Microbial metabolites regulate social novelty via CaMKII neurons in the BNST

Chia Wei Liou, Sin Jhong Cheng, Tzu Hsuan Yao, Tzu Ting Lai, Yu Hsuan Tsai, Che Wei Chien, Yu Lun Kuo, Shih Hsuan Chou, Cheng Chih Hsu, Wei Li Wu

研究成果: Article同行評審

2 引文 斯高帕斯(Scopus)

摘要

Social novelty is a cognitive process that is essential for animals to interact strategically with conspecifics based on their prior experiences. The commensal microbiome in the gut modulates social behavior through various routes, including microbe-derived metabolite signaling. Short-chain fatty acids (SCFAs), metabolites derived from bacterial fermentation in the gastrointestinal tract, have been previously shown to impact host behavior. Herein, we demonstrate that the delivery of SCFAs directly into the brain disrupts social novelty through distinct neuronal populations. We are the first to observe that infusion of SCFAs into the lateral ventricle disrupted social novelty in microbiome-depleted mice without affecting brain inflammatory responses. The deficit in social novelty can be recapitulated by activating calcium/calmodulin-dependent protein kinase II (CaMKII)-labeled neurons in the bed nucleus of the stria terminalis (BNST). Conversely, chemogenetic silencing of the CaMKII-labeled neurons and pharmacological inhibition of fatty acid oxidation in the BNST reversed the SCFAs-induced deficit in social novelty. Our findings suggest that microbial metabolites impact social novelty through a distinct neuron population in the BNST.

原文English
頁(從 - 到)104-123
頁數20
期刊Brain, Behavior, and Immunity
113
DOIs
出版狀態Published - 2023 10月

All Science Journal Classification (ASJC) codes

  • 免疫學
  • 內分泌和自主系統
  • 行為神經科學

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