sleep deprived (REM SD) rats display an enhanced response to dopamine agonists. This action seems to be mediated through a supersensitivity of dopamine post-synaptic receptors. Accordingly, REM SD was performed on rats with an experimental model of Parkinson's disease. The animals were bilaterally lesioned in the nigrostriatal pathway through a stereotaxically directed electrical current. Seven days after the surgery the animals were REM SD for 72 hours and immediately after the end of this period were observed in an open field for ambulation, rearing, grooming, and latency. In comparison with non-deprived rats there was a significant increase in ambulation and rearing, a response that appeared again after a second REM SD period on day 21th after the surgery. These data of improvement of two parameters of an experimental model of Parkinson's disease suggest that SD may be useful in this condition.

Animals↗
PubMed1996

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

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

Adult↗
PubMed1982

Another cause of reversible dementia: sleep deprivation due to prostatism.

A case history is presented of a patient with treatable dementia of unusual pathogenesis. Fear of urinary incontinence associated with nocturia and urgency caused the patient to deprive himself of sleep, resulting in slowed mentation and apathy that was diagnosed as chronic organic brain syndrome for approximately one year. When his benign prostatic hypertrophy was surgically corrected, the patient allowed himself normal sleep, and the "chronic brain syndrome" cleared completely.

Aged↗
PubMed1989

Effects of sleep deprivation on human immune functions.

The effect of 40 h of wakefulness on a variety of immunological parameters in the peripheral blood from 10 normal male subjects was studied. Sleep deprivation led to enhanced nocturnal plasma interleukin 1-like and interleukin 2-like activities. The rise in nocturnal response of lymphocytes to pokeweed mitogen stimulation during a normal 24 h sleep-wake cycle was delayed by sleep deprivation, but the response to the phytohemagglutinin mitogen was unaffected. With resumed nocturnal sleep, there was a prolonged decline in natural killer cell activity (measured as spontaneous cytolytic activity for human tumor cells) and return of an increased response to pokeweed mitogen. The altered patterns in immune functions occurred independently of the cortisol circadian rhythm, which remained unchanged.

Adult↗