细胞松弛素D
细胞骨架
细胞松弛素
鬼臼苷
肌动蛋白
肌动蛋白细胞骨架
生物物理学
细胞生物学
神经元肌动蛋白重塑
微丝
肌动蛋白重塑
MDia1公司
细胞松弛素B
化学
生物
生物化学
细胞
作者
W. H. Wang,Antônio Carlos Cassola,Gerhard Giebisch
出处
期刊:American Journal of Physiology-renal Physiology
[American Physical Society]
日期:1994-10-01
卷期号:267 (4): F592-F598
被引量:61
标识
DOI:10.1152/ajprenal.1994.267.4.f592
摘要
We have employed the patch-clamp technique to investigate the role of the actin cytoskeleton in the modulation of the low-conductance K+ channel in the apical membrane of the rat cortical collecting duct (CCD). This K+ channel is inactivated by application of cytochalasin B or D, both compounds known to disrupt actin filaments. The effect of both cytochalasins, B and D, was fully reversible in cell-attached patches, but channel activity could not be fully restored in excised membrane patches. The effect of cytochalasins on channel activity was specific and resulted from depolymerization of the actin cytoskeleton, since application of 10 microM chaetoglobosin C, a cytochalasin analogue that does not depolymerize the actin filaments, had no effect on channel activity in inside-out patches. Addition of either actin monomers or of the polymerizing actin filaments in inside-out patches to the cytosolic medium had no effect on channel activity. This suggests that cytochalasin B- or D-induced inactivation of apical K+ channels is not caused by obstruction of the channel pore by actin. We also observed that channel inhibition by cytochalasin B or D could be blocked by pretreatment with 5 microM phalloidin, a compound that stabilizes actin filaments. We conclude that apical K+ channel activity depends critically on the integrity of the actin cytoskeleton.
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