Maguire G, Connaughton V, Prat A G, Jackson G R, Cantiello H F
Department of Ophthalmology, University of California at San Diego, 92093, USA.
Neuroreport. 1998 Mar 9;9(4):665-70. doi: 10.1097/00001756-199803090-00019.
The actin cytoskeleton is an important contributor to the integrity of cellular shape and responses in neurons. However, the molecular mechanisms associated with functional interactions between the actin cytoskeleton and neuronal ion channels are largely unknown. Whole-cell and single channel recording techniques were thus applied to identified retinal bipolar neurons of the tiger salamander (Ambystoma tigrinum) to assess the role of acute changes in actin-based cytoskeleton dynamics in the regulation of voltage-gated ion channels. Disruption of endogenous actin filaments after brief treatment (20-30 min) with cytochalasin D (CD) activated voltage-gated K+ currents in bipolar cells, which were largely prevented by intracellular perfusion with the actin filament-stabilizer agent, phalloidin. Either CD treatment under cell-attached conditions or direct addition of actin to excised, inside-out patches of bipolar cells activated and/or increased single K+ channels. Thus, acute changes in actin-based cytoskeleton dynamics regulate voltage-gated ion channel activity in bipolar cells.
肌动蛋白细胞骨架对神经元细胞形态的完整性和反应起着重要作用。然而,肌动蛋白细胞骨架与神经元离子通道之间功能相互作用的分子机制在很大程度上尚不清楚。因此,采用全细胞和单通道记录技术,对虎螈(Ambystoma tigrinum)已鉴定的视网膜双极神经元进行研究,以评估基于肌动蛋白的细胞骨架动力学急性变化在电压门控离子通道调节中的作用。用细胞松弛素D(CD)短暂处理(20 - 30分钟)后破坏内源性肌动蛋白丝,可激活双极细胞中的电压门控钾电流,而通过向细胞内灌注肌动蛋白丝稳定剂鬼笔环肽可在很大程度上阻止这种激活。在细胞贴附条件下进行CD处理或直接向双极细胞的内向外膜片添加肌动蛋白,均可激活和/或增加单个钾通道。因此,基于肌动蛋白的细胞骨架动力学急性变化可调节双极细胞中的电压门控离子通道活性。