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A specific circuit in the midbrain detects stress and induces restorative sleep

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 GABA-somatostatin (VTA(Vgat-Sst)) cells that sense st...

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Detalles Bibliográficos
Autores principales: Yu, Xiao, Zhao, Guangchao, Wang, Dan, Wang, Sa, Li, Rui, Li, Ao, Wang, Huan, Nollet, Mathieu, Chun, You Young, Zhao, Tianyuan, Yustos, Raquel, Li, Huiming, Zhao, Jianshuai, Li, Jiannan, Cai, Min, Vyssotski, Alexei L., Li, Yulong, Dong, Hailong, Franks, Nicholas P., Wisden, William
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7612951/
https://www.ncbi.nlm.nih.gov/pubmed/35771921
http://dx.doi.org/10.1126/science.abn0853
Descripción
Sumario: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 GABA-somatostatin (VTA(Vgat-Sst)) cells that sense stress and drive NREM and REM sleep via 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 levels remained elevated after stress. Thus, a specific circuit allows animals to restore mental and body functions via sleeping, potentially providing a refined route for treating anxiety disorders.