The regulation of extracellular K+ levels,[K+],, in the central nervous system (CNS) is essential for the maintenance of neuronal function. Spatial buffering by glial cells is believed to play an important role in this process." 2 As suggested originally by Orkand, Nicholls, and Kuffler,) excess K+ deposited into interstitial space as a result of neuronal activity will enter K+-permeable cells in regions of raised [K+],. In order to maintain net electrical neutrality, an equal amount of K+ will exit from these cells, or from cells electrically coupled to them, in regions where [K+], is lower. The effect of this K+-mediated current flow is to transfer K+ from regions where [K'l0 is high to regions where [K+], is low.

Astrocytes, which are almost exclusively permeable to K+ 4* 5 and which form large syncytia of cells coupled together by low-resistance gap junctions, 6" are thought to mediate K+ spatial buffering in the brain. In the vertebrate retina, astrocytes are relatively sparse. Instead, the principal glial element is the Miiller cell, a specialized radial glial cell that resembles astrocytes in many respects? Miiller cells extend from the inner (vitreal) surface of the retina to the outer limiting membrane (at the level of the photoreceptor inner segments)? The membrane properties of these cells make them ideally suited to regulate [K+], in the retina through the process of K+ spatial buffering. As I will demonstrate below, the membrane conductance of Muller cells is highly selective for K+. This K+ conductance is not distributed uniformly over the cell surface, but rather is concentrated in specific regions of the cell. This nonuniform conductance distribution serves to greatly enhance the effectiveness of K+ spatial buffering in the retina. Furthermore, Miiller cells possess voltage-dependent ion channels that may also function to amplify spatial buffering currents.