Recent experimental evidence on the clustering of glutamate and GABA transporters on astrocytic processes surrounding synaptic terminals pose the question of the functional relevance of the astrocytes in the regulation of neural activity. In this perspective, we introduce a new computational model that embeds recent findings on neuron–astrocyte coupling at the mesoscopic scale intra- and inter-layer local neural circuits. The model consists of a mass model for the neural compartment and an astrocyte compartment which controls dynamics of extracellular glutamate and GABA concentrations. By arguments based on bifurcation theory, we use the model to study the impact of deficiency of astrocytic glutamate and GABA uptakes on neural activity. While deficient astrocytic GABA uptake naturally results in increased neuronal inhibition, which in turn results in a decreased neuronal firing, deficient glutamate uptake by astrocytes may either decrease or increase neuronal firing either transiently or permanently. Given the relevance of neuronal hyperexcitability (or lack thereof) in the brain pathophysiology, we provide biophysical conditions for the onset identifying different physiologically relevant regimes of operation for astrocytic uptake transporters.

中文翻译：

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新型神经元神经胶质团模型对星形胶质细胞活动在神经元过度兴奋中作用的理论研究。

关于谷氨酸和GABA转运蛋白聚集在突触末端周围的星形细胞过程中的最新实验证据提出了星形胶质细胞在调节神经活动中的功能相关性的问题。从这个角度出发，我们引入了一种新的计算模型，该模型将有关中子层内和层间局部神经回路的神经元-星形胶质细胞偶联的最新发现嵌入其中。该模型由神经区室和星形胶质细胞区室的质量模型组成，该模型控制细胞外谷氨酸和GABA浓度的动态。通过基于分叉理论的论证，我们使用该模型研究星形细胞谷氨酸和GABA摄取不足对神经活动的影响。虽然缺乏星形细胞的GABA摄取自然会导致神经元抑制作用增加，继而导致神经元放电减少，星形胶质细胞摄取谷氨酸不足可能会暂时或永久性降低或增加神经元放电。考虑到神经元过度兴奋性（或缺乏神经兴奋性）在脑部病理生理中的相关性，我们提供了生物物理条件，可用于确定星形胶质摄取转运蛋白的不同生理相关操作方式。