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PubMed2001

Sleep deprivation decreases phase-shift responses of circadian rhythms to light in the mouse: role of serotonergic and metabolic signals.

The circadian pacemaker in the suprachiasmatic nuclei is primarily synchronized to the daily light-dark cycle. The phase-shifting and synchronizing effects of light can be modulated by non-photic factors, such as behavioral, metabolic or serotonergic cues. The present experiments examine the effects of sleep deprivation on the response of the circadian pacemaker to light and test the possible involvement of serotonergic and/or metabolic cues in mediating the effects of sleep deprivation. Photic phase-shifting of the locomotor activity rhythm was analyzed in mice transferred from a light-dark cycle to constant darkness, and sleep-deprived for 8 h from Zeitgeber Time 6 to Zeitgeber Time 14. Phase-delays in response to a 10-min light pulse at Zeitgeber Time 14 were reduced by 30% in sleep-deprived mice compared to control mice, while sleep deprivation without light exposure induced no significant phase-shifts. Stimulation of serotonin neurotransmission by fluoxetine (10 mg/kg), a serotonin reuptake inhibitor that decreases light-induced phase-delays in non-deprived mice, did not further reduce light-induced phase-delays in sleep-deprived mice. Impairment of serotonin neurotransmission with p-chloroamphetamine (three injections of 10 mg/kg), which did not increase light-induced phase-delays in non-deprived mice significantly, partially normalized light-induced phase-delays in sleep-deprived mice. Injections of glucose increased light-induced phase-delays in control and sleep-deprived mice. Chemical damage of the ventromedial hypothalamus by gold-thioglucose (600 mg/kg) prevented the reduction of light-induced phase-delays in sleep-deprived mice, without altering phase-delays in control mice. Taken together, the present results indicate that sleep deprivation can reduce the light-induced phase-shifts of the mouse suprachiasmatic pacemaker, due to serotonergic and metabolic changes associated with the loss of sleep.

Animals↗
PubMed1998

Sleep deprivation alters body temperature dynamics to mild cooling and heating not sweating threshold in women.

Sleep deprivation alters thermoregulatory responses. We used control of skin temperature to produce mild thermal challenge, both cool (32 degrees C) and warm (38 degrees C), and recorded esophageal and rectal temperatures, sweat rate and forearm blood flow in six healthy young women at rest. We discovered that after one night of sleep deprivation (1) both mean esophageal and rectal temperatures were reduced, (2) the mean threshold for sweating was not altered, and (3) there was no direct indication that skin blood flow was set at different levels with skin temperature neutral or cool. Peripheral vasodilation was attenuated when skin temperature was held at 38 degrees C. Following this period of mild hyperthermia, esophageal and rectal temperatures decreased much more rapidly in sleep-deprived subjects when skin temperature was cooled and held constant at 32 degrees C. We conclude that sleep-deprived women lose heat rapidly in response to a mild cooling stimulus. Sleep-deprived humans may be more vulnerable to heat loss with reduced ability to warm even at temperatures thought to be associated with thermal comfort.

Adult↗
PubMed1980

The microstructure of dual-task interaction. 4. Sleep deprivation and the control of attention.

The experiment was designed to investigate attention-switching behaviour in sleep-deprived subjects and involved the same dual-task paradigm reported in earlier studies. The task specified by instructions to be the main task, was the five-choice serial-response task; the secondary task was an auditory-verbal digit task which occurred at random time intervals. A surprising result was that, in terms of overall response rates, the sleep-deprived group, although slower, preserved the dual-task priority structure better than the control group, who slowed on both tasks in the combined condition. The control result was different in this respect from control data from previous research, but it is important that within the sleep-deprived group there was evidence that ability to preserve the priority structure was unaffected. Analysis of the intervals in which the two tasks concurred gave a different result. Sleep-deprived subjects seemed less able to control the fine structure of the interval and tended to persist in producing serial responses at the expense of the secondary-task response. The evidence supported the view that both sleep-deprived and control subjects were not able to process information in parallel and, thus, the difference in interval patterning was due to the difference in attention-switching processes. The possibility that sleep deprivation might result in loss of attentional control is considered briefly.

Adult↗
PubMed2004

Sleep deprivation in honey bees.

Rest at night in forager honey bees (Apis mellifera) meets essential criteria of sleep. This paper reports the effect of a 12-h total sleep deprivation (SD) by forced activity on the behaviour of these animals. The behaviour of sleep-deprived animals is compared with that of control animals under LD [periodic alternation between light (L) and darkness (D)] 12 : 12 hours. SD for 12 h during the first D period resulted in a significant difference with respect to the parameter 'hourly amount of antennal immobility' between sleep-deprived and control animals during the remaining L and D periods. This difference did not occur in the L period following the deprivation night, but rather it became obvious at the beginning of the following D period. The increase of the amount of antennal immobility in sleep-deprived bees was accompanied by an increase of the duration of episodes of antennal immobility. Moreover, the latency from 'lights off' to the first episode of antennal immobility lasting 20 s or longer ('deep sleep latency') tended to be shorter in sleep-deprived than in control animals. Disturbing the bees during the day (L period) did not result in such differences between disturbed and control animals. Highest reaction thresholds in sleeping honey bees occur during long episodes of antennal immobility. We therefore conclude that honey bees compensate a sleep deficit by intensification (deepening) of the sleep process and thus that sleep in honey bees, like that in other arthropods and mammals, is controlled by regulatory mechanisms.

Animals↗
PubMed2005

[EEG recording after sleep deprivation in a series of patients with juvenile myoclonic epilepsy].

Seizures in Juvenile Myoclonic Epilepsy (JME) are dependent on the sleep-wake cycle and precipitant factors, among which sleep deprivation (SD) is one of the most important. Still an under diagnosed syndrome, misinterpretation of the EEGs contributes to diagnostic delay. Despite this, a quantitative EEG investigation of SD effects has not been performed. We investigated the effect of SD on EEGs in 41 patients, aged 16-50 yr. (mean 25.4), who had not yet had syndromic diagnosis after a mean delay of 8.2 yr. Two EEG recordings separated by a 48-hour interval were taken at 7 a.m. preceded by a period of 6 hours of sleep (routine EEG) and after SD (sleep-deprived EEG). The same protocol was followed and included a rest wakefulness recording, photic stimulation, hyperventilation and a post-hyperventilation period. The EEGs were analyzed as to the effect of SD on the number, duration, morphology, localization and predominance of abnormalities in the different stages. A discharge index (DI) was calculated. Out of the 41 patients, 4 presented both normal EEG recordings. In 37 (90.2%) there were epileptiform discharges (ED). The number of patients with ED ascended from 26 (70.3%) in the routine EEG to 32 (86.5%) in the sleep-deprived exam. The presence of generalized spike-wave and multispike-wave increased from 20 (54.1%) and 13 (35.1%) in the first EEG to 29 (78.4%) and 19 (51.4%) in the second, respectively (p<0.05 and p<0.01). As to localization, the number of generalized, bilateral and synchronous ED increased from 21 (56.8%) to 30 (81.1%) (p<0.01). The DI also increased; while 8 patients (21.6%) presented greater rate in the routine EEG, 25 (67.6%) did so in the sleep-deprived EEG mainly during somnolence and sleep (p<0.01). Moreover, the paroxysms were also longer in the sleep-deprived EEG. Sleep-deprived EEG is a powerful tool in JME and can contribute significantly to the syndromic characterization of this syndrome.

Adolescent↗
PubMed1984

[The effects of REM sleep deprivation on the motor behavior of rats].

The effects of rapid-eye-movement (REM) sleep deprivation for 72 h on motor behaviour of rats have been studied. It has been shown both an increased spontaneous locomotor activity and an enhanced rotational behaviour after unilateral intrastriatal injection of dopamine 24 h and 48 h after the end of REM sleep deprivation. The enhancement of motor activity after REM sleep deprivation points to changes in the dopaminergic transmission system. But it is not yet clear, if the main cause of these effects is the development of a super-sensitivity of postsynaptic dopaminergic receptors. In the same way interactions between the dopaminergic system and other inhibitory transmission systems may play an important role, explaining effects of REM sleep deprivation.

Animals↗
PubMed2001

Prolonged sedation with propofol in the rat does not result in sleep deprivation.

UNLABELLED: The use of propofol provides sedation without prolonging emergence in patients in the Intensive Care Unit. When prolonged, however, continuous sedation may overlap with naturally occurring sleep periods and potentially increase the risk of sleep deprivation. We modified an established rat model of sleep to determine whether prolonged, continuous sedation results in sleep deprivation. Rats were continuously sedated for a 12-h period overlapping completely with their normal sleep phase. Electroencephalogram (EEG) and movement data were collected before and after the sedation period. Rats were evaluated for EEG and movement evidence of sleep deprivation after sedation. When compared with baseline, the time spent in rapid eye movement (REM) and non-REM sleep was decreased during the first 4 h after sedation. The duration of non-REM sleep bouts was not altered. Power in the delta band (0.5-4 Hz) during non-REM sleep was diminished during the first 2 h only. Movements were reduced during the first hour after emergence from sedation only. In summary, no EEG or behavioral evidence of sleep deprivation was observed on emergence from sedation. These results imply that sedation is associated with a restorative process reversing the natural accumulation of sleep need that occurs during wakefulness. IMPLICATIONS: Prolonged sedation in the Intensive Care Unit may alter the restorative effects of naturally occurring sleep. We sedated rats during their sleep phase to determine whether sedation interferes with sleep. Upon emergence, no evidence of sleep deprivation was observed. Sedation may thus be associated with a restorative effect similar to sleep.

Animals↗
PubMed2005

Sleep deprivation, cognitive performance, and hormone therapy in postmenopausal women.

OBJECTIVE: To study the effects of sleep deprivation on cognitive performance in postmenopausal women and to evaluate whether hormone therapy (HT) has a modifying effect on coping. DESIGN: Twenty-six postmenopausal women, aged 58 to 72 years (mean 64 years), volunteered for the study (HT users, n = 16; nonusers, n = 10). They spent four consecutive nights in the sleep laboratory. The cognitive tests were performed three times: after the baseline night, after one night of sleep deprivation, and after the rebound night. The cognitive measures included visual episodic memory, visuomotor performance, verbal attention, and shared attention. RESULTS: The practice effect typically occurring in cognitive tests was blunted during sleep deprivation, which indicated deterioration of performance. At rebound, performance improved in visual episodic memory (immediate recall P < 0.01; delayed recall P < 0.05), visuomotor performance (P < 0.001), verbal attention (P < 0.0001), and shared attention (P < 0.05). HT users performed better than nonusers in the visual episodic memory test (P < 0.05) and in one of three subtests of shared attention (cancellation P = 0.040). Otherwise hormone therapy did not influence the results. CONCLUSIONS: In postmenopausal women, sleep deprivation impaired visual functions and attention. However, this effect was not prolonged because after one rebound night the performance was improved, compared with baseline. Hormone therapy did not modify the cognitive performance during sleep deprivation.

Aged↗
PubMed1993

Influence of partial sleep deprivation on the secretion of thyrotropin, thyroid hormones, growth hormone, prolactin, luteinizing hormone, follicle stimulating hormone, and estradiol in healthy young women.

The influence of partial sleep deprivation during the second half of the night on the secretion of thyroid stimulating hormone (TSH), thyroxin (T4), free T4 (fT4), triiodothyronine (T3), prolactin (PRL), growth hormone (GH), luteinizing hormone (LH), follicle stimulating hormone (FSH), and estradiol (E2) was investigated in 10 healthy young women. Blood samples were drawn at hourly intervals over a 64-hour period (i.e., 3 consecutive days and nights). During night 2, all subjects were awakened at 1:30 a.m. During partial sleep deprivation, TSH concentrations increased significantly and remained elevated throughout the following day. Levels of T4, fT4, and T3 were enhanced during the partial sleep deprivation hours only, and changes in these hormones seemed to be independent of TSH. PRL levels decreased, LH and E2 concentrations increased, and GH and FSH secretion remained unchanged during partial sleep deprivation. This pattern of change of different endocrine axes during partial sleep deprivation resembles those seen after total sleep deprivation, suggesting that similar neurochemical changes are induced by both forms of antidepressant therapy. The late evening GH peak occurred almost exclusively before the onset of sleep. Partial sleep deprivation did not influence the chronobiological profiles of any of the hormones investigated. The chemical changes underlying these alterations are speculated to involve enhancement of central norepinephrine and dopamine activity with a concomitant increase in the activity of the sympathetic nervous system.

Adult↗
PubMed1992

Parsing attentional components during a simple reaction time task using sleep deprivation and amphetamine intervention.

To examine the independent contributions of the attentional components of arousal and activation in performance, sleep deprivation was used as the attentional manipulation in a reaction time (RT) task. The subjects were 18 men who underwent 63 hr. of sleep deprivation during which time they periodically performed a simple auditory RT task with manipulations of temporal uncertainty and intensity. After 48 hr. sleep deprivation, subjects ingested either 20 mg d-amphetamine or placebo, then continued testing throughout Day 3. During sleep deprivation, performance was more impaired on trials associated with low temporal uncertainty (arousal) and high preparation (activation) than on trials associated with high temporal uncertainty and low preparation. Analysis indicated that sleep deprivation perturbed activation, leaving arousal relatively unimpaired and that amphetamine had a restorative effect on the sleep deprivation-impaired activation system. The stimulus of high intensity was disruptive on Day 1 but facilitative on Day 3, a result which was interpreted as an initial inhibition, then disinhibition of arousal. Results were interpreted to indicate that, in some instances, alterations in the less specific arousal and activation systems may underlie impairment or changes in the more specific information processing and motor output stages.

Adult↗
PubMed1986

Effects of partial food restriction on nocturnal meal size and feeding speed are counteracted by concurrent REM sleep deprivation in the rat.

Effects of rapid eye movement (REM) sleep deprivation on meal size and feeding speed were investigated by means of the cuff pedestal technique in 9 male rats exposed to partial food restriction. Reduction of available food by 50% alone, when accomplished by providing the pellets at the beginning of each dark period, during 7 consecutive days, induced a quite linear increase both in the meal size and feeding speed. When the same feeding schedule was repeated in combination with REM sleep deprivation, the meal size remained smaller and the feeding time was prolonged (during the first 3-4 days) when compared to those during food restriction alone, although losses of body weight were almost doubled. These findings are in agreement with the effects of REM sleep deprivation on the meal pattern in rats on ad libitum diet and provide further support for the suggestion of the importance of REM sleep in the generation of the light/dark rhythm of feeding in the rat.

Animals↗
PubMed2002

The cyclic alternating pattern decreases as a consequence of total sleep deprivation and correlates with EEG arousals.

The aim of this study was to assess the sensitivity of the cyclic alternating pattern (CAP) parameters to the increased need for recuperation that follows one night of sleep deprivation. Nine normal male subjects were recorded for 3 nights [adaptation, baseline (BSL) and recovery (REC)]. BSL and REC nights were separated by a 40-hour sleep deprivation. Recovery after sleep deprivation was characterized by a decrease in stage 1, stage 2 and sleep latency, and an increase in slow wave sleep (SWS) and the sleep efficiency index, while rapid eye movement (REM) and non-REM (NREM) time did not differ as compared to BSL sleep. CAP parameters were significantly affected by sleep deprivation, and the main results were the following: (1) the CAP rate (time spent in CAP phases/NREM time) significantly decreased from 38.85 to 31.47%, and (2) within phase A subtypes, there was a significant decrease in A3 subtypes (from 38.11 to 19.57). Furthermore, the number of arousals scored according to American Sleep Disorders Association rules strongly correlated with A3 subtypes during both the BSL (r = 0.79) and REC nights (r = 0.95). These results indicate that recuperative processes after sleep deprivation are also associated with a lesser arousal instability as defined by the reduction of the CAP rate, which is strongly correlated with EEG arousals.

Adult↗
PubMed1992

Growth hormone-releasing hormone antibodies suppress sleep and prevent enhancement of sleep after sleep deprivation.

Previous reports suggest that the hypothalamic growth hormone-releasing hormone (GHRH) promotes sleep, especially non-rapid-eye-movement sleep (NREMS). To evaluate the role of endogenous GHRH in sleep regulation, the effects of antibodies to rat GHRH (GHRH-ab) were studied on normal sleep, brain temperature (Tbr), and GH secretion in experiment I and on enhanced sleep after sleep deprivation in experiment II. In experiment I, affinity-purified GHRH-ab (50 and 200 micrograms) raised in goats and a control goat immunoglobulin G (IgG) preparation were injected intracerebroventricularly (icv) in rats 1 h before the onset of the light cycle, and sleep-wake activity and Tbr were recorded for the next 12 or 23 h. Both doses of GHRH-ab suppressed NREMS and REMS throughout the light cycle. Sleep durations at night were normal. Electroencephalographic (EEG) slow-wave activity, characterized by EEG slow-wave amplitudes, was reduced after GHRH-ab during both the light and the dark cycles. Plasma GH concentrations measured 6-12 h after injection of GHRH-ab (200 micrograms) were diminished. Both the control IgG and GHRH-ab elicited fever. In experiment II, the sleep-wake activity and Tbr of rats were recorded for 24 h in three experimental conditions: base-line with icv injection of IgG, 3-h sleep deprivation with icv IgG injection, and 3-h sleep deprivation with icv GHRH-ab (200 micrograms). After sleep deprivation (+IgG), a prompt increase in EEG slow-wave activity (power density analysis) and late increases in NREMS and REMS durations were found.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

Cerebral glucose metabolic response to combined total sleep deprivation and antidepressant treatment in geriatric depression.

OBJECTIVE: The treatment of geriatric depression is complicated by a variable and delayed response to antidepressant treatment. The present study was undertaken to test the hypothesis that combined total sleep deprivation and paroxetine treatment would produce a persistent reduction in glucose metabolism in the anterior cingulate cortex similar to that reported after long-term antidepressant treatment. METHOD: Six elderly depressed patients who met the DSM-IV criteria for major depressive disorder and six age-matched comparison subjects underwent serial positron emission tomography (PET) studies at baseline, after total sleep deprivation, after recovery sleep (after the initial paroxetine dose), and after 2 weeks of paroxetine treatment (patients only). The PET data were analyzed by using statistical parametric mapping methods. RESULTS: The patients' scores on a 13-item version of the Hamilton Depression Rating Scale were decreased after total sleep deprivation, after recovery sleep, and after 2 weeks of treatment. The Hamilton depression scores of the comparison subjects were not significantly altered. In the patients, the greatest reductions in normalized, relative glucose metabolism after sleep deprivation were observed in the anterior cingulate cortex (Brodmann area 24), and they persisted after recovery sleep and antidepressant treatment. The comparison subjects demonstrated increased metabolism in these areas. CONCLUSIONS: Improvement in the patients' depressive symptoms was accompanied by reduced glucose metabolism in the right anterior cingulate cortex and right medial frontal cortex. These preliminary data indicate that in elderly depressed patients, total sleep deprivation may accelerate the clinical and glucose metabolic response to antidepressant treatment.

Age Factors↗
PubMed1995

Are postoperative complications related to resident sleep deprivation?

This real-world study compares the outcome of surgery and the sleep-deprivation status of the resident surgeon. Residents who operated the day after a 24-hour on-call period were considered sleep deprived; all other resident surgeons were considered non-sleep-deprived. We retrospectively reviewed data on 6,371 surgical cases and identified 351 postoperative complications. The complication data were analyzed using logistic regression analysis, with outcome being the presence or absence of surgical complications. No statistically significant change in complication incidence was noted when the resident surgeon was sleep deprived.

Clinical Competence↗
PubMed1983

Evidence for REM sleep deprivation as the mechanism of action of antidepressant drugs.

In the treatment of endogenous depression REM sleep deprivation and imipramine have similar efficacy. Across drugs, efficacy of antidepressant activity is directly related to capacity of drugs to produce large and sustained reductions of REM sleep. Endogenous depression unimproved by REM sleep deprivation is unimproved by imipramine. Endogenous depression improvement by REM sleep deprivation and by amitriptyline have the same biological correlate, viz, REM rebound. In animals REM sleep deprivation produces several behavioral changes (e.g., increased motor, sexual, aggressive, pleasure seeking, feeding activities) which are the reverse of behavioral changes of human endogenous depression.

Amitriptyline↗