Sodium transport in astrocytes

Abstract

Sodium transport in astrocytes in homogenous primary cultures from mouse brain cortex were investigated with radiotracer (²²Na) and electrophysiological methods. The equilibrated Na⁺ content was 190 nmol × mg⁻¹ protein and the influx and efflux rates were identical at about 560 nmol × mg⁻¹ × min⁻¹. No significant change was observed in Na⁺ efflux or influx when external K⁺ was raised from 5.4 to 12 or 54 mM, but the Na⁺ content decreased. Intracellular Na⁺ loading, evoked by previous exposure to ice‐cold K⁺‐free medium, doubled the Na⁺ efflux. Ouabain, a Na⁺ ‐K⁺ exchange inhibitor, exerted a small, nonsignificant inhibition of Na⁺ efflux at both 5.4 and 12 mM K⁺ and caused a large increase in Na⁺ content. At 5.4 mM K⁺, amiloride, a Na⁺‐H⁺ exchange inhibitor, decreased both influx and efflux of Na⁺ and caused an increase in Na⁺ content. Furosemide, an inhibitor of a cation‐Cl⁻ carrier, decreased both content and influx of Na⁺ slightly but had no significant effect on Na⁺ efflux. The effects of amiloride or furosemide on Na⁺ influx were abolished at elevated (12 and 54 mM) K⁺. Attempts to stimulate the Na⁺−K⁺ pump with elevated external K⁺ or internal Na⁺ produced no electrogenic component of the membrane potential. Probably owing to the high K⁺ permeability. Based on the present results and earlier experiments on K⁺ influx, it is concluded that 1) the Na⁺−K⁺ pump of astrocytes under normal conditions transports more K⁺ than Na⁺; 2) intracellular Na⁺ loading increases Na⁺ efflux; 3) some Na⁺−H⁺ exchange and cotransport of Na⁺ and Cl⁻ seem to occur at 5.4 mM K⁺; and 4) neither of the latter two transport mechanisms is enhanced at elevated K⁺ concentrations.