| 注册
首页|期刊导航|军事医学|基底前脑Oxtr+神经元在慢性社交挫败应激中的功能研究

基底前脑Oxtr+神经元在慢性社交挫败应激中的功能研究

宁书艺 李灏 李燊 杨睿 余燕 吴海涛

军事医学2026,Vol.50Issue(6):408-416,9.
军事医学2026,Vol.50Issue(6):408-416,9.DOI:10.7644/j.issn.1674-9960.2026-00004

基底前脑Oxtr+神经元在慢性社交挫败应激中的功能研究

Functional investigation of Oxtr+ neurons in the basal forebrain during chronic social defeat stress

宁书艺 1李灏 1李燊 1杨睿 1余燕 2吴海涛3

作者信息

  • 1. 军事科学院军事医学研究院,北京 100850
  • 2. 青岛大学基础医学院,山东 青岛 266071
  • 3. 军事科学院军事医学研究院,北京 100850||青岛大学基础医学院,山东 青岛 266071
  • 折叠

摘要

Abstract

Objective To investigate the regulatory role of oxytocin receptors(Oxtr)in the basal forebrain in chronic social defeat stress(CSDS)-induced social avoidance behavior.Methods c-Fos immunofluorescence staining,stereotaxic injection,fiber photometry calcium recording,and RNAscope in situ hybridization were employed to compare behavioral performance and neural activity between wild-type mice and those with basal forebrain-specific Oxtr deletion under the CSDS model.Results Compared with the control group without CSDS exposure,CSDS-exposed mice had their social interactions with unfamiliar CD1 mice significantly shortened,accompanied by a marked increase in the proportion of c-Fos-positive neurons in the basal forebrain.Fiber photometry recordings suggested that calcium activity in Oxtr+ neurons of the basal forebrain was significantly enhanced during social interactions in CSDS mice.Notably,selective deletion of Oxtr in the basal forebrain significantly alleviated CSDS-induced social avoidance and effectively attenuated stress-induced neuronal hyperactivation.Conclusion Basal forebrain Oxtr+neurons play a key regulatory role in chronic social defeat stress-induced social avoidance and the processing of social fear-related cues.

关键词

基底前脑/催产素受体/慢性社交挫败应激/社交回避/社交恐惧

Key words

basal forebrain/oxytocin receptor/chronic social defeat stress/social avoidance/social fear

分类

生物科学

引用本文复制引用

宁书艺,李灏,李燊,杨睿,余燕,吴海涛..基底前脑Oxtr+神经元在慢性社交挫败应激中的功能研究[J].军事医学,2026,50(6):408-416,9.

基金项目

国家自然科学基金面上项目(32171148) (32171148)

国家自然科学基金杰出青年科学基金项目(32325025) (32325025)

军事医学

1674-9960

访问量0
|
下载量0
段落导航相关论文