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A specific circuit in the midbrain detects stress and induces restorative sleep
Author(s) -
Xiao Yu,
Guangchao Zhao,
Dan Wang,
Sa Wang,
Rui Li,
Ao Li,
Huan Wang,
Mathieu Nollet,
You Young Chun,
Tian-Yuan Zhao,
Raquel Yustos,
Huiming Li,
Jianshuai Zhao,
Jiannan Li,
Min Cai,
Alexei L. Vyssotski,
Yulong Li,
Hailong Dong,
Nicholas P. Franks,
William Wisden
Publication year - 2022
Publication title -
science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 12.556
H-Index - 1186
eISSN - 1095-9203
pISSN - 0036-8075
DOI - 10.1126/science.abn0853
Subject(s) - ventral tegmental area , sleep (system call) , midbrain , neuroscience , sleep deprivation , stress (linguistics) , psychology , sleep restriction , neuropeptide , dopamine , circadian rhythm , medicine , dopaminergic , computer science , central nervous system , operating system , linguistics , philosophy , receptor
In mice, social defeat stress (SDS), an ethological model for psychosocial stress, induces sleep. Such sleep could enable resilience, but how stress promotes sleep is unclear. Activity-dependent tagging revealed a subset of ventral tegmental area γ-aminobutyric acid (GABA)-somatostatin (VTA Vgat-Sst ) cells that sense stress and drive non-rapid eye movement (NREM) and REM sleep through the lateral hypothalamus and also inhibit corticotropin-releasing factor (CRF) release in the paraventricular hypothalamus. Transient stress enhances the activity of VTA Vgat-Sst cells for several hours, allowing them to exert their sleep effects persistently. Lesioning of VTA Vgat-Sst cells abolished SDS-induced sleep; without it, anxiety and corticosterone concentrations remained increased after stress. Thus, a specific circuit allows animals to restore mental and body functions by sleeping, potentially providing a refined route for treating anxiety disorders.

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