期刊
EUROPEAN JOURNAL OF NEUROSCIENCE
卷 29, 期 9, 页码 1820-1829出版社
WILEY
DOI: 10.1111/j.1460-9568.2009.06723.x
关键词
energy metabolism; human polymorphism; knock-out mice; rhythms; sleep deprivation
资金
- University of Lausanne
- Swiss National Science Foundation
- National Institute of Mental Health [MH67752]
- Biotechnology and Biological Sciences Research Council BBSRC [BB/F022883/1]
- Wellcome Trust [069714/Z/02/Z, 0760667/Z04/Z]
- AFOSR [FA9550-08-1-0080]
- BBSRC [BB/F022883/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/F022883/1] Funding Source: researchfish
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH067752] Funding Source: NIH RePORTER
Circadian and sleep-homeostatic processes both contribute to sleep timing and sleep structure. Elimination of circadian rhythms through lesions of the suprachiasmatic nuclei (SCN), the master circadian pacemaker, leads to fragmentation of wakefulness and sleep but does not eliminate the homeostatic response to sleep loss as indexed by the increase in EEG delta power. In humans, EEG delta power declines during sleep episodes nearly independently of circadian phase. Such observations have contributed to the prevailing notion that circadian and homeostatic processes are separate but recent data imply that this segregation may not extend to the molecular level. Here we summarize the criteria and evidence for a role for clock genes in sleep homeostasis. Studies in mice with targeted disruption for core circadian clock genes have revealed alterations in circadian rhythmicity as well as changes in sleep duration, sleep structure and EEG delta power. Clock-gene expression in brain areas outside the SCN, in particular the cerebral cortex, depends to a large extent on prior sleep-wake history. Evidence for effects of clock genes on sleep homeostasis has also been obtained in Drosophila and humans, pointing to a phylogenetically preserved pathway. These findings suggest that, while within the SCN clock genes are utilized to set internal time-of-day, in the forebrain the same feedback circuitry may be utilized to track time spent awake and asleep. The mechanisms by which clock-gene expression is coupled to the sleep-wake distribution could be through cellular energy charge whereby clock genes act as energy sensors. The data underscore the interrelationships between energy metabolism, circadian rhythmicity, and sleep regulation.
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