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 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 language | English (US) |
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Pages (from-to) | 195-208 |
Number of pages | 14 |
Journal | Molecular neurobiology |
Volume | 28 |
Issue number | 2 |
DOIs | |
State | Published - 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.
Keywords
- Dystrophin
- Glia
- Müller cells
- Potassium channel
- Potassium spatial buffering
- Retina
- Syntrophin