Volume-activated Rb+ transport in astrocytes in culture.
Volume-activated Rb+ transport in astrocytes in culture.
复制标题
培养物中星形胶质细胞中容量激活的 Rb 转运。
DOI：
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发表时间：
1993
影响因子：
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通讯作者：
H. Pasantes‐Morales
中科院分区：
文献类型：
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作者：
R. Sánchez;J. Morán;A. Martı́nez;H. Pasantes‐Morales
以~(86)Rb为示踪剂，研究K~+在星形胶质细胞体积调节过程中的作用。在细胞肿胀后表现出体积调节反应的过程中，渗透压分别从320降至160或220molM后，细胞内约70%和30%的86Rb被释放。在渗透压降低的情况下，86Rb外排未见明显增加。86Rb外流不依赖于钙离子，对温度不敏感。速尿可抑制胞内氯离子的释放，而布美他尼对其无抑制作用，当硝酸盐而不是葡萄糖酸取代胞内氯离子时，该作用不受影响。奎尼丁和4，4‘-二异硫氰基二苯乙烯-2，2’-二磺酸可显著抑制外排。奎尼丁也能阻止细胞体积调节性下降，当革兰西丁施加大的阳离子渗透性时，这种作用被克服。在等渗条件下，N-乙基马来酰亚胺不能激活86Rb的外流，但对低渗激活的释放有强烈的抑制作用。这些发现表明，星形胶质细胞的86Rb外流与细胞肿胀相关，不是由电中和共转运体介导的，而是一种可能是钙非依赖性K+通道的传导性退出途径。
The involvement of K+ on the volume regulatory process in astrocytes was investigated by characterizing the hyposmolarity-induced efflux of K+ using 86Rb as a tracer. About 70 and 30% of the intracellular content of 86Rb was released after reductions in osmolarity from 320 to 160 or 220 mosM, respectively, during the time in which cells exhibit a volume regulatory response subsequent to swelling. No significant increase in 86Rb efflux was observed with lower reductions in osmolarity. The 86Rb efflux was Ca2+ independent and insensitive to temperature. It was inhibited by furosemide but not by bumetanide and was unaffected when nitrate, but not gluconate, replaced intracellular Cl-. The efflux was markedly inhibited by quinidine and by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. Quinidine also prevented the volume regulatory decrease of cells, and this effect was overcome when a large cation permeability was imposed by gramicidin. In isosmotic conditions 86Rb efflux was not activated by N-ethylmaleimide, but this drug strongly inhibited the hyposmolarity-activated release. These findings suggest that 86Rb efflux from astrocytes associated to cell swelling is not mediated by an electroneutral cotransporter and rather favor the implication of a conductive exit pathway that may be a Ca(2+)-independent K+ channel.