Neuron-specific mechanisms for epilepsy self-termination

Jin-Hui Wang, Wei Lu, Bo Wen
{"title":"Neuron-specific mechanisms for epilepsy self-termination","authors":"Jin-Hui Wang, Wei Lu, Bo Wen","doi":"10.14800/MCE.716","DOIUrl":null,"url":null,"abstract":"Epilepsy as a common neurological disorder appears the sudden onset and self-termination in the cerebral cortical ictal discharges and tonic muscle contractions within a few minutes. The seizure onset is believed to be initiated by the synchronous activity of excitatory neurons and the weakness of inhibitory synapses. Current medications to suppress the seizure onset are applying exogenous reagents to enhance inhibitory synaptic transmission and block spike generation. After the treatments, many epileptic patients become insensitive to original medications and the pathogenesis in the elevated ratio of cortical excitation to inhibition is still present. The reasons for lack of long-term medical efficiency may include that the medical treatment is not neuron-specific and the seizure self-termination has not been taken into account. Therefore, new therapeutic strategies against epilepsy remains to be explored based on strengthening the endogenous mechanisms of seizure self-termination in a neuron-specific manner. We review the potential mechanism of seizure self-termination and give our thought in anti-epilepsy by strengthening endogenous seizure self-termination in different neuronal compartments.","PeriodicalId":18603,"journal":{"name":"Molecular & Cellular Epilepsy","volume":"67 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2015-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"14","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular & Cellular Epilepsy","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.14800/MCE.716","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 14

Abstract

Epilepsy as a common neurological disorder appears the sudden onset and self-termination in the cerebral cortical ictal discharges and tonic muscle contractions within a few minutes. The seizure onset is believed to be initiated by the synchronous activity of excitatory neurons and the weakness of inhibitory synapses. Current medications to suppress the seizure onset are applying exogenous reagents to enhance inhibitory synaptic transmission and block spike generation. After the treatments, many epileptic patients become insensitive to original medications and the pathogenesis in the elevated ratio of cortical excitation to inhibition is still present. The reasons for lack of long-term medical efficiency may include that the medical treatment is not neuron-specific and the seizure self-termination has not been taken into account. Therefore, new therapeutic strategies against epilepsy remains to be explored based on strengthening the endogenous mechanisms of seizure self-termination in a neuron-specific manner. We review the potential mechanism of seizure self-termination and give our thought in anti-epilepsy by strengthening endogenous seizure self-termination in different neuronal compartments.
癫痫自我终止的神经元特异性机制
癫痫作为一种常见的神经系统疾病,在几分钟内表现为大脑皮层皮层性放电和强直性肌肉收缩的突然发作和自我终止。癫痫发作被认为是由兴奋性神经元的同步活动和抑制性突触的衰弱引起的。目前抑制癫痫发作的药物是使用外源性试剂来增强抑制性突触传递和阻断spike的产生。治疗后,许多癫痫患者对原有药物不敏感,其发病机制仍然存在于皮层兴奋抑制比升高。缺乏长期医疗效率的原因可能包括药物治疗不是神经元特异性的,并且没有考虑到癫痫发作的自我终止。因此,在加强癫痫发作自我终止的内源性神经元特异性机制的基础上,新的治疗策略仍有待探索。本文综述了癫痫发作自我终止的潜在机制,并对加强不同神经室的内源性癫痫发作自我终止在抗癫痫中的作用进行了思考。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信