Potassium homeostasis in the brain at the organ and cell level

Abstract

Publisher Summary This chapter reviews that potassium ion has a crucial role in neuronal excitability. Its distribution across neuronal membranes determines the resting membrane potential features, transmitter release, and the kinetics of voltage-gated ion channels. Thus, small absolute changes of the normally low extracellular but not necessarily of the higher intracellular concentration of potassium can play havoc with excitability and neuronal information transfer. It discusses that active neurons release potassium ions into the extracellular space. The resulting increase in extracellular potassium concentration is high enough to interfere with ion channel gating, and therefore information transfer in neurons. The excess potassium is not released across the blood–brain barrier into the blood. Astrocytes are also acknowledged to be the major site of the clearance of excess extracellular potassium. The chapter reviews that spatial buffering by potassium currents across astrocytic membranes works only over short distances due to the small length constant and does therefore, not contribute significantly. The only exception might be the periphery of the retina. After injury, reactive astrocytes express chloride conductances that allow KCl accumulation via Donnan forces in addition to the carrier-mediated accumulation. Thus, KCl accumulation into astrocytes by active and passive (after injury) means is now a well established cellular mechanism in the nervous system.