Molecular Substrates of Potassium Spatial Buffering in Glial Cells

Paulo Kofuji, Nathan C. Connors

Research output: Contribution to journalArticlepeer-review

28 Scopus citations


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 non-uniform 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.

Original languageEnglish (US)
Pages (from-to)195-208
Number of pages14
JournalMolecular neurobiology
Issue number2
StatePublished - Oct 2003

Bibliographical note

Funding Information:
This work was supported by National Institutes of Health Grants EY12949 to P.K. and Vision Training Grant EY07133 to N.C.C.


  • Dystrophin
  • Glia
  • Müller cells
  • Potassium channel
  • Potassium spatial buffering
  • Retina
  • Syntrophin


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