The pathophysiology of epilepsy has been historically grounded on hyperexcitability attributed to the oversimplified imbalance between excitation (E) and inhibition (I) in the brain. The decreased inhibition is mostly attributed to deficits in gamma-aminobutyric acid-containing (GABAergic) interneurons, the main source of inhibition in the central nervous system. However, the cell diversity, the wide range of spatiotemporal connectivity, and the distinct effects of the neurotransmitter GABA especially during development, must be considered to critically revisit the concept of hyperexcitability caused by decreased inhibition as a key characteristic in the development of epilepsy. Here, we will discuss that behind this known mechanism, there is a heterogeneity of GABAergic interneurons with distinct functions and sources, which have specific roles in controlling the neural network activity within the recruited microcircuit and altered network during the epileptogenic process. This article is part of the Special Issue "NEWroscience 2018.

中文翻译：

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癫痫中的 GABA 能中间神经元：不仅仅是抑制的简单变化

癫痫的病理生理学历史上一直基于过度兴奋，这归因于大脑中兴奋 (E) 和抑制 (I) 之间的过度简化失衡。抑制作用的降低主要归因于含 γ-氨基丁酸 (GABAergic) 中间神经元的缺陷，中间神经元是中枢神经系统抑制的主要来源。然而，必须考虑细胞多样性、广泛的时空连通性以及神经递质 GABA 的独特作用，尤其是在发育过程中的独特作用，以批判性地重新审视由抑制减少引起的过度兴奋的概念，这是癫痫发展的一个关键特征。在这里，我们将讨论在这种已知机制的背后，存在具有不同功能和来源的 GABA 能中间神经元的异质性，在癫痫发生过程中，它们在控制募集的微电路和改变的网络内的神经网络活动方面具有特定作用。本文是特刊“NEWroscience 2018”的一部分。