AUTHOR=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 

TITLE=Beclin1 Deficiency Suppresses Epileptic Seizures

JOURNAL=Frontiers in Molecular Neuroscience

VOLUME=Volume 15 - 2022

YEAR=2022

URL=https://www.frontiersin.org/journals/molecular-neuroscience/articles/10.3389/fnmol.2022.807671

DOI=10.3389/fnmol.2022.807671

ISSN=1662-5099

ABSTRACT=Epilepsy is a common disease of the nervous system. Autophagy is a degradation process involved in epilepsy, and in turn, seizures can activate autophagy. As a critical role in autophagy, Beclin1 participates in numerous physiological and pathological processes. However, how Beclin1 influences epilepsy remains unclear. In this study, we detected increased expression of Beclin1 in brain tissues from patients with temporal lobe epilepsy. And heterozygous disruption of beclin1 decreased susceptibility to epilepsy, suppressed seizure activity in two mouse epileptic models. We further illustrated for the first time that heterozygous disruption of beclin1 suppresses excitatory synaptic transmission, which may be caused by the decreased dendritic spine density. These findings provide a new clue that the regulation of Beclin1, may serve as a strategy for antiepileptic therapy. Besides, Beclin1 participates in synaptic transmission, and the development of dendritic spines may be a biological function independent of autophagy.