期刊
CURRENT BIOLOGY
卷 19, 期 5, 页码 386-390出版社
CELL PRESS
DOI: 10.1016/j.cub.2009.01.040
关键词
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资金
- National Institutes of Health (NIH) [R01 NS052903, MH067870]
- Burroughs Wellcome Fund
- NIH
- Center for Sleep and Circadian Biology at Northwestern University [T32HL07909]
- National Institute of Neurological Disorders and Stroke [F31NS062551]
Sleep is regulated by a circadian clock that times sleep and wake to specific times of day and a homeostat that drives sleep as a function of prior wakefulness [1]. To analyze the role of the circadian clock, we have used the fruit fly Drosophila [2]. Flies display the core behavioral features of sleep, including relative immobility, elevated arousal thresholds, and homeostatic regulation [2,3]. We assessed sleep-wake modulation by a core set of circadian pacemaker neurons that express the neuropeptide PDF. We find that disruption of PDF function increases sleep during the late night in light:dark and the first subjective day of constant darkness. Flies deploy genetic and neurotransmitter pathways to regulate sleep that are similar to those of their mammalian counterparts, including GABA [4]. We find that RNA interference-mediated knockdown of the GABA(A) receptor gene, Resistant to dieldrin (Rdl), in PDF neurons reduces sleep, consistent with a role for GABA in inhibiting PDF neuron function. Patch-clamp electrophysiology reveals GABA-activated picrotoxin-sensitive chloride currents on PDF+ neurons. In addition, RDL is detectable most strongly on the large subset of PDF+ pacemaker neurons. These results suggest that GABAergic inhibition of arousal-promoting PDF neurons is an important mode of sleep-wake regulation in vivo.
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