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Publication Detail
Endfeet of retinal glial cells have higher densities of ion channels that mediate K+ buffering.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Brew H, Gray PT, Mobbs P, Attwell D
  • Publication date:
    04/12/1986
  • Pagination:
    466, 468
  • Journal:
    Nature
  • Volume:
    324
  • Issue:
    6096
  • Status:
    Published
  • Country:
    England
  • Print ISSN:
    0028-0836
  • Language:
    eng
  • Keywords:
    Ambystoma, Animals, Ion Channels, Membrane Potentials, Microelectrodes, Potassium, Retina, Retinal Ganglion Cells
Abstract
A major function of glial cells in the central nervous system is to buffer the extracellular potassium concentration, [K+]o. A local rise in [K+]o causes potassium ions to enter glial cells, which have membranes that are highly permeable to K+; potassium then leaves the glial cells at other locations where [K+]o has not risen. We report here the first study of the individual ion channels mediating potassium buffering by glial cells. The patch-clamp technique was employed to record single channel currents in Müller cells, the radial glia of the vertebrate retina. Those cells have 94% of their potassium conductance in an endfoot apposed to the vitreous humour, causing K+ released from active retinal neurones to be buffered preferentially to the vitreous. Recordings from patches of endfoot and cell body membrane show that a single type of inward-rectifying K+ channel mediates potassium buffering at both cell locations. The non-uniform density of K+ conductance is due to a non-uniform distribution of one type of K+ channel, rather than to the cell expressing high conductance channels at the endfoot and low conductance channels elsewhere on the cell.
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