Glia use multiple mechanisms to mediate potassium fluxes that support neuronal function. In addition to changes in potassium levels within synapses, these ions are dynamically dispersed through the interstitial parenchyma, perivascular spaces, leptomeninges, cerebrospinal fluid, choroid plexus, blood, vitreous, and endolymph. Neural circuits drive diversity in the glia that buffer potassium and this is reciprocal. Glia mediate buffering of potassium locally at glial-neuronal interfaces and via widespread networked connections. Control of potassium levels in the central nervous system is mediated by mechanisms operating at various loci with complexity that is difficult to model. However, major components of networked glial buffering are known. The role that potassium buffering plays in homeostasis of the CNS underlies some pathologic phenomena. An overview of potassium fluxes in the CNS is relevant for understanding consequences of pathogenic sequence variants in genes that encode potassium buffering proteins. Potassium flows in the CNS are described as follows: K1, the coordinated potassium fluxes within the astrocytic cradle around the synapse; K2, temporary storage of potassium within astrocytic processes in proposed microdomains; K3, potassium fluxes between oligodendrocytes and astrocytes; K4, potassium fluxes between astrocytes; K5, astrocytic potassium flux mediation of neurovasular coupling; K6, CSF delivery of potassium to perivascular spaces with dispersion to interstitial fluid between astrocytic endfeet; K7, astrocytic delivery of potassium to CSF and K8, choroid plexus (modified glia) regulation of potassium at the blood-CSF barrier. Components, mainly potassium channels, transporters, connexins and modulators, and the pathogenic sequence variants of their genes with the associated diseases are described.

胶质细胞使用多种机制来介导支持神经元功能的钾通量。除了突触中钾水平的变化外，这些离子还通过间质实质，血管周间隙，软脑膜，脑脊液，脉络丛，血液，玻璃体和内淋巴动态分散。神经回路驱动胶质细胞的多样性，以缓冲钾，这是相互的。胶质细胞介导神经胶质-神经元界面处钾离子的局部缓冲和广泛的网络连接。中枢神经系统中钾水平的控制是由在各种基因座上运行的机制介导的，这种机制难以建模。但是，网络化神经胶质缓冲的主要组成部分是已知的。钾缓冲在中枢神经系统稳态中的作用是一些病理现象的基础。中枢神经系统钾通量的概述与理解编码钾缓冲蛋白的基因中致病性序列变异的后果有关。CNS中的钾流量描述如下：K1，突触周围星形细胞摇篮内的协调钾通量；K2，拟议的微域中星形细胞过程中钾的临时储存；K3，少突胶质细胞和星形胶质细胞之间的钾通量；K4，星形胶质细胞之间的钾通量；K5，星形细胞钾通量介导的神经血管耦合；K6，脑脊液将钾扩散到血管周围间隙，并分散到星形胶质终极之间的组织液中；K7，钾向CSF和K8的星形细胞递送，脉络丛（修饰的神经胶质）调节血液CSF屏障处的钾。成分，主要是钾通道