Beclin1 Deficiency Suppresses Epileptic Seizures
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 underlyi...
| Main Authors: | , , , , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2022-07-01
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| Series: | Frontiers in Molecular Neuroscience |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fnmol.2022.807671/full |
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| author | 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 |
| author_facet | 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 |
| author_sort | Min Yang |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-04-13T20:30:42Z |
| format | Article |
| id | doaj.art-8a5ba9fb67954c14a19edf19709da235 |
| institution | Directory Open Access Journal |
| issn | 1662-5099 |
| language | English |
| last_indexed | 2024-04-13T20:30:42Z |
| publishDate | 2022-07-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Molecular Neuroscience |
| spelling | doaj.art-8a5ba9fb67954c14a19edf19709da2352022-12-22T02:31:11ZengFrontiers Media S.A.Frontiers in Molecular Neuroscience1662-50992022-07-011510.3389/fnmol.2022.807671807671Beclin1 Deficiency Suppresses Epileptic SeizuresMin Yang0Peijia Lin1Wei Jing2Haokun Guo3Hongnian Chen4Yuanyuan Chen5Yi Guo6Yixue Gu7Miaoqing He8Junhong Wu9Xuejun Jiang10Xuejun Jiang11Zhen Zou12Zhen Zou13Xin Xu14Chengzhi Chen15Chengzhi Chen16Fei Xiao17Xuefeng Wang18Xin Tian19Chongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, ChinaChongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, ChinaChongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, ChinaChongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, ChinaChongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, ChinaChongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, ChinaChongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, ChinaChongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, ChinaChongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, ChinaChongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, ChinaCenter of Experimental Teaching for Public Health, Experimental Teaching and Management Center, Chongqing Medical University, Chongqing, ChinaResearch Center for Environment and Human Health, School of Public Health, Chongqing Medical University, Chongqing, ChinaMolecular Biology Laboratory of Respiratory Diseases, Institute of Life Sciences, Chongqing Medical University, Chongqing, ChinaResearch Center for Environment and Human Health, School of Public Health, Chongqing Medical University, Chongqing, ChinaChongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, ChinaResearch Center for Environment and Human Health, School of Public Health, Chongqing Medical University, Chongqing, ChinaDepartment of Occupational and Environmental Health, School of Public Health and Management, Chongqing Medical University, Chongqing, ChinaChongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, ChinaChongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, ChinaChongqing Key Laboratory of Neurology, Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, ChinaEpilepsy 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.https://www.frontiersin.org/articles/10.3389/fnmol.2022.807671/fullepilepsyBeclin1transgenic miceexcitatory synaptic transmissiondendritic spines |
| spellingShingle | 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 Beclin1 Deficiency Suppresses Epileptic Seizures Frontiers in Molecular Neuroscience epilepsy Beclin1 transgenic mice excitatory synaptic transmission dendritic spines |
| title | Beclin1 Deficiency Suppresses Epileptic Seizures |
| title_full | Beclin1 Deficiency Suppresses Epileptic Seizures |
| title_fullStr | Beclin1 Deficiency Suppresses Epileptic Seizures |
| title_full_unstemmed | Beclin1 Deficiency Suppresses Epileptic Seizures |
| title_short | Beclin1 Deficiency Suppresses Epileptic Seizures |
| title_sort | beclin1 deficiency suppresses epileptic seizures |
| topic | epilepsy Beclin1 transgenic mice excitatory synaptic transmission dendritic spines |
| url | https://www.frontiersin.org/articles/10.3389/fnmol.2022.807671/full |
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