蓝斑
肠-脑轴
神经科学
肠道菌群
生物
脑干
去甲肾上腺素
多巴胺
背运动核
酪氨酸羟化酶
细胞生物学
化学
药理学
核心
生物化学
迷走神经
刺激
作者
Hayatte-Dounia Mir,Qingning Yang,Elise Maximin,Quentin Montardy,Shuqin Ji,Qi Cheng,Xiaochun Shan,Liping Wang,Laurent Naudon,Sylvie Rabot,Lei Li
标识
DOI:10.1016/j.nbd.2024.106606
摘要
The gut microbiota produces metabolites that enrich the host metabolome and play a part in host physiology, including brain functions. Yet the biological mediators of this gut-brain signal transduction remain largely unknown. In this study, the possible role of the gut microbiota metabolite indole, originating from tryptophan, was investigated. Oral administration of indole to simulate microbial overproduction of this compound in the gut consistently led to impaired locomotion and anxiety-like behaviour in both C3H/HeN and C57BL/6J mice. By employing c-Fos protein expression mapping in mice, we observed a noticeable increase in brain activation within the dorsal motor nucleus of the vagus nerve (DMX) and the locus coeruleus (LC) regions in a dose-dependent manner. Further immune co-labelling experiments elucidated that the primary cells activated within the LC were tyrosine hydroxylase positive. To delve deeper into the mechanistic aspects, we conducted chemogenetic activation experiments on LC norepinephrine neurons with two doses of clozapine N-oxide (CNO). Low dose of CNO at 0.5 mg/kg induced no change in locomotion but anxiety-like behaviour, while high dose of CNO at 2 mg/kg resulted in locomotion impairment and anxiety-like behaviour. These findings support the neuroactive roles of indole in mediating gut-brain communication. It also highlights the LC as a novel hub in the gut-brain axis, encouraging further investigations.
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