Loss of transient receptor potential channel 5 causes obesity and postpartum depression

生物 瞬时受体电位通道 肥胖 萧条(经济学) 受体 瞬态(计算机编程) 内分泌学 内科学 遗传学 医学 计算机科学 经济 宏观经济学 操作系统
作者
Yongxiang Li,Tessa Cacciottolo,Na Yin,Yang He,Hesong Liu,Hailan Liu,Yuxue Yang,Elana Henning,Julia M. Keogh,Katherine Lawler,Edson Mendes de Oliveira,Eugene J. Gardner,Katherine A. Kentistou,Panayiotis Laouris,Rebecca Bounds,Ken K. Ong,John R. B. Perry,Inês Barroso,Longlong Tu,Jonathan C. Bean,Meng Yu,Kristine M. Conde,Sheng Wang,Olivia Ginnard,Xing Fang,Lydia Tong,Junying Han,Tia Darwich,Kevin W. Williams,Yongjie Yang,Chunmei Wang,Shelagh Joss,Helen V. Firth,Yong Xu,I. Sadaf Farooqi
出处
期刊:Cell [Elsevier]
卷期号:187 (16): 4176-4192.e17 被引量:7
标识
DOI:10.1016/j.cell.2024.06.001
摘要

Hypothalamic neural circuits regulate instinctive behaviors such as food seeking, the fight/flight response, socialization, and maternal care. Here, we identified microdeletions on chromosome Xq23 disrupting the brain-expressed transient receptor potential (TRP) channel 5 (TRPC5). This family of channels detects sensory stimuli and converts them into electrical signals interpretable by the brain. Male TRPC5 deletion carriers exhibited food seeking, obesity, anxiety, and autism, which were recapitulated in knockin male mice harboring a human loss-of-function TRPC5 mutation. Women carrying TRPC5 deletions had severe postpartum depression. As mothers, female knockin mice exhibited anhedonia and depression-like behavior with impaired care of offspring. Deletion of Trpc5 from oxytocin neurons in the hypothalamic paraventricular nucleus caused obesity in both sexes and postpartum depressive behavior in females, while Trpc5 overexpression in oxytocin neurons in knock-in mice reversed these phenotypes. We demonstrate that TRPC5 plays a pivotal role in mediating innate human behaviors fundamental to survival, including food seeking and maternal care.
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