期刊
SCIENCE
卷 350, 期 6263, 页码 957-961出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aad1023
关键词
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资金
- Japan Science and Technology Agency PRESTO program
- Ministry of Education, Cutlure, Sports, Science, and Technology of Japan (MEXT) World Premier International Research Center Initiative (WPI)
- MEXT KAKENHI [23115724, 26115503]
- Japan Society for the Promotion of Science KAKENHI [23700403, 21800090]
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Astellas Foundation for Research on Metabolic Disorders
- Sumitomo Foundation
- SENSHIN Medical Research Foundation
- Japan Foundation for Applied Enzymology (TMFC)
- RIKEN Special Postdoctoral Researcher Program
- Funding Program for World-Leading Innovative R&D on Science and Technology (FIRST Program) - Council for Science and Technology Policy (CSTP)
- RIKEN intramural fund
- Grants-in-Aid for Scientific Research [23700403, 21800090, 26115503] Funding Source: KAKEN
Mammalian sleep comprises rapid eye movement (REM) sleep and non-REM (NREM) sleep. To functionally isolate from the complex mixture of neurons populating the brainstem pons those involved in switching between REM and NREM sleep, we chemogenetically manipulated neurons of a specific embryonic cell lineage in mice. We identified excitatory glutamatergic neurons that inhibit REM sleep and promote NREM sleep. These neurons shared a common developmental origin with neurons promoting wakefulness; both derived from a pool of proneural hindbrain cells expressing Atoh1 at embryonic day 10.5. We also identified inhibitory gamma-aminobutyric acid-releasing neurons that act downstream to inhibit REM sleep. Artificial reduction or prolongation of REM sleep in turn affected slow-wave activity during subsequent NREM sleep, implicating REM sleep in the regulation of NREM sleep.
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