Beclin1 Deficiency Suppresses Epileptic Seizures

作者全名："Yang, Min; Lin, Peijia; Jing, Wei; Guo, Haokun; Chen, Hongnian; Chen, Yuanyuan; Guo, Yi; Gu, Yixue; He, Miaoqing; Wu, Junhong; Jiang, Xuejun; Zou, Zhen; Xu, Xin; Chen, Chengzhi; Xiao, Fei; Wang, Xuefeng; Tian, Xin"

作者地址："[Yang, Min; Lin, Peijia; Jing, Wei; Guo, Haokun; Chen, Hongnian; Chen, Yuanyuan; Guo, Yi; Gu, Yixue; He, Miaoqing; Wu, Junhong; Xu, Xin; Xiao, Fei; Wang, Xuefeng; Tian, Xin] Chongqing Med Univ, Affiliated Hosp 1, Dept Neurol, Chongqing Key Lab Neurol, Chongqing, Peoples R China; [Jiang, Xuejun] Chongqing Med Univ, Ctr Expt Teaching Publ Hlth, Expt Teaching & Management Ctr, Chongqing, Peoples R China; [Zou, Zhen] Chongqing Med Univ, Inst Life Sci, Mol Biol Lab Resp Dis, Chongqing, Peoples R China; [Jiang, Xuejun; Zou, Zhen; Chen, Chengzhi] Chongqing Med Univ, Res Ctr Environm & Human Hlth, Sch Publ Hlth, Chongqing, Peoples R China; [Chen, Chengzhi] Chongqing Med Univ, Sch Publ Hlth & Management, Dept Occupat & Environm Hlth, Chongqing, Peoples R China"

通信作者："Xiao, F; Wang, XF; Tian, X (通讯作者)，Chongqing Med Univ, Affiliated Hosp 1, Dept Neurol, Chongqing Key Lab Neurol, Chongqing, Peoples R China.; Chen, CZ (通讯作者)，Chongqing Med Univ, Res Ctr Environm & Human Hlth, Sch Publ Hlth, Chongqing, Peoples R China.; Chen, CZ (通讯作者)，Chongqing Med Univ, Sch Publ Hlth & Management, Dept Occupat & Environm Hlth, Chongqing, Peoples R China."

来源：FRONTIERS IN MOLECULAR NEUROSCIENCE

ESI学科分类：NEUROSCIENCE & BEHAVIOR

WOS号：WOS:000837097100001

JCR分区：Q2

影响因子：4.8

年份：2022

卷号：15

期号：　

开始页：　

结束页：　

文献类型：Article

关键词：epilepsy; Beclin1; transgenic mice; excitatory synaptic transmission; dendritic spines

摘要："Epilepsy is a common disease of the nervous system. Autophagy is a degradation process involved in epilepsy, and in turn, seizures can activate autophagy. Beclin1 plays a critical role in autophagy and participates in numerous physiological and pathological processes. However, the mechanism underlying the effect of Beclin1 on epilepsy remains unclear. In this study, we detected increased expression of Beclin1 in brain tissues from patients with temporal lobe epilepsy (TLE). Heterozygous disruption of beclin1 decreased susceptibility to epilepsy and suppressed seizure activity in two mouse epilepsy models. We further illustrated for the first time that heterozygous disruption of beclin1 suppresses excitatory synaptic transmission, which may be caused by a decreased dendritic spine density. These findings suggest for the first time that the regulation of Beclin1 may serve as a strategy for antiepileptic therapy. In addition, Beclin1 participates in synaptic transmission, and the development of dendritic spines may be a biological function of Beclin1 independent of its role in autophagy."

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