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Review
. 2003 Oct;28(2):195-208.
doi: 10.1385/MN:28:2:195.

Molecular substrates of potassium spatial buffering in glial cells

Paulo Kofuji  1 , Nathan C Connors
Affiliations
Review

Molecular substrates of potassium spatial buffering in glial cells

Paulo Kofuji et al. Mol Neurobiol. 2003 Oct.

Abstract

It is generally accepted that the foremost mechanism for the buffering of K+ from the extracellular space ([K+]o) in the brain is "K+ spatial buffering." This is the process by which glial cells dissipate local K+ gradients by transferring K+ ions from areas of high to low [K+]o. These glial K+ fluxes are mediated mainly by inwardly rectifying K+ (Kir) channels. The K+ spatial buffering hypothesis has been tested and confirmed in the retina, in which is has been termed as "K+ siphoning". In Müller cells, the primary glial cells of the retina, Kir channels are distributed in a highly non-uniform manner, exhibiting high concentrations in membrane domains facing the vitreous humor (endfeet) and in proximity to the blood vessels (perivascular processes). Such nonuniform distribution of Kir channels facilitates directed K+ fluxes in the retina from the synaptic plexiform layers to the vitreous humor and blood vessels. Recent molecular and electrophysiological studies in Müller cells have revealed a high degree of complexity in terms of Kir channel subunit composition, mechanisms of subcellular localization, and regulation. How such complexity fits into their proposed role in buffering [K+]o in retina is the main topic of this article.

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