Regulation of potassium by glial cells in the central nervous system

Research output: Chapter in Book/Report/Conference proceedingChapter

14 Scopus citations


Rapid changes in extracellular K+ concentration ([K+]o) in the mammalian central nervous system (CNS) are counteracted by simple passive diffusion as well as by cellular mechanisms of K+ clearance. Regulation of [K+]o can occur via glial or neuronal uptake of K+ ions through transporters or K+-selective ion channels. The best studied mechanism of [K+]o regulation in the brain is K+ spatial buffering, wherein the glial syncytium disperses local extracellular K+ increases by transferring K+ from sites of elevated [K+]o to those with lower [K+]o. In recent years, K+ spatial buffering has been implicated or directly demonstrated by a variety of experimental approaches, including electrophysiological and optical methods. A specialized form of spatial buffering termed K+ siphoning takes place in the vertebrate retina, where glial Müller cells express inwardly rectifying K+ channels (Kir channels) positioned in membrane domains near to the vitreous humor and blood vessels. This highly compartmentalized distribution of Kir channels in retinal glia directs K+ ions from the synaptic layers to the vitreous humor and blood vessels. Here, we review the principal mechanisms of [K+]o regulation in the CNS and recent molecular studies on the structure and function of glial Kir channels. We also discuss intriguing new data that suggest a close physical and functional relationship between Kir and water channels in glial cells.

Original languageEnglish (US)
Title of host publicationAstrocytes in (Patho)Physiology of the Nervous System
PublisherSpringer US
Number of pages25
ISBN (Electronic)9780387794921
ISBN (Print)9780387794914
StatePublished - 2009


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