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Neurochem Res. 2012 Nov;37(11):2299-309. doi: 10.1007/s11064-012-0731-3. Epub 2012 Feb 26.

Glial K⁺ clearance and cell swelling: key roles for cotransporters and pumps.

Author information

1
Department of Cellular and Molecular Medicine, Faculty of Health Sciences, University of Copenhagen, Blegdamsvej 3, Copenhagen, Denmark. macaulay@sund.ku.dk

Abstract

An important feature of neuronal signalling is the increased concentration of K(+) in the extracellular space. The K(+) concentration is restored to its original basal level primarily by uptake into nearby glial cells. The molecular mechanisms by which K(+) is transferred from the extracellular space into the glial cell are debated. Although spatial buffer currents may occur, their quantitative contribution to K(+) clearance is uncertain. The concept of spatial buffering of K(+) precludes intracellular K(+) accumulation and is therefore (i) difficult to reconcile with the K(+) accumulation repeatedly observed in glial cells during K(+) clearance and (ii) incompatible with K(+)-dependent glial cell swelling. K(+) uptake into non-voltage clamped cultured glial cells is carried out by the Na(+)/K(+)-ATPase and the Na(+)/K(+)/Cl(-) cotransporter in combination. In brain slices and intact optic nerve, however, only the Na(+)/K(+)-ATPase has been demonstrated to be involved in stimulus-evoked K(+) clearance. The glial cell swelling associated with K(+) clearance is prevented under conditions that block the activity of the Na(+)/K(+)/Cl(-) cotransporter. The Na(+)/K(+)/Cl(-) cotransporter is activated by increased K(+) concentration and cotransports water along with its substrates. It thereby serves as a K(+)-dependent molecular water pump under conditions of increased extracellular K(+) load.

PMID:
22367475
DOI:
10.1007/s11064-012-0731-3
[Indexed for MEDLINE]

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