Sodium transport in astrocytes

✍ Scribed by Dr. Wolfang Walz; L. Hertz

• Book ID: 102909453
• Publisher: John Wiley and Sons
• Year: 1984
• Tongue: English
• Weight: 582 KB
• Volume: 11
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/jnr.490110303

✦ Synopsis

Sodium transport in astrocytes in homogenous primary cultures from mouse brain cortex were investigated with radiotracer ('*Na) and electrophysiological methods. The equilibrated Na+ content was 190 nmol X mg-' protein and the influx and efflux rates were identical at about 560 nmol X mg-' X min-'. No significant change was observed in Nat 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 Naf 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 Nat content. Furosemide, an inhibitor of a cation-CI-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 f . Attempts to stimulate the Na+-K+ pump with elevated external Kf 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 C1-seem to occur at 5.4 mM K + ; and 4) neither of the latter two transport mechanisms is enhanced at elevated K + concentrations.