慢性心理社会压力会触发微质/巨细胞诱导的炎症反应,导致神经元功能障碍和与抑郁相关的行为
Alexandros G Kokkosis1, Miguel M Madeira1, Zachary Hage1
1Department of Pharmacological Sciences, Renaissance School of Medicine at Stony Brook University, Stony Brook, New York, USA.
Glia
|September 7, 2023
概括
慢性压力会激活大脑中的微质细胞和巨细胞,导致神经炎症和与抑郁症相关的突触损伤. 抑制这些细胞可以改善压力引起的行为缺陷,揭示了它在情绪障碍中的关键作用.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 精神病学是一个精神病学.
背景情况:
- 慢性压力和创伤是主要抑郁症 (MDD) 和焦虑症的危险因素.
- 中间前额皮层 (mPFC) 中的神经炎症和突触可塑性的改变与与压力有关的疾病有关.
- 微质在调解压力诱导的行为变化中的确切作用尚不清楚.
研究的目的:
- 调查微质激活和神经炎症在慢性心理社会压力期间mPFC中的作用.
- 确定微质细胞如何调节神经元可塑性和行为结果,以应对压力.
- 评估向微质在与压力相关的行为缺陷中的治疗潜力.
主要方法:
- 利用重复社会失败压力 (RSDS) 鼠标模型来模拟慢性心理社会压力.
- 在mPFC中检查了微质和巨细胞的激活,增殖和透,使用免疫组织化学.
- 评估了神经元激活和突触可塑性标记物.
- 使用CSF1R抑制剂 (PLX5622和PLX73086) 调节微质/巨细胞活动.
- 评估压力诱导的行为变化.
主要成果:
- 慢性压力迅速激活mPFC中的微质和巨细胞,与神经元激活空间相关.
- 微质炎症反应与对慢性压力的易感性或弹性有关.
- 压力加剧了突触元细胞分裂和神经元可塑性受损.
- 使用CSF1R抑制剂抑制微质/巨细胞可以改善mPFC中压力诱导的行为缺陷.
结论:
- 微细胞和巨细胞在调解与慢性心理社会压力相关的神经炎症和神经可塑性变化方面发挥着关键作用.
- 针对mPFC中的微质和巨细胞活动,为抑郁症和焦虑障碍提供了潜在的治疗策略.
- 这些发现阐明了先天免疫细胞对与压力相关的精神疾病病理生理学的贡献.
关键词:
慢性压力是一种慢性压力.与抑郁相关的行为.这是先天免疫力.巨细胞是什么?巨细胞是什么?微质细胞中的微质细胞神经炎症是一种神经炎症.神经元功能障碍是指神经元功能障碍.对压力的敏感性/弹性.突触剪切是指突触的剪切.更多相关视频
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