Sleep deprivation: Effect on sleep stages and EEG power density in man

Borbély, Alexander A.; Baumann, Fritz; Brandeis, Daniel; Strauch, Inge; Lehmann, Dietrich

doi:10.1016/0013-4694(81)90225-x

Cited by 915 publications

(491 citation statements)

References 21 publications

Supporting

Mentioning

429

Contrasting

Unclassified

Order By: Relevance

“…These data confirm the results obtained in mice of other lines (Franken et al, 2001;Lena et al, 2004;Tobler et al, 1997), and are consistent with those in humans after one night of sleep deprivation (Borbely et al, 1981;Dijk and Beersma, 1989).…”

Section: Effect Of Sleep Deprivationsupporting

confidence: 92%

“…It has been well documented that sleep regulation depends on a homeostatic drive (Borbely et al, 1981). During recovery from sleep deprivation, this homeostatic drive notably causes an increase of slow wave activity (SWA) assessed by quantitative EEG measures, in humans (Borbely et al, 1981), rats (Borbely et al, 1981;Tobler and Borbely, 1990), as well as mice (Franken et al, 2001;Lena et al, 2004;Tobler et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

“…During recovery from sleep deprivation, this homeostatic drive notably causes an increase of slow wave activity (SWA) assessed by quantitative EEG measures, in humans (Borbely et al, 1981), rats (Borbely et al, 1981;Tobler and Borbely, 1990), as well as mice (Franken et al, 2001;Lena et al, 2004;Tobler et al, 1997). The magnitude of SWA depends on the duration of prior waking (Tobler and Borbely, 1990), which suggests that SWA is a marker for sleep intensity (Borbely et al, 1981). On the other hand, it has been shown that stress-elicited activation of the hypothalamo-pituitary-adrenocortical (HPA) axis triggers a REM sleep rebound (Boutrel et al, 2002;Lena et al, 2004;Rampin et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Homeostatic Regulation of Sleep in a Genetic Model of Depression in the Mouse: Effects of Muscarinic and 5-HT1A Receptor Activation

Popa

Yacoubi²,

Vaugeois³

et al. 2005

Neuropsychopharmacol

View full text Add to dashboard Cite

In depressed patients, sleep undergoes marked alterations, especially sleep onset insomnia, sleep fragmentation, and disturbances of the Rapid Eye Movement (REM) sleep. Abnormalities of rest-activity rhythms and of hypothalamic-pituitary-adrenocortical function have also been described in these patients. In the present study, we examined the presence of such abnormalities in a recently developed line of mice (Helpless mice-H) that exhibit depression-like behaviors in validated tests, compared to the nonhelpless (NH) line derived from the same colony. Experiments were essentially carried out in females for which previous studies showed marked differences between H and NH lines. Compared to NH mice, the H line exhibited (i) lower basal locomotor activity, (ii) sleep fragmentation, shift towards lighter sleep stages, and facilitation of REM sleep reflected by increased amounts and decreased latency, (iii) larger response to the REM sleep promoting effect of muscarinic receptor stimulation (by arecoline). In contrast, H and NH mice were equally responsive to the REM sleep inhibitory effect of 5-HT 1A receptor stimulation (by 8-OH-DPAT). In addition, a deficiency in delta power enhancement after sleep deprivation was observed in the H group, and acute immobilization stress in this group failed to elicit a REM sleep rebound and was associated with a long-lasting raise in serum corticosterone levels. These results further validate H mice as a depression model and suggest they might be of particular interest for investigating the neurobiological mechanisms and possibly genetic substrates underlying sleep alterations associated with depression.

show abstract

Section: Effect Of Sleep Deprivationsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Homeostatic Regulation of Sleep in a Genetic Model of Depression in the Mouse: Effects of Muscarinic and 5-HT1A Receptor Activation

Popa

Yacoubi²,

Vaugeois³

et al. 2005

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…Recovery sleep after sleep deprivation occurs with reduced latency, and is prolonged and more intense than baseline sleep. The duration of slow wave sleep and initial low-frequency (delta/theta) activity rise as a function of time awake, while spindle frequency activity is typically reduced after sleep loss (Borbély and Achermann, 2005;Borbély et al, 1981).…”

Section: Sleep-wake Regulationmentioning

confidence: 99%

“…A powerful tool to quantify amplitude and prevalence of EEG oscillations with distinct frequencies is power spectral analysis based on the Fast-Fourier Transform (FFT) (Borbély et al, 1981). This method faithfully reveals the EEG characteristics of wakefulness, NREM sleep, and REM sleep.…”

Section: Introductionmentioning

confidence: 99%

Genetic determination of sleep EEG profiles in healthy humans

Landolt

2011

Progress in Brain Research

View full text Add to dashboard Cite

The contribution of slow brain oscillations including delta, theta, alpha, and sigma frequencies to the sleep electroencephalography (EEG) is finely regulated by circadian and homeostatic influences, and reflects functional aspects of wakefulness and sleep. Accumulating evidence demonstrates that individual sleep EEG patterns in non-rapid-eye-movement (NREM) sleep and rapid-eye-movement (REM) sleep are heritable traits. More specifically, multiple recordings in the same individuals, as well as studies in monozygotic and dizygotic twins suggest that a very high percentage of the robust interindividual variation and the high intraindividual stability of sleep EEG profiles can be explained by genetic factors (> 90% in distinct frequency bands). Still little is known about which genes contribute to different sleep EEG phenotypes in healthy humans. The genetic variations that have been identified to date include functional polymorphisms of the clock gene PER3 and of genes contributing to signal transduction pathways involving adenosine (ADA, ADORA2A), brain-derived neurotrophic factor (BDNF), dopamine (COMT), and prion protein (PRNP). Some of these polymorphisms profoundly modulate sleep EEG profiles; their effects are reviewed here. It is concluded that the search for genetic contributions to slow sleep EEG oscillations constitutes a promising avenue to identify molecular mechanisms underlying sleep-wake regulation in humans.

show abstract