Walz W, Hertz L
J Neurosci Res. 1984;11(3):231-9. doi: 10.1002/jnr.490110303.
Sodium transport in astrocytes in homogeneous primary cultures from mouse brain cortex were investigated with radiotracer (22Na) and electrophysiological methods. The equilibrated Na+ content was 190 nmol X mg-1 protein and the influx and efflux rates were identical at about 560 nmol X mg-1 X 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, double 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.
利用放射性示踪剂（²²Na）和电生理方法，对来自小鼠大脑皮层的均匀原代培养星形胶质细胞中的钠转运进行了研究。平衡后的Na⁺含量为190 nmol·mg⁻¹蛋白质，流入和流出速率相同，约为560 nmol·mg⁻¹·min⁻¹。当细胞外K⁺从5.4 mM升高到12 mM或54 mM时，Na⁺流出或流入未观察到显著变化，但Na⁺含量降低。先前暴露于冰冷的无K⁺培养基引起的细胞内Na⁺负载，使Na⁺流出增加了一倍。哇巴因，一种Na⁺-K⁺交换抑制剂，在5.4 mM和12 mM K⁺时对Na⁺流出有轻微的、不显著的抑制作用，并导致Na⁺含量大幅增加。在5.4 mM K⁺时，氨氯地平，一种Na⁺-H⁺交换抑制剂，降低了Na⁺的流入和流出，并导致Na⁺含量增加。呋塞米，一种阳离子-Cl⁻载体抑制剂，略微降低了Na⁺含量和流入，但对Na⁺流出没有显著影响。在升高的（12 mM和54 mM）K⁺浓度下，氨氯地平或呋塞米对Na⁺流入的影响被消除。试图用升高的细胞外K⁺或细胞内Na⁺刺激Na⁺-K⁺泵，未产生膜电位的电生成成分，这可能是由于高K⁺通透性所致。根据目前结果和早期关于K⁺流入的实验，得出以下结论：1）正常条件下星形胶质细胞的Na⁺-K⁺泵转运的K⁺比Na⁺多；2）细胞内Na⁺负载增加Na⁺流出；3）在5.4 mM K⁺时似乎发生了一些Na⁺-H⁺交换以及Na⁺和Cl⁻的共转运；4）后两种转运机制在升高的K⁺浓度下均未增强。
