Neurophysiology and Neurochemistry of Neuronal Excitability and Synaptic Plasticity Laboratory, Department of Biochemistry, ICBS, Universidade Federal do Rio Grande do Sul, Porto Alegre 90035-003, RS, Brazil; Graduate Program in Biological Science: Biochemistry, Universidade Federal do Rio Grande do Sul, Porto Alegre 90035-003, RS, Brazil.
Neurophysiology and Neurochemistry of Neuronal Excitability and Synaptic Plasticity Laboratory, Department of Biochemistry, ICBS, Universidade Federal do Rio Grande do Sul, Porto Alegre 90035-003, RS, Brazil; Graduate Program in Biological Science: Biochemistry, Universidade Federal do Rio Grande do Sul, Porto Alegre 90035-003, RS, Brazil; Graduate Program in Neuroscience, Universidade Federal do Rio Grande do Sul, Porto Alegre 90046-900, RS, Brazil.
Epilepsy Behav. 2021 Aug;121(Pt B):106935. doi: 10.1016/j.yebeh.2020.106935. Epub 2020 Feb 5.
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.
癫痫的病理生理学历史上基于过度兴奋，这归因于大脑中兴奋（E）和抑制（I）之间过于简单的失衡。抑制的减少主要归因于含γ-氨基丁酸（GABAergic）中间神经元的缺陷，GABAergic 中间神经元是中枢神经系统中抑制的主要来源。然而，必须考虑到细胞多样性、广泛的时空连接以及神经递质 GABA 的独特作用，尤其是在发育过程中，以批判性地重新审视由抑制减少引起的过度兴奋作为癫痫发展的关键特征的概念。在这里，我们将讨论在这个已知的机制背后，存在着具有不同功能和来源的 GABAergic 中间神经元的异质性，它们在控制募集的微电路内的神经网络活动以及在致痫过程中改变的网络中具有特定的作用。本文是“NEWroscience 2018 特刊”的一部分。
