期刊
CELL REPORTS
卷 24, 期 9, 页码 2231-+出版社
CELL PRESS
DOI: 10.1016/j.celrep.2018.07.082
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资金
- Japan Agency for Medical Research and Development (AMED)-Core Research for Evolution Science and Technology (CREST) (AMED/Ministry of Education, Culture, Sports, Science and Technology [MEXT]) [JP17gm0610006]
- CREST (Japan Science and Technology Agency [JST]/MEXT)
- Brain Mapping by Integrated Neurotechnologies for Disease Studies (Brain/MINDS) (AMED/MEXT)
- Basic Science and Platform Technology Program for Innovative Biological Medicine (AMED/MEXT)
- Japan Society for the Promotion of Science [JSPS] KAKENHI [25221004]
- JSPS KAKENHI [15H04408, 23115006, 26113720]
- RIKEN
- RIKEN Quantitative Biology Center
- RIKEN Special Postdoctoral Research Program
- ECARD grant from Queensland University of Technology
- strategic programs for R&D (President's Discretionary Fund) of RIKEN
- [25560427]
- [13J01565]
- [16K21619]
- Grants-in-Aid for Scientific Research [15H04408, 26113720] Funding Source: KAKEN
Sleep regulation involves interdependent signaling among specialized neurons in distributed brain regions. Although acetylcholine promotes wakefulness and rapid eye movement (REM) sleep, it is unclear whether the cholinergic pathway is essential (i.e., absolutely required) for REM sleep because of redundancy from neural circuits to molecules. First, we demonstrate that synaptic inhibition of TrkA+ cholinergic neurons causes a severe short-sleep phenotype and that sleep reduction is mostly attributable to a shortened sleep duration in the dark phase. Subsequent comprehensive knockout of acetylcholine receptor genes by the triple-target CRISPR method reveals that a similar short-sleep phenotype appears in the knockout of two Gq-type acetylcholine receptors Chrm1 and Chrm3. Strikingly, Chrm1 and Chrm3 double knockout chronically diminishes REM sleep to an almost undetectable level. These results suggest that muscarinic acetylcholine receptors, Chrm1 and Chrm3, are essential for REM sleep.
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