期刊
JOURNAL OF NEUROSCIENCE
卷 36, 期 13, 页码 3709-3721出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3906-15.2016
关键词
adenosine; adenosine kinase; delta power; glia; SWS; sleep
资金
- National Institutes of Health [MH06777, NS075545]
- Department of Veterans Affairs, Dallas Veterans Administration Medical Center [MH79710, MH083711, DA016672]
- University of Texas Southwestern Medical Center
- Intra-Cellular Therapies, Inc.
- Japan Society for the Promotion of Science through the Funding Program for World-Leading Innovative R&D on Science and Technology (FIRST)
Sleep homeostasis reflects a centrally mediated drive for sleep, which increases during waking and resolves during subsequent sleep. Here we demonstrate that mice deficient for glial adenosine kinase (AdK), the primary metabolizing enzyme for adenosine (Ado), exhibit enhanced expression of this homeostatic drive by three independent measures: (1) increased rebound of slow-wave activity; (2) increased consolidation of slow-wave sleep; and (3) increased time constant of slow-wave activity decay during an average slow-wave sleep episode, proposed and validated here as a new index for homeostatic sleep drive. Conversely, mice deficient for the neuronal adenosine A1 receptor exhibit significantly decreased sleep drive as judged by these same indices. Neuronal knock-out of AdK did not influence homeostatic sleep need. Together, these findings implicate a glial-neuronal circuit mediated by intercellular Ado, controlling expression of homeostatic sleep drive. Because AdK is tightly regulated by glial metabolic state, our findings suggest a functional link between cellular metabolism and sleep homeostasis.
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