Contribution of the circadian pacemaker and the sleep homeostat to sleep propensity, sleep structure, electroencephalographic slow waves, and sleep spindle activity in humans

Dijk, Derk‐Jan; Czeisler, Charles A.

doi:10.1523/jneurosci.15-05-03526.1995

Cited by 1,168 publications

(927 citation statements)

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“…Sigma activity, which correlates well with sleep spindle activity (Dijk and Czeisler, 1995), was reduced in PER3 5/5 individuals. Sleep spindles comprise the interplay of reticular thalamic, thalamocortical, and cortical pyramidal cells (Steriade et al, 1993), and are under circadian control (Dijk and Czeisler, 1995;Wei et al, 1999), such that the circadian pacemaker actively promotes spindles during the night, presumably to promote sleep consolidation (Dijk and Czeisler, 1995).…”

Section: Discussionmentioning

confidence: 67%

Interindividual differences in circadian rhythmicity and sleep homeostasis in older people: effect of a PER3 polymorphism

Viola

Chellappa

Archer

et al. 2012

Neurobiology of Aging

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Aging is associated with marked changes in the timing, consolidation and structure of sleep. Older people wake up frequently, get up earlier and have less slow wave sleep than young people, although the extent of these age-related changes differs considerably between individuals. Interindividual differences in homeostatic sleep regulation in young volunteers are associated with the variable-number, tandem-repeat (VNTR) polymorphism (rs57875989) in the coding region of the circadian clock gene PERIOD3 (PER3). However, predictors of these interindividual differences have yet to be identified in older people. Sleep electroencephalographic (EEG) characteristics and circadian rhythms were assessed in 26 healthy older volunteers (55-75 years) selected on the basis of homozygosity for either the long or short allele of the PER3 polymorphism. Homozygosity for the longer allele (PER3 5/5 ) associated with a phase-advance in the circadian melatonin profile and an earlier occurrence of the melatonin peak within the sleep episode. Furthermore, older PER3 5/5 participants accumulated more nocturnal wakefulness, had increased EEG frontal delta activity (0.75-1.50 Hz), and decreased EEG frontal sigma activity (11-13 Hz) during non-rapid eye movement (REM) sleep compared with PER3 4/4 participants. Our results indicate that the polymorphism in the clock gene PER3 may contribute to interindividual differences in sleep and circadian physiology in older people.

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Section: Discussionmentioning

confidence: 67%

Interindividual differences in circadian rhythmicity and sleep homeostasis in older people: effect of a PER3 polymorphism

Viola

Chellappa

Archer

et al. 2012

Neurobiology of Aging

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“…Since circadian phase has a profound effect on both the efficiency and structure of sleep [6], this finding must be interpreted only for conditions of the current experiment, where anchor sleeps occurred in the nocturnal portion of the circadian cycle and nap sleep in the diurnal portion. A separate experiment in which anchor and nap sleep placements are reversed in circadian time is being completed and will provide needed information on the extent to which circadian placement of split sleeps affects total sleep obtained and its recovery potential.…”

Section: Discussionmentioning

confidence: 86%

“…Unlike the psychomotor vigilance task and the Stanford sleepiness scale, the digit symbol substitution task displays considerable learning effects [2]. As such, subtle differences among conditions in sleep architecture associated with the different placements of the sleep episodes [6] may have differentially affected the learning curve [18].…”

Section: Discussionmentioning

confidence: 99%

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Response surface mapping of neurobehavioral performance: Testing the feasibility of split sleep schedules for space operations

et al. 2008

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The demands of sustaining high levels of neurobehavioral performance during space operations necessitate precise scheduling of sleep opportunities in order to best preserve optimal performance. We report here the results of the first split-sleep, dose-response experiment involving a range of sleep/wake scenarios with chronically reduced nocturnal sleep, augmented with a diurnal nap. To characterize performance over all combinations of split sleep in the range studied, we used response surface mapping methodology. Waking neurobehavioral performance was studied in N=90 subjects each assigned to one of 18 sleep regimens consisting of a restricted nocturnal anchor sleep period and a diurnal nap. Psychomotor vigilance task performance and subjective assessments of sleepiness were found to be primarily a function of total time in bed per 24 h regardless of how sleep was divided among nocturnal anchor sleep and diurnal nap periods. Digit symbol substitution task performance was also found to be primarily a function of total time in bed per 24 h; however, accounting for nocturnal sleep duration and nap duration separately provided a small but significant enhancement in the variance explained. The results suggest that reductions in total daily sleep result in a near-linear accumulation of impairment regardless of whether sleep is scheduled as a consolidated nocturnal sleep period or split into a nocturnal anchor sleep period and a diurnal nap. Thus, split sleep schedules are feasible and can be used to enhance the flexibility of sleep/work schedules for space operations involving restricted nocturnal sleep due to mission-critical task scheduling. These results are generally applicable to any continuous industrial operation that involves sleep restriction, night operations, and shift work.

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“…The timing of sleep and wakefulness and the structure of sleep are regulated by the interaction of a homeostatic, sleep-wake-dependent process S and the circadian pacemaker located in the hypothalamus Dijk and Czeisler 1995). Similar mechanisms may underlie the regulation of mood (Boivin et al 1997;Wirz-Justice and Van den Hoofdakker 1999).…”

mentioning

confidence: 99%

Different Effects of Phenelzine Treatment on EEG Topography in Waking and Sleep in Depressed Patients

Landolt

Gillin

2002

Neuropsychopharmacology

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A novel approach to investigate the relationship between depression and changes in sleep-wake regulatory mechanisms used the monoamine oxidase inhibitor (MAOI) phenelzine that is known to suppress rapid-eye-movement (REM) sleep. Sleep architecture and EEG topography during wakefulness and sleep were studied in eight depressed patients before and after five weeks of treatment with phenelzine (30-90 mg/day), which induced a significant alleviation of depressive symptoms. Theta power (4.75-7.5 Hz) during a 5-min wake EEG prior to sleep increased two-fold during administration of phenelzine. REM sleep was almost completely eliminated. This latter effect was compensated by increased duration of stage 2, whereas total sleep time was not shortened. In non-REM sleep (stages 2, 3, and 4), treatment slightly reduced EEG power between 2. Hz band increased. Activity in the delta band Mood and the regulation of sleep are closely related. This notion is supported by the presence of frequent sleep abnormalities in depressed patients, which may affect both rapid-eye-movement (REM) sleep and nonrapid-eye-movement (non-REM) sleep (Benca et al. 1992). A tight association between sleep and mood is further suggested by the beneficial action of total and partial sleep deprivation, as well as phase advance therapies of sleep in many patients with depression (Gillin and Borbély 1985; Wirz-Justice and Van den Hoofdakker 1999). Different theories have been proposed to account for the antidepressant effects of sleep manipulations. They include prolonged major suppression of REM sleep (Vogel 1975;Vogel et al. 1990), elevation of sleep propensity (Borbély and Wirz-Justice 1982), and reduction of non-REM sleep intensity (Beersma and Van den Hoofdakker 1992).The timing of sleep and wakefulness and the structure of sleep are regulated by the interaction of a homeostatic, sleep-wake-dependent process S and the circadian pacemaker located in the hypothalamus et al. 1981;Daan et al. 1984;Dijk et al. 1987;Achermann et al. 1993). Recent studies have indicated that an EEG correlate of sleep propensity can also be measured during wakefulness. Power in the theta band ( ‫ف‬ 5-8 Hz) of the wake EEG increases during sleep deprivation (Cajochen et al. 1995;Aeschbach et al. 1997;Finelli et al. 2000). The time constant of this increase is similar to that obtained for the wake-dependent rise of delta power as measured in non-REM sleep. Furthermore, topographical analyses of the EEG during prolonged wakefulness have shown that the increase of theta activity in waking and delta activity ( ‫ف‬ 1-4 Hz) in non-REM sleep are largest in frontal EEG derivations and positively correlated (Werth et al. 1998;Cajochen et al. 1999aCajochen et al. , 1999bFinelli et al. 2000). These findings suggest that sleep regulation may exhibit local features. In other words, frontal parts of the cortex may be particularly susceptible to sleep loss and reflect the homeostatic process of sleep regulation more sensitively than other cortical regions. The monoamine oxidase inhibitor...

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Contribution of the circadian pacemaker and the sleep homeostat to sleep propensity, sleep structure, electroencephalographic slow waves, and sleep spindle activity in humans

Abstract: We thank Al l an E. Ward and Davi d W. Rimmer for supervising the studies, the research and student technicians for data collection, Joseph M

Cited by 1,168 publications

References 79 publications

Interindividual differences in circadian rhythmicity and sleep homeostasis in older people: effect of a PER3 polymorphism

Interindividual differences in circadian rhythmicity and sleep homeostasis in older people: effect of a PER3 polymorphism

Response surface mapping of neurobehavioral performance: Testing the feasibility of split sleep schedules for space operations

Different Effects of Phenelzine Treatment on EEG Topography in Waking and Sleep in Depressed Patients

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