Otassium Buffering in the Central Nervous System

bstract —Rapid changes in extracellular K concentration [K ]o) in the mammalian CNS are counteracted by simple assive diffusion as well as by cellular mechanisms of K learance. Buffering of [K ]o can occur via glial or neuronal ptake of K ions through transporters or K -selective chanels. The best studied mechanism for [K ]o buffering in the rain is called K spatial buffering, wherein the glial syncyium disperses local extracellular K increases by transfering K ions from sites of elevated [K ]o to those with lower K ]o. In recent years, K spatial buffering has been impliated or directly demonstrated by a variety of experimental pproaches including electrophysiological and optical methds. A specialized form of spatial buffering named K sihoning takes place in the vertebrate retina, where glial üller cells express inwardly rectifying K channels (Kir hannels) positioned in the membrane domains near to the itreous humor and blood vessels. This highly compartmenalized distribution of Kir channels in retinal glia directs K ons from the synaptic layers to the vitreous humor and blood essels. Here, we review the principal mechanisms of [K ]o uffering in the CNS and recent molecular studies on the tructure and functions of glial Kir channels. We also discuss ntriguing new data that suggest a close physical and funcional relationship between Kir and water channels in glial ells. © 2004 IBRO. Published by Elsevier Ltd. All rights eserved.