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Circadian and homeostatic regulation...

Wurts, Sarah Wilder.

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Circadian and homeostatic regulation of rapid-eye-movement sleep in the rat.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Circadian and homeostatic regulation of rapid-eye-movement sleep in the rat./
Author:	Wurts, Sarah Wilder.
Description:	171 p.
Notes:	Source: Dissertation Abstracts International, Volume: 61-01, Section: B, page: 0131.
Contained By:	Dissertation Abstracts International61-01B.
Subject:	Biology, Neuroscience. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9957853
ISBN:	0599609710

Circadian and homeostatic regulation of rapid-eye-movement sleep in the rat.
Wurts, Sarah Wilder.

Circadian and homeostatic regulation of rapid-eye-movement sleep in the rat. - 171 p.

Source: Dissertation Abstracts International, Volume: 61-01, Section: B, page: 0131.

Thesis (Ph.D.)--University of California, Los Angeles, 2000.

The daily organization of arousal states can be influenced by the circadian pacemaker located in the suprachiasmatic nucleus (SCN), a homeostatic process that induces compensatory sleep in response to sleep loss, and the mutual competition between rapid-eye-movement (REM) and non-REM (NREM) sleep states for expression. Whether the circadian variation in REM sleep propensity is due to active promotion, inhibition, or passive gating of REM sleep homeostasis by the SCN is unknown. To investigate these possibilities, compensatory responses to 24-h REM sleep deprivation (RSD) were compared between SCN-lesioned (SCNx) and sham-lesioned rats at different times of day in constant dark. The attempts to enter REM sleep increased during RSD in all rats, and were modulated by circadian phase in sham-lesioned, but not SCNx rats. REM attempts doubled during the rest phase in sham-lesioned rats relative to SCNx rats, but were indistinguishable between SCNx and sham-lesioned rats during the activity phase. By contrast, the amount of compensatory REM sleep after RSD did not depend on circadian phase. Thus, transitions into REM sleep are promoted during the rest phase and are not inhibited during the activity phase, but the amount of REM sleep, once initiated, is determined primarily by homeostatic mechanisms. Circadian modulation of power in all frequency bands of the REM and NREM sleep EEG was observed. However, EEG power in REM sleep did not fluctuate with changes in REM sleep homeostasis in any frequency band. Therefore, daily oscillations in REM sleep EEG power cannot be attributed to changes in REM sleep homeostasis. NREM delta power decreased during RSD, and NREM duration abated for 4 h post-RSD, showing the homeostatic drive for REM sleep suppresses the expression of NREM sleep. The dynamics between arousal states after total sleep deprivation are sensitive to adenosine antagonism. Caffeine slowed the rate of NREM recovery, did not influence the amount of compensatory NREM, but shifted the onset of REM recovery and permitted substantially more compensatory REM sleep. Recovery sleep after caffeine occurred preferentially during the activity phase. Most importantly, these studies support a role for the SCN in the active promotion of cortical desynchronization that manifests as wakefulness or REM sleep at specific times of day.

ISBN: 0599609710Subjects--Topical Terms:

1017680
Biology, Neuroscience.

Circadian and homeostatic regulation of rapid-eye-movement sleep in the rat.
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245 1 0 $a Circadian and homeostatic regulation of rapid-eye-movement sleep in the rat.
300 $a 171 p.
500 $a Source: Dissertation Abstracts International, Volume: 61-01, Section: B, page: 0131.
500 $a Co-Chairs: Jerome Siegel; Dale M. Edgar.
502 $a Thesis (Ph.D.)--University of California, Los Angeles, 2000.
520 $a The daily organization of arousal states can be influenced by the circadian pacemaker located in the suprachiasmatic nucleus (SCN), a homeostatic process that induces compensatory sleep in response to sleep loss, and the mutual competition between rapid-eye-movement (REM) and non-REM (NREM) sleep states for expression. Whether the circadian variation in REM sleep propensity is due to active promotion, inhibition, or passive gating of REM sleep homeostasis by the SCN is unknown. To investigate these possibilities, compensatory responses to 24-h REM sleep deprivation (RSD) were compared between SCN-lesioned (SCNx) and sham-lesioned rats at different times of day in constant dark. The attempts to enter REM sleep increased during RSD in all rats, and were modulated by circadian phase in sham-lesioned, but not SCNx rats. REM attempts doubled during the rest phase in sham-lesioned rats relative to SCNx rats, but were indistinguishable between SCNx and sham-lesioned rats during the activity phase. By contrast, the amount of compensatory REM sleep after RSD did not depend on circadian phase. Thus, transitions into REM sleep are promoted during the rest phase and are not inhibited during the activity phase, but the amount of REM sleep, once initiated, is determined primarily by homeostatic mechanisms. Circadian modulation of power in all frequency bands of the REM and NREM sleep EEG was observed. However, EEG power in REM sleep did not fluctuate with changes in REM sleep homeostasis in any frequency band. Therefore, daily oscillations in REM sleep EEG power cannot be attributed to changes in REM sleep homeostasis. NREM delta power decreased during RSD, and NREM duration abated for 4 h post-RSD, showing the homeostatic drive for REM sleep suppresses the expression of NREM sleep. The dynamics between arousal states after total sleep deprivation are sensitive to adenosine antagonism. Caffeine slowed the rate of NREM recovery, did not influence the amount of compensatory NREM, but shifted the onset of REM recovery and permitted substantially more compensatory REM sleep. Recovery sleep after caffeine occurred preferentially during the activity phase. Most importantly, these studies support a role for the SCN in the active promotion of cortical desynchronization that manifests as wakefulness or REM sleep at specific times of day.
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