Microglial deletion and inhibition alleviate behavior of post-traumatic stress disorder in mice.
Microglial deletion and inhibition alleviate behavior of post-traumatic stress disorder in mice.
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小胶质细胞缺失和抑制可减轻小鼠创伤后应激障碍的行为
DOI：
10.1186/s12974-020-02069-9
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发表时间：
2021-01-05
影响因子：
9.3
通讯作者：
Yuan Z
中科院分区：
文献类型：
--
作者：
Li S;Liao Y;Dong Y;Li X;Li J;Cheng Y;Cheng J;Yuan Z
BackgroundAlteration of immune status in the central nervous system (CNS) has been implicated in the development of post-traumatic stress disorder (PTSD). However, the nature of overall changes in brain immunocyte landscape in PTSD condition remains unclear.MethodsWe constructed a mouse PTSD model by electric foot-shocks followed by contextual reminders and verified the PTSD-related symptoms by behavior test (including contextual freezing test, open-field test, and elevated plus maze test). We examined the immunocyte panorama in the brains of the naïve or PTSD mice by using single-cell mass cytometry. Microglia number and morphological changes in the hippocampus, prefrontal cortex, and amygdala were analyzed by histopathological methods. The gene expression changes of those microglia were detected by quantitative real-time PCR. Genetic/pharmacological depletion of microglia or minocycline treatment before foot-shocks exposure was performed to study the role of microglia in PTSD development and progress.ResultsWe found microglia are the major brain immune cells that respond to PTSD. The number of microglia and ratio of microglia to immunocytes was significantly increased on the fifth day of foot-shock exposure. Furthermore, morphological analysis and gene expression profiling revealed temporal patterns of microglial activation in the hippocampus of the PTSD brains. Importantly, we found that genetic/pharmacological depletion of microglia or minocycline treatment before foot-shock exposure alleviated PTSD-associated anxiety and contextual fear.ConclusionOur results demonstrated a critical role for microglial activation in PTSD development and a potential therapeutic strategy for the clinical treatment of PTSD in the form of microglial inhibition.
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影响因子：
25.8
作者：
Eraly, Satish A.;Nievergelt, Caroline M.;Maihofer, Adam X.;Barkauskas, Donald A.;Biswas, Nilima;Agorastos, Agorastos;O'Connor, Daniel T.;Baker, Dewleen G.
通讯作者：
Baker, Dewleen G.
影响因子：
11
作者：
Fox ME;Chandra R;Menken MS;Larkin EJ;Nam H;Engeln M;Francis TC;Lobo MK
通讯作者：
Lobo MK
小胶质细胞中自噬以磷酸化依赖性方式调节 MAVS 信号激活。
影响因子：
12.4
作者：
Cheng, Jinbo;Liao, Yajin;Yuan, Zengqiang
通讯作者：
Yuan, Zengqiang
影响因子：
6.2
作者：
De Haas, Alexander H.;Boddeke, Hendrikus W. G. M.;Biber, Knut
通讯作者：
Biber, Knut
影响因子：
6.2
作者：
Blank, Thomas;Prinz, Marco
通讯作者：
Prinz, Marco