期刊
ELIFE
卷 8, 期 -, 页码 -出版社
ELIFE SCIENCES PUBLICATIONS LTD
DOI: 10.7554/eLife.44928
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资金
- Ministry of Education, Culture, Sports, Science, and Technology [17H05563, 18KK0223, 18H05124, 16H01271, 18H02523, 19H05016]
- Japan Science and Technology Agency [JPMJCR1656]
- Grants-in-Aid for Scientific Research [18H02523, 16H01271, 18KK0223, 18H05124, 17H05563, 19H05016] Funding Source: KAKEN
Sleep/wakefulness cycle is regulated by coordinated interactions between sleep- and wakefulness-regulating neural circuitry. However, the detailed mechanism is far from understood. Here, we found that glutamic acid decarboxylase 67-positive GABAergic neurons in the ventral tegmental area (VTA(Gad67+)) are a key regulator of non-rapid eye movement (NREM) sleep in mice. VTA(Gad67+) project to multiple brain areas implicated in sleep/wakefulness regulation such as the lateral hypothalamus (LH). Chemogenetic activation of VTA(Gad67+) promoted NREM sleep with higher delta power whereas optogenetic inhibition of these induced prompt arousal from NREM sleep, even under highly somnolescent conditions, but not from REM sleep. VTA(Gad67+) showed the highest activity in NREM sleep and the lowest activity in REM sleep. Moreover, VTA(Gad67+) directly innervated and inhibited wake-promoting orexin/hypocretin neurons by releasing GABA. As such, optogenetic activation of VTA(Gad67+) terminals in the LH promoted NREM sleep. Taken together, we revealed that VTA(Gad67+) play an important role in the regulation of NREM sleep.
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