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PubMed2006

Transition to daylight saving time reduces sleep duration plus sleep efficiency of the deprived sleep.

Daylight saving time (DST) is widely adopted. We explored the effects of transition to daylight saving time on sleep. With the use of wrist-worn accelerometers, we monitored the rest-activity cycles on a sample of 10 healthy adults for 10 days around the transition to summer time. Identical measurement protocols were carried out twice on the same individuals during the transitions in the years of 2003 and 2004, yielding data on 200 person-days for analysis. Both sleep duration and sleep efficiency were reduced after the transition both years. After the transition sleep time was shortened by 60.14min (P<0.01) and sleep efficiency was reduced by 10% (P<0.01) on average. Transition to daylight saving time appears to compromise the process of sleep by decreasing both sleep duration and sleep efficiency.

Adaptation, Physiological↗

PubMed1997

Decreased attentional responsivity during sleep deprivation: orienting response latency, amplitude, and habituation.

Ever increasing societal demands for uninterrupted work are causing unparalleled amounts of sleep deprivation among workers. Sleep deprivation has been linked to safety problems ranging from medical misdiagnosis to industrial and vehicular accidents. Microsleeps (very brief intrusions of sleep into wakefulness) are usually cited as the cause of the performance decrements during sleep deprivation. Changes in a more basic physiological phenomenon, attentional shift, were hypothesized to be additional factors in performance declines. The current study examined the effects of 36 hours of sleep deprivation on the electrodermal-orienting response (OR), a measure of attentional shift or capture. Subjects were 71 male undergraduate students, who were divided into sleep deprivation and control (non-sleep deprivation) groups. The expected negative effects of sleep deprivation on performance were noted in increased reaction times and increased variability in the sleep-deprived group on attention-demanding cognitive tasks. OR latency was found to be significantly delayed after sleep deprivation, OR amplitude was significantly decreased, and habituation of the OR was significantly faster during sleep deprivation. These findings indicate impaired attention, the first revealing slowed shift of attention to novel stimuli, the second indicating decreased attentional allocation to stimuli, and the third revealing more rapid loss of attention to repeated stimuli. These phenomena may be factors in the impaired cognitive performance seen during sleep deprivation.

Attention↗

PubMed2004

Recovery from sleep deprivation occurs during propofol anesthesia.

BACKGROUND: Some neurophysiologic similarities between sleep and anesthesia suggest that an anesthetized state may reverse effects of sleep deprivation. The effect of anesthesia on sleep homeostasis, however, is unknown. To test the hypothesis that recovery from sleep deprivation occurs during anesthesia, the authors followed 24 h of sleep deprivation in the rat with a 6-h period of either ad libitum sleep or propofol anesthesia, and compared subsequent sleep characteristics. METHODS: With animal care committee approval, electroencephalographic/electromyographic electrodes and intrajugular cannulae were implanted in 32 rats. After a 7-day recovery and 24-h baseline electroencephalographic/electromyographic recording period, rats were sleep deprived for 24 h by the disk-over-water method. Rats then underwent 6 h of either propofol anesthesia (n = 16) or ad libitum sleep with intralipid administration (n = 16), followed by electroencephalographic/electromyographic monitoring for 72 h. RESULTS: In control rats, increases above baseline in non-rapid eye movement sleep, rapid eye movement sleep, and non-rapid eye movement delta power persisted for 12 h after 24 h of sleep deprivation. Recovery from sleep deprivation in anesthetized rats was similar in timing to that of controls. No delayed rebound effects were observed in either group for 72 h after deprivation. CONCLUSION: These data show that a recovery process similar to that occurring during naturally occurring sleep also takes place during anesthesia and suggest that sleep and anesthesia share common regulatory mechanisms. Such interactions between sleep and anesthesia may allow anesthesiologists to better understand a potentially important source of variability in anesthetic action and raise the possibility that anesthetics may facilitate sleep in environments where sleep deprivation is common.

Anesthesia Recovery Period↗

PubMed2004

Total sleep deprivation decreases immobility in the forced-swim test.

Sleep deprivation can exert antidepressant effects in humans in less than 24 h, making it the fastest acting antidepressant treatment. However, it is rarely used clinically because the effect disappears once the subject goes back to sleep. An understanding of the neurobiological mechanisms underlying the antidepressant effect of sleep deprivation should help to develop new rapidly acting antidepressant strategies. In the present report, an animal model of depression (the forced-swim test) was used to determine whether the effects of total sleep deprivation parallel those obtained with antidepressant drugs. Using the disk-over-water method, rats deprived of sleep for 24 h exhibited increased swimming behavior when compared to cage control rats, mimicking the effects of serotonergic antidepressants. After 48 h, sleep-deprived rats exhibited increased swimming when compared to both cage control and stimulus control rats, demonstrating that the effect is due to sleep deprivation per se, and not to extraneous factors inherent in the sleep deprivation protocol (such as stress and movement). We believe that this paradigm can be used to study the neurobiological mechanisms of rapid antidepressant effects induced by sleep deprivation.

Analysis of Variance↗

PubMed1987

Effect of 64-hour sleep deprivation on the circadian waveform of thyrotropin (TSH): further evidence of sleep-related inhibition of TSH release.

Half-hourly sampling of plasma TSH was done across 3 days in four normal young men. Sleep was denied for 64 h from 0700 h on awakening from accommodation sleep until polygraphic sleep was resumed at 7100 h of the third day (D3) such that 2 consecutive nights of usual 2300-0700 h sleep were missed. This protocol allowed examination of any modulatory effects on the daily patterns in TSH concentrations during sleep deprivation on D1-2 (1100-3500, 3500-5900 h) or during resumption of usual nightly sleep on D3 (5900-8300) compared to that of a previously studied group of normal young men. The circadian nature of the daily TSH waveform was evidenced by its daily repetition within a subject both basally and during D1-2 sleep deprivation and by its synchronization within the basal, deprived, or resumed sleep days. The peaks in each subject's daily TSH patterns on D1-2 were consistently longer, and the daily maxima and cosine acrophases on D1-2 were consistently later than those on D3 when basal sleep was resumed. About half the daily TSH concentration maxima and daily cosinor amplitudes on D1-2 were greater than those of the respective sleep-resumed TSH patterns of D3. Both the group mean TSH patterns and the cosinor 95% confidence ellipses also indicated the daily peak in the TSH waveform to be significantly longer, later, and larger during D1-2 sleep deprivation than during the basal or D3 periods. These results indicate that significant alteration of the daily TSH waveform can occur in response to absence of sleep and are compatible with the existence of an inhibitory effect in early nightly sleep on TSH release. The TSH patterns during the 1700-2300 h intervals of rising TSH levels were congruent in the basal, deprived, and resumed sleep periods. Prompt reversion to the basal TSH pattern also occurred when sleep was resumed on D3. Both of these observations suggest the alteration in TSH waveform during sleep deprivation to have arisen from an inhibitory effect in sleep rather than from a change in period or phase of a generating oscillator.

Adult↗

PubMed1983

Sleep deprivation and the control of ventilation.

Sleep deprivation is common in acutely ill patients because of their underlying disease and can be compounded by aggressive medical care. While sleep deprivation has been shown to produce a number of psychological and physiologic events, the effects on respiration have been minimally evaluated. We therefore studied resting ventilation and ventilatory responses to hypoxia and hypercapnia before and after 24 h of sleeplessness in 13 healthy men. Hypoxic ventilatory responses (HVR) were measured during progressive isocapnic hypoxia, and hypercapnic ventilatory responses (HCVR) were measured using a rebreathing technique. Measures of resting ventilation, i.e., minute ventilation, tidal volume, arterial oxygen saturation, and end-tidal gas concentrations, did not change with short-term sleep deprivation. Both HVR and HCVR, however, decreased significantly after a single night without sleep. The mean hypoxic response decreased 29% from a slope of 1.20 +/- 0.22 (SEM) to 0.85 +/- 0.15 L/min/% saturation (p less than 0.02), and the slope of the HCVR decreased 24% from 2.07 +/- 0.17 to 1.57 +/- 0.15 L/min/mmHg PCO2 (p less than 0.01). These data indicate that ventilatory chemosensitivity may be substantially attenuated by even short-term sleep deprivation. This absence of sleep could therefore contribute to hypoventilation in acutely ill patients.

Adult↗

PubMed2000

Preliminary evidence of an association between increased REM density and poor antidepressant response to partial sleep deprivation.

BACKGROUND: One night of total sleep deprivation or of late-night partial sleep deprivation (PSD) produces a temporary remission in approximately 40-60% of patients with major depressive disorder; however, little is known about polysomnography (PSG) characteristics of responders to these types of sleep deprivation (SD). METHODS: Twenty-three unmedicated unipolar patients (17-item Hamilton Depression Rating Scale (HDRS17) >16) and 14 normal controls underwent 1 night of late-night PSD (awake after 3 a.m.) Subjects underwent baseline PSG and received the HDRS17 at standard times before and after PSD. Clinical response was defined as a reduction of >30% in the modified HDRS17 (omitting sleep and weight loss items) following PSD. RESULTS: The 12 responders and 11 nonresponders did not differ from each other significantly on baseline HDRS17 or PSG variables. The only PSG variable correlating with percent decrease in modified HDRS17 was baseline REM density (Pearson's r=-0.52, n=23, P=0.01.) In other words, the lower the baseline REM density, the more robust the antidepressant response was. LIMITATIONS: Subject numbers are relatively small. CONCLUSIONS: Increased REM density, which reflects the number of rapid eye movements per epoch of REM sleep, may be a physiological marker for severity or poor prognosis in a variety of psychiatric disorders, including relapse in recovering alcoholics, suicidality in schizophrenia, and poor response to PSD or interpersonal psychotherapy in depression.

Adult↗

PubMed1976

[Y-maze learning in two strains of mice. Effects of instrumental and pharmacologic sleep deprivation].

Effects of instrumental and pharmacological deprivation of sleep on Y-maze learning have been studied in two inbred strains of mice (C57BR/cd/Orl and C57BL/6/Orl), having identical sleep rhythms, but mainly differing in their ability to learn. Administration of alpha-methyl-DOPA (100 mg/kg) provokes complete suppression of paradoxical sleep (PS) for 9-11 h. Injection immediately after each training session over the first 5 days caused a delay in acquisition of an active avoidance task in C57BR mice. Treated C57BL/6 mice exhibited a significant facilitation of acquisition. Similar results were obtained by instrumental deprivation of sleep for 10 h.

Animals↗

PubMed1999

Nuclear factor-kappaB-like activity increases in murine cerebral cortex after sleep deprivation.

Several well-defined sleep regulatory substances, e.g., interleukin-1beta, activate the heterodimeric transcription factor nuclear factor-kappaB (NF-kappaB). Several substances that inhibit sleep, e.g., interleukin-4, inhibit NF-kappaB activation. NF-kappaB activation promotes production of several additional substances thought to be involved in sleep regulation, e.g., nitric oxide. We investigated, therefore, whether there are diurnal rhythms of NF-kappaB activation in brain and changes in the activation after sleep deprivation. Mice were kept on a 12:12-h light-dark cycle. In one experiment, groups of mice were killed every 3 h across the 24-h cycle. In another experiment, mice were killed at 1500 after 6 h of sleep deprivation, and a group of control mice were killed at the same time. Nuclear proteins were extracted from each brain tissue sample, and NF-kappaB-like activity was determined with an electrophoretic mobility shift assay. In cerebral cortex, but not other areas of brain, there was a diurnal rhythm in NF-kappaB-like activation; highest levels were found during the light period. NF-kappaB-like activation was higher in cerebral cortex after sleep deprivation compared with values obtained from control mice. The results are consistent with the hypothesis that sleep regulation involves multiple gene events, some of which include enhanced production of sleep regulatory substances, the actions of which involve NF-kappaB activation.

Animals↗

PubMedDate not supplied

Response covariation of escape-maintained aberrant behavior correlated with sleep deprivation.

We examined the relation between sleep deprivation and changes in level and allocation of aberrant behavior (aggression and self-injury) for a child with moderate mental retardation. First, a series of functional analyses identified that self-injury (SIB) and aggression were maintained by escape from demands (i.e., were members of the same response class). Escape from demand conditions were then held constant over time while natural levels of sleep deprivation occurred. This final analysis demonstrated a correlation between sleep deprivation and increases in escape-maintained aberrant behavior. Sleep deprivation seemed to be related to increases in levels of self-injury but did not seem to influence levels of aggression.

Aggression↗

PubMed1995

[Humoral aspects of sleep deprivation].

The effects of an antidepressant sleep deprivation on humoral systems and neurotransmitter systems are reviewed (cortisol, endorphins, thyroidea, growth hormone, prolactin, catecholamines, sexual hormones, melatonin, serotonin). The main results are: Depressed patients have a physiological response similar to controls with some differences between responders and nonresponders (responders are more similar to controls). TSH is more activated in responders than in nonresponders. The dopamine system is more activated in responders than in nonresponders and less activated in responders before sleep deprivation. The glucocorticoid-axis in more activated in responders after sleep deprivation. In conclusion, patients who profit from sleep deprivation can activate systems correlated with arousal or stress.

Arousal↗

PubMed2003

Seasonal effects of sleep deprivation on thermoregulatory responses in a hot environment.

Effects of sleep deprivation and season on thermoregulation during 60 min. of leg-bathing (water temperature of 42 degrees C, air temperature of 30 degrees C, and relative humidity of 70%) were studied in eight men who completed all 4 experiments for normal sleep and sleep deprivation in summer and winter. Rectal temperature (T(re)), skin temperature, total body sweating rate (M(sw-t)), local sweating rate on the back (M(sw-back)) and forearm (M(sw-forearm)), and skin blood flow on the back (SBF(back)) and forearm (SBF(forearm)) were measured. The changes in T(re) (DeltaT(re)) were smaller (P<0.05) for sleep deprivation than for normal sleep regardless of the season. This decrease in DeltaT(re) was significant only in summer (P<0.05). Mean skin temperature (T(mean of)(sk)) was higher (P<0.05) for sleep deprivation than for normal sleep regardless of the season. M(sw-t) was smaller (P<0.05) for sleep deprivation than for normal sleep regardless of season, although M(sw-back) and M(sw-forearm) were similar. SBF(back) and SBF(forearm) tended to be higher for sleep deprivation than normal sleep. The sensitivity of SBF to T(re) was higher (P<0.05) for sleep deprivation than for normal sleep. These data indicate that seasonal differences in thermoregulation were small because of morning time. Sleep deprivation increased dry heat loss and restrained T(re) rise, in spite of decreased sweating rate.

Acclimatization↗

PubMed1996

Food deprivation and hypothermia in desynchronized sleep-deprived rats.

Reports of the effect of desynchronized sleep (DS) deprivation on body temperature (Tb) of rats in the literature are contradictory. Since conspicuous body weight loss is common in such deprivation, the effect of food plus DS deprivation on Tb of adult male Wistar rats was studied. DS deprivation carried out by the small platform method with food ad libitum (N = 8) induced hyperthermia (Tb above 38.5 degrees C) in 1 to 3 rats daily until the 8th day, when a case of discrete hypothermia (Tb below 36.9 degrees C) appeared. Food deprivation alone started to induce hypothermia on the third day in one (20%) out of five rats. Fasting imposed from the 5th to the 8th day of DS deprivation (N = 12) caused hypothermia in 33% and 67% of the animals on the second and third day of starvation, respectively. DS compensatory manifestations in 6 starved rats intensified (N = 2) or precipitated (N = 2) hypothermia after the end of sleep deprivation. It is concluded that the hypothermia is not a primary effect of DS deprivation, and this state of sleep seems to have its particular functional role which is independent of thermoregulation.

Animals↗

PubMed1990

Sleep and EEG spectra in the rabbit under baseline conditions and following sleep deprivation.

The 24-hr sleep-wake distribution and power spectra of the electroencephalogram were determined in rabbits that had been implanted with cortical and hippocampal electrodes. A diurnal preference for sleep was observed. The spectral power density in nonrapid eye movement sleep (NREM sleep) of the cortex showed a decreasing trend in most frequencies within the 12-hr light period. In the 12-hr dim period no clear trend was present. Most hippocampal EEG frequencies decreased in NREM sleep in the first two hours of the light period, and thereafter stayed on a constant level. Sleep deprivation elicited the following changes: a prolonged increase of NREM sleep and a short increase of REM sleep; in the cortex, an increase of slow-wave activity (SWA; power density in the 0.25-2.0 Hz frequency band) in NREM sleep, which declined in the course of recovery; an enhancement of slow-wave (1.25-3 Hz) and theta (6.25-7 Hz) activity in REM sleep. The hippocampus showed an increase in NREM sleep power density in almost all frequencies. In REM sleep the hippocampus exhibited an increase in power density in the 6.25-7 Hz and 12.25-13 Hz bands, whereas in the 7.25-8 Hz band the values were below baseline. The results show that SWA in NREM sleep and theta activity in REM sleep are enhanced by sleep deprivation, as has been observed in other mammalian species. The EEG changes in the hippocampus resembled those in the cortex.

Animals↗

PubMed1990

Sleep and EEG slow-wave activity in the domestic cat: effect of sleep deprivation.

The 24-h sleep-wake distribution, the vigilance states and the time course of EEG slow-wave activity was investigated in 8 adult domestic cats individually maintained in isolation under 14-h light (06.00-20.00 h)/10-h dim conditions. The frontal EEG and motor activity were continuously recorded for 22 h (during the daily cleaning and food-replenishing period between 07.00 and 09.00 h the cats were only observed). Sleep was prevented for 14 h (07.00-21.00 h) by playing with the animals. Recovery from sleep deprivation was recorded for the remaining 10 h of the dim period. Non-rapid eye movement (non-REM) sleep, REM sleep and waking were uniformly distributed over the light and dim period, with the exception of the 2-h feeding period where the cats were always awake. EEG power density in the delta band (0.75-4.5 Hz; slow-wave activity) was computed in non-REM sleep. The values in the light period were higher than in the dim period. In neither of the lighting periods was a trend observed. After sleep deprivation a small increase of non-REM sleep and REM sleep was present. EEG slow-wave activity was initially enhanced and then declined progressively. We conclude that despite the small circadian difference in the sleep-wake pattern observed in our cats, sleep homeostasis is similar to that observed in other mammalian species.

Animals↗

PubMed1989

Sleep deprivation in the rat: IX. Recovery.

Eight rats were subjected to total sleep deprivation, paradoxical sleep deprivation, or high amplitude sleep deprivation until they showed major deprivation-induced changes. Then they were allowed to sleep ad lib. Three rats that had shown the largest temperature declines died within two to six recovery days. During the first 15 days of ad lib sleep, surviving rats showed complete or almost complete reversal of the following deprivation-induced changes: debilitated appearance, lesions on the paws and tail, high energy expenditure, large decreases in peritoneal temperature, high plasma epinephrine and norepinephrine levels, and low thyroxine levels. The most prominent features of recovery sleep in all rats were immediate and large rebounds of paradoxical sleep to far above baseline levels, followed by lesser temporally extended rebounds. Rebounds of high amplitude non-rapid eye movement (NREM) sleep occurred only in some rats and were smaller and less immediate.

Adrenal Cortex Hormones↗

PubMed1999

Circadian and homeostatic influences on sleep in the squirrel monkey: sleep after sleep deprivation.

A series of sleep deprivation (SD) experiments were performed to examine the relative influence of circadian and homeostatic factors on the timing of sleep in squirrel monkeys free-running in constant illumination. All SDs started at the beginning of subjective night and lasted 0, 1/4, 1/2, 1, 1 1/4, or 1 1/2 circadian cycles. These six lengths represented three pairs: (0.1), (1/4, 1 1/4), (1/2, 1 1/2). Within each pair, SD ended at the same circadian phase but differed by one circadian cycle in duration. Both before and after SD, consolidated sleep (CS) episodes occurred predominantly during subjective night, even after long SDs ending at the beginning of subjective day. CS duration was strongly influenced by circadian phase but had no overall correlation with prior wake duration. Sleep loss incurred during SDs longer than 1/4 cycle was only partially recovered over the next two circadian cycles, though total sleep duration was closer to baseline levels after the second circadian cycle after SD. There was a trend toward a positive correlation between prior wake duration and the amount of NREM and delta activity measures during subjective day. Delta activity was not increased in the first 2 hours of CS after the SD. Relatively high levels of delta activity occurred immediately after the SD ended and again at the time of baseline CS onset. These data indicate that the amount of sleep and delta activity after SD in squirrel monkeys is weakly dependent on prior wake duration. Circadian factors appear to dominate homeostatic processes in determining the timing, duration and content of sleep in these diurnal primates.

Animals↗

PubMed2003

Total sleep deprivation increases extracellular serotonin in the rat hippocampus.

Sleep deprivation exerts antidepressant effects after only one night of deprivation, demonstrating that a rapid antidepressant response is possible. In this report we tested the hypothesis that total sleep deprivation induces an increase in extracellular serotonin (5-HT) levels in the hippocampus, a structure that has been proposed repeatedly to play a role in the pathophysiology of depression. Sleep deprivation was performed using the disk-over-water method. Extracellular levels of 5-HT were determined in 3 h periods with microdialysis and measured by high performance liquid chromatography coupled with electrochemical detection. Sleep deprivation induced an increase in 5-HT levels during the sleep deprivation day. During an additional sleep recovery day, 5-HT remained elevated even though rats displayed normal amounts of sleep. Stimulus control rats, which had been allowed to sleep, did not experience a significant increased in 5-HT levels, though they were exposed to a stressful situation similar to slee-deprived rats. These results are consistent with a role of 5-HT in the antidepressant effects of sleep deprivation.

Analysis of Variance↗