Sodium transport in astrocytes

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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.