Decoupling of Sleepiness from Sleep Time and Intensity during Chronic Sleep Restriction: Evidence for a Role of the Adenosine System

Kim, Youngsoo; Bolortuya, Yunren; Chen, Lichao; Basheer, Radhika; McCarley, Robert W.; Strecker, Robert E.

doi:10.5665/sleep.1890

Cited by 46 publications

(91 citation statements)

References 35 publications

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“…However, our finding of a sustained NREMS rebound during SOs across 4 days of CSR disagrees sharply with these studies in which NREMS amount during daily SOs was either decreased (35,36) or not significantly changed (40) across CSR. This discrepancy suggests that different CSR methods used in these studies may differentially affect NREMS and REMS rebound during CSR.…”

Section: Sleep Patterns During Csrcontrasting

confidence: 99%

“…The sustained REMS rebound during SOs across the 4-day CSR is consistent with three recent studies in which rats were sleep deprived for 20 or 18 h daily for 5 days using either activity wheels (35,36) or disk-over-water methods with continuous observation (40). However, our finding of a sustained NREMS rebound during SOs across 4 days of CSR disagrees sharply with these studies in which NREMS amount during daily SOs was either decreased (35,36) or not significantly changed (40) across CSR.…”

Section: Sleep Patterns During Csrsupporting

confidence: 90%

“…One reported preservation of homeostatic responses to CSR (40). The other study reported generally muted homeostatic responses to CSR and emphasized allostatic adjustments (36), a result also observed in a study that restricted sleep to 6 h daily (35). The basis for this discrepancy is not clear, but possible factors include differences in electrode derivations used for electroencephalogram (EEG) recordings, sleep deprivation (SD) procedures, the extent of EEG artifacts, and the strains of rat studied.…”

mentioning

confidence: 99%

“…In humans, several studies reported that homeostatic sleep responses were virtually absent during 4 -14 days of restriction to 3-6 h of sleep per night (5,18,23,61), whereas other studies using 4 -5 days of restriction to 4 h of sleep per night reported the presence of homeostatic responses (1,15). A number of studies used animal models to study alterations in sleep-wake patterns during CSR (17,24,35,36,39,40,43). Two recent studies restricted sleep in rats for 5 days to a single daily interval of 4 h starting at the beginning of the daily light phase (36,40) and reported contradictory results.…”

mentioning

confidence: 99%

“…The use of a single daily 4-or 6-h sleep opportunity (SO) (35,36,40) does not permit analysis of time-of-day effects on responses to sleep loss. While providing valuable information about homeostatic regulation of sleep, this model is limited because sleep propensity is known to be modulated by both homeostatic and circadian processes.…”

mentioning

confidence: 99%

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Time-of-day modulation of homeostatic and allostatic sleep responses to chronic sleep restriction in rats

Deurveilher

Rusak

Semba

2012

American Journal of Physiology-Regulatory, Integrative and Comp

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To study sleep responses to chronic sleep restriction (CSR) and time-of-day influences on these responses, we developed a rat model of CSR that takes into account the polyphasic sleep patterns in rats. Adult male rats underwent cycles of 3 h of sleep deprivation (SD) and 1 h of sleep opportunity (SO) continuously for 4 days, beginning at the onset of the 12-h light phase (“3/1” protocol). Electroencephalogram (EEG) and electromyogram (EMG) recordings were made before, during, and after CSR. During CSR, total sleep time was reduced by ∼60% from baseline levels. Both rapid eye movement sleep (REMS) and non-rapid eye movement sleep (NREMS) during SO periods increased initially relative to baseline and remained elevated for the rest of the CSR period. In contrast, NREMS EEG delta power (a measure of sleep intensity) increased initially, but then declined gradually, in parallel with increases in high-frequency power in the NREMS EEG. The amplitude of daily rhythms in NREMS and REMS amounts was maintained during SO periods, whereas that of NREMS delta power was reduced. Compensatory responses during the 2-day post-CSR recovery period were either modest or negative and gated by time of day. NREMS, REMS, and EEG delta power lost during CSR were not recovered by the end of the second recovery day. Thus the “3/1” CSR protocol triggered both homeostatic responses (increased sleep amounts and intensity during SOs) and allostatic responses (gradual decline in sleep intensity during SOs and muted or negative post-CSR sleep recovery), and both responses were modulated by time of day.

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Section: Sleep Patterns During Csrcontrasting

confidence: 99%

Section: Sleep Patterns During Csrsupporting

confidence: 90%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Time-of-day modulation of homeostatic and allostatic sleep responses to chronic sleep restriction in rats

Deurveilher

Rusak

Semba

2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Neurobiology of REM Sleep, NREM Sleep Homeostasis, and Gamma Band Oscillations

Mckenna¹,

Zielinski²,

McCarley³

2017

Sleep Disorders Medicine

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Mechanisms of the psychostimulant effects of caffeine: implications for substance use disorders

2016

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Background The psychostimulant properties of caffeine are reviewed and compared with those of prototypical psychostimulants, able to cause substance use disorders (SUD). Caffeine produces psychomotor activating, reinforcing and arousing effects, which depend on its ability to disinhibit the brake that endogenous adenosine imposes on the ascending dopamine and arousal systems. Objectives A model that considers the striatal adenosine A2A-dopamine D2 receptor heteromer as a key modulator of dopamine-dependent striatal functions (reward-oriented behavior and learning of stimulus-reward and reward-response associations) is introduced, which should explain most of the psychomotor and reinforcing effects of caffeine. Highlights The model can explain the caffeine-induced rotational behavior in rats with unilateral striatal dopamine denervation and the ability of caffeine to reverse the adipsic-aphagic syndrome in dopamine-deficient rodents. The model can also explain the weaker reinforcing effects and low abuse liability of caffeine, compared with prototypical psychostimulants. Finally the model can explain the actual major societal dangers of caffeine: the ability of caffeine to potentiate the addictive and toxic effects of drugs of abuse, with the particularly alarming associations of caffeine (as adulterant) with cocaine, amphetamine derivatives and synthetic cathinones and energy drinks with alcohol; and the higher sensitivity of children and adolescents to the psychostimulants effects of caffeine and its possible increase in the vulnerability to develop SUD. Conclusions The striatal A2A-D2 receptor heteromer constitutes an unequivocal main pharmacological target of caffeine and provides the main mechanisms by which caffeine potentiates the acute and long-term effects of prototypical psychostimulants.

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Decoupling of Sleepiness from Sleep Time and Intensity during Chronic Sleep Restriction: Evidence for a Role of the Adenosine System

Cited by 46 publications

References 35 publications

Time-of-day modulation of homeostatic and allostatic sleep responses to chronic sleep restriction in rats

Time-of-day modulation of homeostatic and allostatic sleep responses to chronic sleep restriction in rats

Neurobiology of REM Sleep, NREM Sleep Homeostasis, and Gamma Band Oscillations

Mechanisms of the psychostimulant effects of caffeine: implications for substance use disorders

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