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癫痫发作起始的协同正反馈机制。

Synergistic Positive Feedback Mechanisms Underlying Seizure Initiation.

作者信息

Trevelyan Andrew J, Graham Robert T, Parrish R Ryley, Codadu Neela K

机构信息

Newcastle University Biosciences Institute, Medical School, Framlington Place, Newcastle upon Tyne, United Kingdom.

Queen Square Institute of Neurology, University College London, United Kingdom.

出版信息

Epilepsy Curr. 2022 Sep 27;23(1):38-43. doi: 10.1177/15357597221127163. eCollection 2023 Jan-Feb.

DOI:10.1177/15357597221127163
PMID:36923333
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10009126/
Abstract

Investigations into seizure initiation, in recent years, have focused almost entirely upon alterations of interneuronal function, chloride homeostasis, and extracellular potassium levels. In contrast, little attention has been directed toward a possible role of dendritic plateau potentials in the actual ictogenic transition, despite a substantial literature dating back 40 years regarding its importance generally in epilepsy. Here, we argue that an increase in dendritic excitability, coordinated across the population of pyramidal cells, is a key stage in ictogenesis.

摘要

近年来,关于癫痫发作起始的研究几乎完全集中在中间神经元功能、氯离子稳态和细胞外钾离子水平的改变上。相比之下,尽管有大量可追溯到40年前的文献表明树突状平台电位在癫痫发生中普遍具有重要性,但对于其在实际致痫转变过程中可能发挥的作用却很少有人关注。在此,我们认为,在锥体细胞群体中协同发生的树突兴奋性增加是癫痫发生的关键阶段。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa83/10009126/8b581e622b8f/10.1177_15357597221127163-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa83/10009126/5a9c46de87cd/10.1177_15357597221127163-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa83/10009126/9f842442d433/10.1177_15357597221127163-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa83/10009126/8b581e622b8f/10.1177_15357597221127163-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa83/10009126/5a9c46de87cd/10.1177_15357597221127163-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa83/10009126/9f842442d433/10.1177_15357597221127163-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa83/10009126/8b581e622b8f/10.1177_15357597221127163-fig3.jpg

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Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels as Drug Targets for Neurological Disorders.超极化激活环核苷酸门控通道作为神经紊乱的药物靶点。
论癫痫中的脑刺激
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