Potassium buffering in the central nervous system

Abstract

Rapid changes in extracellular K + concentration ([K +] o) in the mammalian CNS are counteracted by simple passive diffusion as well as by cellular mechanisms of K + clearance. Buffering of [K +] o can occur via glial or neuronal uptake of K + ions through transporters or K +-selective channels. The best studied mechanism for [K +] o buffering in the brain is called K + spatial buffering , wherein the glial syncytium disperses local extracellular K + increases by transferring K + ions from sites of elevated [K +] o to those with lower [K +] o. In recent years, K + spatial buffering has been implicated or directly demonstrated by a variety of experimental approaches including electrophysiological and optical methods. A specialized form of spatial buffering named K + siphoning takes place in the vertebrate retina, where glial Müller cells express inwardly rectifying K + channels (Kir channels) positioned in the membrane domains near to the vitreous humor and blood vessels. This highly compartmentalized distribution of Kir channels in retinal glia directs K + ions from the synaptic layers to the vitreous humor and blood vessels. Here, we review the principal mechanisms of [K +] o buffering in the CNS and recent molecular studies on the structure and functions of glial Kir channels. We also discuss intriguing new data that suggest a close physical and functional relationship between Kir and water channels in glial cells.