期刊
NEURON
卷 61, 期 2, 页码 213-219出版社
CELL PRESS
DOI: 10.1016/j.neuron.2008.11.024
关键词
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资金
- NIA NIH HHS [P01 AG017628-070006, P01 AG017628] Funding Source: Medline
- NINDS NIH HHS [R01 NS054770, R01 NS054770-04, F31 NS059091-02, R37 NS037585-11, F31 NS059091, R01 NS037585, R37 NS037585, R01 NS043142, R01 NS043142-09] Funding Source: Medline
Astrocytes modulate neuronal activity by releasing chemical transmitters via a process termed gliotransmission. The role of this process in the control of behavior is unknown. Since one outcome of SNARE-dependent gliotransmission is the regulation of extracellular adenosine and because adenosine promotes sleep, we genetically inhibited the release of gliotransmitters and asked if astrocytes play an unsuspected role in sleep regulation. Inhibiting gliotransmission attenuated the accumulation of sleep pressure, assessed by measuring the slow wave activity of the EEG during NREM sleep, and prevented cognitive deficits associated with sleep loss. Since the sleep-suppressing effects of the A1 receptor antagonist CPT were prevented following inhibition of gliotransmission and because intracerebroventricular delivery of CPT to wild-type mice mimicked the transgenic phenotype, we conclude that astrocytes modulate the accumulation of sleep pressure and its cognitive consequences through a pathway involving All receptors.
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