Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SLEEP DEPRIVATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 955 records · Page 53Linked to original sources
PubMed1980

Study on the effects of L-5HTP on the stages of sleep in man as evaluated by using sleep deprivation.

The effects of L-5HTP 200 mg on the EEG sleep pattern were investigated in normal subjects. When L-5HTP 200 mg was orally administered, only % S1 significantly decreased in comparison with the baseline. There was no change in any sleep stage on the first recovery night. On the second recovery night, % S1 significantly decreased, while % SR increased significantly. SWS did not show any change. The effects of L-5HTP 200 mg were investigated on the first recovery night after one night of sleep deprivation. SWS significantly increased on the first recovery night when a placebo was given, while this rebound increase of SWS disappeared and % S2 significantly increased on the first recovery night when L-5HTP was given. % SR significantly increased on the next night after the L-5HTP night.

5-Hydroxytryptophan↗
PubMed2003

Human circadian melatonin rhythm phase delay during a fixed sleep-wake schedule interspersed with nights of sleep deprivation.

The human circadian pacemaker, with an intrinsic period between 23.9 and 24.5 hr, can be reset by low levels of light. Biomathematical models of the human clock predict that light-dark cycles consisting of only approximately 3.5 lux during 16 hr of wakefulness and 0 lux during 8 hr of sleep should entrain approximately 45% of the population. However, under real-life conditions, sleep-wake schedules and the associated light-dark exposures are often irregular. It remains unclear whether the phase of the pacemaker would remain stable under such conditions. We investigated the stability of the circadian phase in dim light by assessing the plasma melatonin rhythm during nine consecutive circadian cycles. Ten subjects were scheduled to sleep for 8 hr (0.03 lux) and to be awake for 16 hr (5-13 lux) during all days except on days 4 and 8, during which the subjects were sleep deprived for 40 hr (5-13 lux), either in a sitting/standing or supine body posture. In all subjects, the phase of the melatonin rhythm occurred at a later clock time on day 9 than on day 2 (average delay: 1.4 hr). Largest delays in the melatonin onset were observed in subjects with low amplitude melatonin rhythms. The area under the curve during active melatonin secretion was significantly reduced when subjects were sleep deprived in the 40-hr supine body posture condition compared with either the 40-hr sitting/standing sleep deprivation (SD) or the ambulatory condition under non-SD conditions. Posture differences did not significantly affect the relative phase position of the melatonin profiles. The data indicate that under conditions of reduced zeitgeber strength, the phase of the human circadian pacemaker, using plasma melatonin as a marker, can be phase delayed by one night of SD and the associated dim light exposure.

Biological Clocks↗
PubMed1994

The intrinsic effects of sarmazenil on sleep propensity and performance level of sleep-deprived subjects.

The effect of two dosages of sarmazenil (RO 15-3505) on sleep propensity and performance was investigated in a double-blind, placebo-controlled paradigm. The design included three 24-h testing periods, separated by at least one 7-day rest period, commencing after 24-h of sleep deprivation. Twelve normal, healthy, adult males (mean age 27 +/- 2.8 years) were paid to participate. During the experimental periods, they came to the sleep laboratory at 2100 hours and spent the night awake under close supervision. At 0700 hours, a schedule of 7 min "attempting" sleep in bed, 13 min awake outside the bedroom, began. This schedule was maintained for 24 h. Repeated administrations of 1 mg and 2 mg sarmazenil significantly reduced the 24-h levels of total sleep. This was particularly evident during the period 0700-2300 hours. Sarmazenil also significantly improved reaction time and tended to increase the number of correct responses in the "categories search" task. Sarmazenil tended to improve reaction time in the "Stroop" test but this was significant only for the "easy" version of the test during the night.

Adult↗
PubMed1989

[Disturbance of sports performance after partial sleep deprivation].

The changes in cardiac and ventilatory responses were measured in 7 endurance athletes during physical exercise on a bicycle ergometer, taking place after a control night and after a night with partial sleep deprivation in the middle of the night. The results show that, despite the maximal work load was not modified with control, heart rate, ventilation and VE/VO2 ratio (ERO2) were greater at the submaximal (75% of the VO2 max) and maximal work load and oxygen consumption decreased at maximal work, after the night of partial sleep deprivation as compared to the control. These findings suggest that acute sleep loss may contribute to alter the endurance performance by impairment of aerobic pathways.

Adult↗
PubMed2000

The effects of body posture on resting electroencephalographic activity in sleep-deprived subjects.

OBJECTIVE: This study examined the effects of posture on the resting electroencephalographic (EEG) activity of sleep-deprived volunteers. METHODS: EEG data were collected under two conditions at 13 separate time points. Testing was performed while subjects remained in a normal seated position and then repeated while subjects stood upright. RESULTS: Results indicated that delta and theta activity progressively increased as a function of sleep loss, and that standing upright attenuated this effect. CONCLUSIONS: These results suggest that an upright posture increases EEG arousal and may be useful for counteracting fatigue in sleep-deprived individuals.

Adult↗
PubMed2003

Gene expression during sleep, wakefulness and sleep deprivation.

Studies conducted on genes expression through the sleep-wake cycle and after sleep deprivation have revealed a number of genes that are more active during wakefulness/prolonged wakefulness than sleep, but also a few genes that are more active during sleep than wakefulness. Gene expression profiles during a specific vigilance state can be effectively monitored using microarrays, and when comparing profiles under different vigilance states, state-specific gene expression patterns can be precipitated. As such approach is random, and does not include any assumptions as to which genes would be expressed, it offers a non-biased view on the participation of different factors in the regulation of vigilance states. Combining results from different species offers a powerful tool for the analysis of genes that are involved in sleep-wake cycle regulation. The results of such assays are dependent on what area the tissue for the analysis is collected and the time point of the collection in respect to the duration of the specific vigilance state.

Animals↗
PubMed1995

REM sleep deprivation alters dopamine D2 receptor binding in the rat frontal cortex.

REM sleep deprivation (RSD) of rats results in facilitation of dopaminergic behavior and an increase in striatal D2 receptor density. To determine whether RSD results in changes in D2 receptor in other brain regions, receptor affinity (Kd) and density (Bmax) were measured in the anteromediofrontal (AM), cingulate (CN), and sulcal cortex (SL) in four groups of rats: 1), RSD96 group (RSD for 96 h; small pedestal/water tank method), 2) RSD24 group (large pedestals for 72 h then small pedestals for 24 h), 3) tank control group (TC; large pedestals for 96 h), and 4) cage control group. In separate groups, ambulation was recorded for 30 min following treatments. Group RSD96 showed an increase in activity compared to TC, and TC was increased compared to CC (p < 0.05 for all). In group RSD24, the AM showed an increase in Bmax and Kd (p < 0.05), but there were no effects by RSD96. In the CN, Bmax and Kd were decreased by RSD96 (p < 0.05) but not RSD24. In the SL, Bmax was increased by RSD96, but not RSD24, whereas Kd was increased in both RSD groups (p < 0.05).

Animals↗
PubMed1991

REM sleep deprivation reduces auditory evoked inhibition of dorsolateral pontine neurons.

In many dorsolateral pontine neurons, auditory stimulation produces an initial excitation followed by a sustained inhibition. We now report that rapid eye movement (REM) sleep deprivation, for periods of from 22-48 h, reduced this auditory evoked inhibition of unit discharge. Inhibition returned to baseline levels after recovery REM sleep. Prior work indicates that the auditory evoked inhibition seen in noradrenergic cells in this region is partially mediated by norepinephrine. We hypothesize that the reduction in inhibition that we see is a consequence of either downregulation/desensitization of norepinephrine receptors or reduced norepinephrine release resulting from REM sleep deprivation.

Acoustic Stimulation↗
PubMed1983

The effect of rapid eye movement sleep deprivation on cortical beta-adrenergic receptors.

The relationship between rapid eye movement sleep deprivation (REMD) and rat beta-adrenergic receptors was evaluated. REMD was achieved using the platform method and verified by EEG and EMG recordings. Although the amount of REM sleep was diminished 90%, there was no alteration in either the number of binding sites or their affinity for [3H]-dihydroalprenolol. Periods of stress as well as recovery periods after REMD were also without effect on the cortical beta-adrenergic receptors. Thus no support is garnered for the interaction of REMD and the cortical beta-adrenergic receptor binding parameters, although REMD is sometimes used as a mode of therapy for depression and other antidepressives do in fact affect the beta-adrenergic system. The mechanism of REMD as a potential antidepressive therapy is yet to be elucidated.

Animals↗
PubMed2001

The cloning of a rat peptidoglycan recognition protein (PGRP) and its induction in brain by sleep deprivation.

Peptidoglycan recognition protein (PGRP) binds to peptidoglycan (PG) or live bacteria and is upregulated by PG. PGRP is a ubiquitous protein involved in innate immunity. Tag7, a novel cytokine, is also induced by bacterial products; tag7 is apoptotic to murine L929 cells in a NF-kappaB-independent manner. Both of these genes are expressed in brain, lymphatic and haematopoietic tissues. We provide evidence that murine PGRP and tag7 encode identical transcripts and have structural relationships to lysozymes. Further, we have cloned the cDNA of rat PGRP and analyzed its expression in brains of sleep-deprived and control rats. The mRNA levels of PGRP/tag7 were measured by RT-PCR and compared to the housekeeping gene porphobilinogen deaminase (PBD). PGRP was constitutively expressed in rat brain. PGRP mRNA was increased by 43% and 17% in the brainstem and hypothalamus, respectively, in sleep-deprived rats compared to controls. The upregulation of PGRP expression by sleep deprivation suggests a role for PGRP in a homeostatic regulation of sleep.

Amino Acid Sequence↗
PubMed2004

Malnutrition and REM-sleep deprivation modulate in rats the impairment of spreading depression by a single sub-convulsing dose of pilocarpine.

This study aimed to investigate the effect of a single injection of pilocarpine upon the phenomenon of cortical spreading depression (SD), in adult rats submitted to early malnutrition and/or to REM-sleep deprivation for 72h prior to the SD-recordings. The SD was recorded continuously for 3-4h in 13 well-nourished (W) and 15 early-malnourished (M) adult rats. One to two hours after the beginning of the recording session, a sub-convulsing intraperitoneal (i.p.) injection of pilocarpine (190mg/kg) was applied and its effects on SD were studied during the rest of the recording session. Pilocarpine reduced markedly the ECoG amplitudes in all animals and decreased the SD velocity of propagation in the M-, but not in the W-rats, as compared with the pre-drug values for the same animals. In additional 9W- and 10 M-animals, REM-sleep deprivation was induced during the 72 h preceding the SD-recording session. This condition enhanced the pilocarpine effects on SD in the W-, but not in the M-rats, as compared to the respective non-deprived (ND) groups. The results indicate an important acute cholinergic influence on SD, acting by means of pilocarpine-activated muscarinic receptors. This effect seems to be differentially modulated by sleep deprivation and malnutrition.

Animals↗
PubMed2004

Effects of paradoxical sleep deprivation on blood parameters associated with cardiovascular risk in aged rats.

The effects of 96 h of paradoxical sleep deprivation (PSD) on blood parameters associated with cardiovascular risk were studied in young (3-month old) and aged (22-month old) rats. In general, aging was associated with an overall increase in most measures, irrespective of sleep deprivation condition. The latter manipulation also had significant effects on blood variables, but not in a consistent pattern. Thus, PSD significantly reduced triglyceride levels in both young and aged rats; it reduced blood viscosity in aged but not in young rats, and had no effect on the increased cholesterol levels observed in aged controls. Examinations of cholesterol fractions revealed significant increases in low density lipoprotein and high density lipoprotein in aged PSD rats compared to respective controls, whereas very low density lipoprotein was significant decreased after PSD in both young and aged animals. PSD increased vitamin B(12) levels in aged rats, and significantly decreased homocysteine levels in young but not in aged rats which in turn were already reduced. Folate levels were the only variable that was unaffected by aging and/or PSD. These results indicate that PSD has significant but heterogeneous physiological effects in aged rats and may intensify certain aging-related effects which contribute to cardiovascular disease risk while attenuating others.

Age Factors↗
PubMed2006

Sleep deprivation abolishes the locomotor stimulant effect of ethanol in mice.

The present study aimed to investigate the effects of sleep deprivation (SD) on the dose-dependent stimulant effect of ethanol (ETOH) on the open-field behavior of female and male mice. Sleep-deprived (48 h, multiple platforms method) or home-cage control female mice were treated with saline (SAL) or 1.4, 1.8 or 2.2g/kg ETOH 5 min before behavioral testing. ETOH produced a dose-dependent increase in open-field locomotor behavior. This locomotor stimulant effect did not reflect a general stimulation in motor activity, since it was accompanied by a simultaneous decrease in rearing frequency as well as by no modification in immobility duration. The effects of ETOH on these three behavioral parameters were specifically modified by SD: the locomotor stimulant effect was abolished, the rearing inhibitory effect was potentiated and the lack of effect on immobility was changed to increase in immobility. Similar results were obtained for male mice although the effects of SD had a lower magnitude. The present findings demonstrate that the acute effect of ETOH on mice's motor activity are behaviorally complex and can be specifically modulated by SD.

Analysis of Variance↗
PubMed2006

Growth hormone-releasing hormone and corticotropin-releasing hormone enhance non-rapid-eye-movement sleep after sleep deprivation.

The neuropeptides growth hormone (GH)-releasing hormone (GHRH) and corticotropin-releasing hormone (CRH) regulate sleep and nocturnal hormone secretion in a reciprocal fashion, at least in males. GHRH promotes sleep and GH and inhibits hypothalamo-pituitary-adrenocortical (HPA) hormones. CRH exerts opposite effects. In women, a sexual dimorphism was found because GHRH impairs sleep and stimulates HPA hormones. Sleep deprivation (SD) is the most powerful stimulus for inducing sleep. Studies in rodents show a key role of GHRH in sleep promotion after SD. The effects of GHRH and CRH on sleep-endocrine activity during the recovery night after SD are unknown. We compared sleep EEG, GH, and cortisol secretion between nights before and after 40 h of SD in 48 normal women and men aged 19-67 yr. During the recovery night, GHRH, CRH, or placebo were injected repetitively. After placebo during the recovery night, non-rapid-eye-movement sleep (NREMS) and rapid-eye-movement sleep (REMS) increased and wakefulness decreased compared with the baseline night. After GHRH, the increase of NREMS and the decrease of wakefulness were more distinct than after placebo. Also, after CRH, NREMS increased higher than after placebo, and a positive correlation was found between age and the baseline-related increase of slow-wave sleep. REMS increased after placebo and after GHRH, but not after CRH. EEG spectral analysis showed increases in the lower frequencies and decreases in the higher frequencies during NREMS after each of the treatments. Cortisol and GH did not differ between baseline and recovery nights after placebo. After GHRH, GH increased and cortisol decreased. Cortisol increased after CRH. No sex differences were found in these changes. Our data suggest that GHRH and CRH augment NREMS promotion after SD. Marked differences appear to exist in peptidergic sleep regulation between spontaneous and recovery sleep.

Adult↗
PubMed1988

[Effectiveness of bright light therapy in cyclothymic axis syndromes--a cross-over study in comparison with partial sleep deprivation].

In a preliminary crossover study, fifty patients with a cyclothymic axial syndrome were given bright-light treatment, while fifty other such patients were treated by means of partial sleep deprivation, 60% of the patients responded to bright-light treatment, as opposed to 50% of the patients partially deprived of sleep. The superior results of the bright-light treatment (Hamilton Depression Scale) are confirmed on the Nurses' Observation Scale for Inpatient Evaluation and the Profile of Mood States. Comparatively young patients with a not so extremely marked depression show the best response rates. Bright-light treatment is also effective against depressive disorders in non-seasonal depressions.

Adult↗
PubMed1978

Effects of sleep deprivation on short duration performance measures compared to the Wilkinson auditory vigilance task.

The effects of one night's total sleep deprivation were examined using the Wilkinson vigilance task and four 10 min duration performance tests. A repeated measures design was used in which eight male subjects experienced one night of sleep loss, the order of sleep loss being balanced across subjects. The four short duration performance tests consisted of choice reaction time, simple reaction time, short-term memory, and a motor task, handwriting. The results confirm the effects of one night's sleep deprivation on the vigilance task and also show that performance on the two reaction time tests was significantly impaired by the loss of sleep, but not at such a high level as for the vigilance. The short-term memory test failed to show any adverse effects of sleep loss and similarly for the handwriting. The experiment shows that two portable and brief (10 min) performance tests are sensitive indices of sleep loss and should be particularly useful for assessing levels of alertness in the field.

Adult↗
PubMed1993

Interaction of the alerting effect of noise with partial sleep deprivation and circadian rhythmicity of vigilance.

Only a few studies have been devoted to the interaction of noise with sleep deprivation and time of day. In a previous study we demonstrated that noise had an alerting effect on cognitive performance during the early night but not during the late night. However, it was not clear whether these different effects of noise were related to prior sleep debt or to time of day as both factors varied simultaneously. In the present experiment, we further studied this issue to identify which of these two factors was responsible for the noise effects. Analysis showed that, when performance was tested at different times with an equivalent prior sleep debt, noise improved speed of response at 0500 but not at 0800 at which variability of response time increased. Noise had no effect on errors. It is suggested that the effect of noise depends on the underlying arousal and raises arousal from its low level due either to time of day or to partial sleep deprivation.

Adult↗