Sodium transport in astrocytes

Sodium transport in astrocytes in homogenous primary cultures from mouse brain cortex were investigated with radiotracer ( 22 Na) 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.