生物
乙酰胆碱
背运动核
干细胞
嗜铬细胞
睡眠(系统调用)
肠神经系统
神经科学
睡眠障碍
迷走神经
毒蕈碱乙酰胆碱受体
睡眠剥夺
细胞
内分泌学
内科学
迷走神经电刺激
发病机制
神经干细胞
神经发生
副交感神经系统
信号转导
肠-脑轴
再摄取
胆碱能的
作者
M. Zhang,Xi Wu,Di Liu,Huaxing Li,Xiaofeng Li,Wuqi Yang,Jialin Ye,Liyuan Hou,Shiyang Wang,Ning Ning,Hanfu Zhang,Yuhua Tian,Lu Yu,Kaichun Wu,Linlin Wang,Maksim V. Plikus,Cong Lv,Feng Wang,Zhengquan Yu
出处
期刊:Cell Stem Cell
[Elsevier BV]
日期:2026-02-01
卷期号:33 (2): 306-324.e8
标识
DOI:10.1016/j.stem.2026.01.002
摘要
Sleep disturbances are associated with pathogenesis of numerous chronic disorders, including chronic gastrointestinal diseases. However, the mechanism that transmits sleep disturbance-induced aberrant neural signaling from the brain to the gut remains elusive. We show that acute sleep deprivation (SD) impairs intestinal stem cell (ISC) function, leading to shortening of crypt-villus architecture and Paneth cell loss. We identified the dorsal motor nucleus of vagus (DMV) as the SD-sensitive central nervous system center that transmits sleep effects to the gut. SD aberrantly activates DMV neurons, driving excessive acetylcholine release from the vagus nerve into the gut. Acetylcholine triggers 5-hydroxytryptamine (5-HT) release by enterochromaffin cells and suppresses its reuptake via muscarinic receptors, thereby causing a spike in 5-HT levels. Elevated 5-HT induces excessive oxidative stress in ISCs through its receptor HTR4, promoting gut pathologies. Overall, we reveal an SD-responsive neural circuit that controls ISCs and identify therapeutic strategies for mitigating SD-related gut diseases.
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