Long-term vs. short-term processes regulating REM sleep.
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In cats, rats, and mice, the amount of rapid eye movement sleep (REMS) lost during a sleep deprivation (SD) predicts the subsequent REMS rebound during recovery sleep. This suggests that REMS is homeostatically regulated and that a need or pressure for REMS accumulates in its absence, i.e. during both wakefulness and non-rapid eye movement sleep (NREMS). Conversely, it has been proposed that REMS pressure accumulates exclusively during NREMS [Benington and Heller, Am. J. Physiol. 266 (1994) R1992; Prog. Neurobiol. 44 (1994b) 433]. This hypothesis is based on the analysis of the duration of successive NREMS and REMS episodes and of electroencephalogram (EEG) events preceding REMS. Pre-REMS events (PREs) do not always result in sustained REMS and can thus be regarded as REMS attempts that increase as NREMS progresses. It is assumed that two processes regulating REMS can resolve the apparent contradiction between these two concepts: a 'long-term' process that homeostatically regulates the daily REMS amount and a 'short-term' process that regulates the NREM--REMS cycle. These issues were addressed in two SD experiments in rats. The two SDs varied in length (12 and 24 h) and resulted in very similar compensatory changes in NREMS but evoked very different changes for all REMS parameters studied. The large REMS increase observed after 24-h SD was accompanied by a reduction in unsuccessful PREs and an increase in sustained REMS episodes, together resulting in a threefold increase in the success-rate to enter REMS. Changes in success-rate matched those of a theoretically derived long-term REMS pressure. The SD induced changes in sleep architecture could be reproduced by assuming that the increased long-term REMS pressure interacts with the short-term process by increasing the probability to enter and remain in REMS. (+info)
Short-term homeostasis of REM sleep assessed in an intermittent REM sleep deprivation protocol in the rat.
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An intermittent rapid eye movement (REM) sleep deprivation protocol was applied to determine whether an increase in REM sleep propensity occurs throughout an interval without REM sleep comparable with the spontaneous sleep cycle of the rat. Seven chronically implanted rats under a 12 : 12 light-dark schedule were subjected to an intermittent REM sleep deprivation protocol that started at hour 6 after lights-on and lasted for 3 h. It consisted of six instances of a 10-min REM sleep permission window alternating with a 20-min REM sleep deprivation window. REM sleep increased throughout the protocol, so that total REM sleep in the two REM sleep permission windows of the third hour became comparable with that expected in the corresponding baseline hour. Attempted REM sleep transitions were already increased in the second deprivation window. Attempted transitions to REM sleep were more frequent in the second than in the first half of any 20-min deprivation window. From one deprivation window to the next, transitions to REM sleep changed in correspondence to the amount of REM sleep in the permission window in-between. Our results suggest that: (i) REM sleep pressure increases throughout a time segment similar in duration to a spontaneous interval without REM sleep; (ii) it diminishes during REM sleep occurrence; and (iii) that drop is proportional to the intervening amount of REM sleep. These results are consistent with a homeostatic REM sleep regulatory mechanism that operates in the time scale of spontaneous sleep cycle. (+info)
Slow release caffeine and prolonged (64-h) continuous wakefulness: effects on vigilance and cognitive performance.
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Some long work or shift work schedules necessitate an elevated and prolonged level of vigilance and performance but often result in sleep deprivation (SD), fatigue and sleepiness, which may impair efficiency. This study investigated the effects of a slow-release caffeine [(SRC) at the daily dose of 600 mg] on vigilance and cognitive performance during a 64 h continuous wakefulness period. Sixteen healthy males volunteered for this double-blind, randomised, placebo controlled, two-way crossover study. A total of 300-mg SRC or placebo (PBO) was given twice a day at 21:00 and 9:00 h during the SD period. Vigilance was objectively assessed with continuous electroencephalogram (EEG), the multiple sleep latency tests (MSLT) and wrist actigraphy. Cognitive functions (information processing and working memory), selective and divided attention were determined with computerised tests from the AGARD-NATO STRES Battery (Standardised Tests for Research with Environmental Stressors). Attention was also assessed with a symbol cancellation task and a Stroop's test; alertness was appreciated from visual analogue scales (VAS). Tests were performed at the hypo (02:00-04:00 h, 14:00-16:00 h) and hypervigilance (10:00-12:00 h, 22:00-00:00 h) periods during SD. Central temperature was continuously measured and safety of treatment was assessed from repeated clinical examinations. Compared with PBO, MSLT showed that SRC subjects were more vigilant from the onset (P=0.001) to the end of SD (P < 0.0001) whereas some cognitive functions were improved till the thirty third of SD but others were ameliorated through all the SD period and alertness was better from the thirteenth hour of SD, as shown by Stroop's test (P=0.048). We showed that 300-mg SRC given twice daily during a 64-h SD is able to antagonize the impairment produced on vigilance and cognitive functions. (+info)
The effects of 1 week of REM sleep deprivation on parvalbumin and calbindin immunoreactive neurons in central visual pathways of kittens.
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Many maturational processes in the brain are at high levels prenatally as well as neonatally before eye-opening, when extrinsic sensory stimulation is limited. During these periods of rapid brain development, a large percentage of time is spent in rapid eye movement (REM) sleep, a state characterized by high levels of endogenously produced brain activity. The abundance of REM sleep in early life and its ensuing decline to lower levels in adulthood strongly suggest that REM sleep constitutes an integral part of the activity-dependent processes that enable normal physiological and structural brain development. We examined the effect of REM sleep deprivation during the critical period for visual development on the development of two calcium-binding proteins that are associated with developmental synaptic plasticity and are found in the lateral geniculate nucleus (LGN) and visual cortex. In this study, REM sleep deprivation was carried out utilizing a computer-controlled, cage-shaking apparatus that successfully suppressed REM sleep. Body weight data suggested that this method of REM sleep deprivation produced less stress than the classical multiple-platform-over-water method. In REM sleep-deprived animals with normal binocular vision, the number of parvalbumin-immunoreactive (PV) neurons in LGN was found to be lower compared with control animals but was not affected in visual cortex. The pattern of calbindin-immunoreactivity (CaB) was unchanged at either site after REM sleep deprivation. Parvalbumin-immunoreactivity develops later than calbindin-immunoreactivity in the LGN, and the REM sleep deprivation that we applied from postnatal day 42-49 delayed this essential step in the development of the kitten's visual system. These data suggest that in early postnatal brain development, REM sleep facilitates the usual time course of the expression of PV-immunoreactivity in LGN neurons. (+info)
Driver sleepiness and risk of serious injury to car occupants: population based case control study.
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OBJECTIVES: To estimate the contribution of driver sleepiness to the causes of car crash injuries. DESIGN: Population based case control study. SETTING: Auckland region of New Zealand, April 1998 to July 1999. PARTICIPANTS: 571 car drivers involved in crashes where at least one occupant was admitted to hospital or killed ("injury crash"); 588 car drivers recruited while driving on public roads (controls), representative of all time spent driving in the study region during the study period. MAIN OUTCOME MEASURES: Relative risk for injury crash associated with driver characteristics related to sleep, and the population attributable risk for driver sleepiness. RESULTS: There was a strong association between measures of acute sleepiness and the risk of an injury crash. After adjustment for major confounders significantly increased risk was associated with drivers who identified themselves as sleepy (Stanford sleepiness score 4-7 v 1-3; odds ratio 8.2, 95% confidence interval 3.4 to 19.7); with drivers who reported five hours or less of sleep in the previous 24 hours compared with more than five hours (2.7, 1.4 to 5.4); and with driving between 2 am and 5 am compared with other times of day (5.6, 1.4 to 22.7). No increase in risk was associated with measures of chronic sleepiness. The population attributable risk for driving with one or more of the acute sleepiness risk factors was 19% (15% to 25%). CONCLUSIONS: Acute sleepiness in car drivers significantly increases the risk of a crash in which a car occupant is injured or killed. Reductions in road traffic injuries may be achieved if fewer people drive when they are sleepy or have been deprived of sleep or drive between 2 am and 5 am. (+info)
Sawtooth waves during REM sleep after administration of haloperidol combined with total sleep deprivation in healthy young subjects.
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We sought to examine the possible participation of dopaminergic receptors in the phasic events that occur during rapid eye movement (REM) sleep, known as sawtooth waves (STW). These phasic phenomena of REM sleep exhibit a unique morphology and, although they represent a characteristic feature of REM sleep, little is known about the mechanisms which generate them and which are apparently different from rapid eye movements. STW behavior was studied in 10 male volunteers aged 20 to 35 years, who were submitted to polysomnographic monitoring (PSG). On the adaptation night they were submitted to the first PSG and on the second night, to the basal PSG. On the third night the volunteers received placebo or haloperidol and spent the whole night awake. On the fourth night they were submitted to the third PSG. After a 15-day rest period, the volunteers returned to the sleep laboratory and, according to a double-blind crossover randomized design, received haloperidol or placebo and spent the whole night awake, after which they were submitted to the fourth PSG. The volunteers who were given haloperidol combined with sleep deprivation exhibited an elevation of the duration and density of the STW, without significant alterations of the other REM sleep phasic phenomena such as rapid eye movement. These findings suggest that sawtooth waves must have their own generating mechanisms and that the dopaminergic receptors must exert a modulating role since REM sleep deprivation, as well as administration of neuroleptics, produces supersensitivity of dopaminergic receptors. (+info)
Electrodermal activity during total sleep deprivation and its relationship with other activation and performance measures.
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The present study analyses the variations of the skin resistance level (SRL) during 48 h of total sleep deprivation (TSD) and its relationship to body temperature, self-informed sleepiness in the Stanford Sleepiness Scale (SSS), and reaction time (RT). All of the variables were evaluated every 2 h except for the SSS, which was evaluated every hour. A total of 30 healthy subjects (15 men and 15 women) from 18 to 24 years old participated in the experiment. Analyses of variance (ANOVAs) with TSD days and time-of-day as factors showed a substantial increase of SRL, SSS, and RT, and a decrease in body temperature marked by strong circadian oscillations. The interaction between day by time-of-day was only significant for RT. Furthermore, Pearson's correlations showed that the increase of SRL is associated to the decrease in temperature (mean r=-0.511), the increase of SSS (mean r=0.509), and the deterioration of RT (mean r=0.425). The results support previous TSD reports and demonstrate the sensitivity of SRL to TSD. The non-invasive character of SRL, its simplicity, and its relationships with other activation parameters, widely validated by previous literature, convert SRL into an interesting and useful measure in this field. (+info)
Involvement of 5-HT1A receptors in homeostatic and stress-induced adaptive regulations of paradoxical sleep: studies in 5-HT1A knock-out mice.
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For the last two decades, the involvement of 5-HT(1A) receptors in the regulation of vigilance states has been studied extensively thanks to pharmacological tools, but clear-cut conclusion has not been reached yet. By studying mutant mice that do not express this receptor type (5-HT(1A)-/-) and their wild-type 129/Sv counterparts, we herein demonstrate that 5-HT(1A) receptors play key roles in the control of spontaneous sleep-wakefulness cycles, as well as in homeostatic regulation and stress-induced adaptive changes of paradoxical sleep. Both strains of mice exhibited a diurnal sleep-wakefulness rhythm, but 5-HT(1A)-/- animals expressed higher amounts of paradoxical sleep than wild-type mice during both the light and the dark phases. In wild-type mice, pharmacological blockade of 5-HT(1A) receptors by WAY 100635 (0.5 mg/kg, i.p.) promoted paradoxical sleep, whereas the 5-HT(1A) agonist 8-OH-DPAT (0.25-1 mg/kg, s.c.) had an opposite effect. In contrast, none of the 5-HT(1A) receptor ligands affected sleep significantly in 5-HT(1A)-/- mice. However, 5-HT(1B) receptor stimulation by CP 94253 (1-3 mg/kg, i.p.) induced a reduction in paradoxical sleep in both strains, this effect being more pronounced in 5-HT(1A)-/- mutants. Finally, in contrast to wild-type mice, 5-HT(1A)-/- mutants did not exhibit any rebound of paradoxical sleep after either a 9 hr instrumental paradoxical sleep deprivation or a 90 min immobilization stress. Altogether, these data indicate that, in the mouse, 5-HT(1A) receptors participate in the spontaneous and homeostatic regulation, as well as in stress-induced adaptive changes of paradoxical sleep. (+info)