A non-circadian role for clock-genes in sleep homeostasis: a strain comparison.

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Type
Article: article from journal or magazin.
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Publications
Institution
Title
A non-circadian role for clock-genes in sleep homeostasis: a strain comparison.
Journal
BMC Neuroscience
Author(s)
Franken P., Thomason R., Heller H.C., O'Hara B.F.
ISSN
1471-2202
Publication state
Published
Issued date
2007
Peer-reviewed
Oui
Volume
8
Number
1
Pages
87
Language
english
Abstract
BACKGROUND: We have previously reported that the expression of circadian clock-genes increases in the cerebral cortex after sleep deprivation (SD) and that the sleep rebound following SD is attenuated in mice deficient for one or more clock-genes. We hypothesized that besides generating circadian rhythms, clock-genes also play a role in the homeostatic regulation of sleep. Here we follow the time course of the forebrain changes in the expression of the clock-genes period (per)-1, per2, and of the clock-controlled gene albumin D-binding protein (dbp) during a 6 h SD and subsequent recovery sleep in three inbred strains of mice for which the homeostatic sleep rebound following SD differs. We reasoned that if clock genes are functionally implicated in sleep homeostasis then the SD-induced changes in gene expression should vary according to the genotypic differences in the sleep rebound. RESULTS: In all three strains per expression was increased when animals were kept awake but the rate of increase during the SD as well as the relative increase in per after 6 h SD were highest in the strain for which the sleep rebound was smallest; i.e., DBA/2J (D2). Moreover, whereas in the other two strains per1 and per2 reverted to control levels with recovery sleep, per2 expression specifically, remained elevated in D2 mice. dbp expression increased during the light period both during baseline and during SD although levels were reduced during the latter condition compared to baseline. In contrast to per2, dbp expression reverted to control levels with recovery sleep in D2 only, whereas in the two other strains expression remained decreased. CONCLUSION: These findings support and extend our previous findings that clock genes in the forebrain are implicated in the homeostatic regulation of sleep and suggest that sustained, high levels of per2 expression may negatively impact recovery sleep.
Keywords
Analysis of Variance, Animals, Cell Cycle Proteins, Circadian Rhythm, DNA-Binding Proteins, Gene Expression Regulation, Homeostasis, In Situ Hybridization, Mice, Mice, Inbred Strains, Nuclear Proteins, Prosencephalon, Sleep, Sleep Deprivation, Species Specificity, Time Factors, Trans-Activators, Transcription Factors, Wakefulness
Pubmed
Web of science
Open Access
Yes
Create date
24/01/2008 15:31
Last modification date
20/08/2019 12:59
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