突触修剪
神经科学
前额叶皮质
小胶质细胞
慢性应激
突触
突触后电位
神经传递
兴奋性突触后电位
树突棘
心理学
医学
抑制性突触后电位
炎症
海马结构
内科学
认知
受体
作者
Ji Wang,Hongsheng Chen,Hou‐Hong Li,Huajie Wang,Ruo-Si Zou,Xiao‐Jia Lu,Jie Wang,Binbin Nie,Jinfeng Wu,Shuang Li,Baoci Shan,Pengfei Wu,Bo-Seok Kang,Zhuang‐Li Hu,Jianguo Chen,Fang Wang
标识
DOI:10.1016/j.bbi.2022.12.019
摘要
Synapse loss in medial prefrontal cortex (mPFC) has been implicated in stress-related mood disorders, such as depression. However, the exact effect of synapse elimination in the depression and how it is triggered are largely unknown. Through repeated longitudinal imaging of mPFC in the living brain, we found both presynaptic and postsynaptic components were declined, together with the impairment of synapse remodeling and cross-synaptic signal transmission in the mPFC during chronic stress. Meanwhile, chronic stress also induced excessive microglia phagocytosis, leading to engulfment of excitatory synapses. Further investigation revealed that the elevated complement C3 during the stress acted as the tag of synapses to be eliminated by microglia. Besides, chronic stress induced a reduction of the connectivity between the mPFC and neighbor regions. C3 knockout mice displayed significant reduction of synaptic pruning and alleviation of disrupted functional connectivity in mPFC, resulting in more resilience to chronic stress. These results indicate that complement-mediated excessive microglia phagocytosis in adulthood induces synaptic dysfunction and cortical hypo-connectivity, leading to stress-related behavioral abnormality.
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