Beclin1 Deficiency Suppresses Epileptic Seizures

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

doi:10.3389/fnmol.2022.807671

Frontiers in Molecular Neuroscience (Jul 2022)

Beclin1 Deficiency Suppresses Epileptic Seizures

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

Affiliations

Min Yang: Chongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
Peijia Lin: Chongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
Wei Jing: Chongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
Haokun Guo: Chongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
Hongnian Chen: Chongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
Yuanyuan Chen: Chongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
Yi Guo: Chongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
Yixue Gu: Chongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
Miaoqing He: Chongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
Junhong Wu: Chongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
Xuejun Jiang: Center of Experimental Teaching for Public Health, Experimental Teaching and Management Center, Chongqing Medical University, Chongqing, China
Xuejun Jiang: Research Center for Environment and Human Health, School of Public Health, Chongqing Medical University, Chongqing, China
Zhen Zou: Molecular Biology Laboratory of Respiratory Diseases, Institute of Life Sciences, Chongqing Medical University, Chongqing, China
Zhen Zou: Research Center for Environment and Human Health, School of Public Health, Chongqing Medical University, Chongqing, China
Xin Xu: Chongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
Chengzhi Chen: Research Center for Environment and Human Health, School of Public Health, Chongqing Medical University, Chongqing, China
Chengzhi Chen: Department of Occupational and Environmental Health, School of Public Health and Management, Chongqing Medical University, Chongqing, China
Fei Xiao: Chongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
Xuefeng Wang: Chongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
Xin Tian: Chongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China

DOI: https://doi.org/10.3389/fnmol.2022.807671
Journal volume & issue: Vol. 15

Abstract

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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.

Published in Frontiers in Molecular Neuroscience

ISSN: 1662-5099 (Online)
Publisher: Frontiers Media S.A.
Country of publisher: Switzerland
LCC subjects: Medicine: Internal medicine: Neurosciences. Biological psychiatry. Neuropsychiatry
Website: https://www.frontiersin.org/journals/molecular-neuroscience

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