期刊
SCIENCE
卷 335, 期 6076, 页码 1617-1621出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1212476
关键词
-
资金
- NIH [NS053087, GM054339]
- Jane Coffin Childs Memorial Fund for Medical Research
- Merck fellowship
How and why the brain reversibly switches from a waking to a sleep state remain among the most intriguing questions in biology. We show that cyclin A (CycA) and regulator of cyclin A1, essential cell cycle factors, function in postmitotic neurons to promote sleep in Drosophila melanogaster. Reducing the abundance of CycA in neurons delayed the wake-sleep transition, caused multiple arousals from sleep, and reduced the homeostatic response to sleep deprivation. CycA is expressed in similar to 40 to 50 neurons in the adult brain, most of which are intermingled with circadian clock neurons, suggesting functional interactions among neurons controlling sleep and circadian behavior.
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