title: Endfeet of retinal glial cells have higher densities of ion channels that mediate K+ buffering.
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.
mesh_terms: D000557:Ambystoma; D000818:Animals; D007473:Ion Channels / Q000502:physiology*; D008564:Membrane Potentials; D008839:Microelectrodes; D011188:Potassium / Q000378:metabolism*; D012160:Retina / Q000502:physiology*; D012165:Retinal Ganglion Cells / Q000502:physiology*
chemical_list: D007473:Ion Channels; D011188:Potassium