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. These cells have 94% of their potassium conductance in an endfoot apposed to the vitreous humour¹, causing K⁺ released from active retinal neurones to be buffered preferentially to the vitreous^2,3. 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.