Actin filaments regulate voltage-gated ion channels in salamander retinal ganglion cells

被引:34
作者
Schubert, T
Akopian, A
机构
[1] NYU, Sch Med, Dept Ophthalmol, New York, NY 10016 USA
[2] Carl von Ossietzky Univ Oldenburg, Dept Neurobiol, D-2900 Oldenburg, Germany
关键词
cytoskeleton; calcium channel; potassium channel; retina; latrunculin; patch clamp;
D O I
10.1016/j.neuroscience.2004.02.009
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The regulation of voltage-activated K+, and Ca2+ currents by actin filaments was studied in salamander retinal ganglion cells, using the whole-cell patch clamp technique and Ca2+ imaging. Disruption of F-actin by cytochalasin B or latrunculin B resulted in a reduction of L-type Ca2+ current by 55 +/- 4%, and a sustained outward K+ current (I-k) by 41 +/- 3%. The effect was diminished when the F-actin stabilizing agent phalloidin was present in the patch pipette. In a group of cells where I-K exhibited a small degree of inactivation, the effect of F-actin disruption on current was dual; it increased it by 89 +/- 16%, at -10 mV, and reduced it by 37 +/- 5% at +50 mV voltage step from the same holding potential of -70 mV. This was accompanied by a shift in a voltage of half-maximal activation toward negative potentials by approximately 20 mV. In Ca2+ imaging experiments, 30 min incubation of isolated neurons with latrunculin A reduced a depolarization-induced Ca2+ accumulation by 45 5%. These results suggest a role for the actin cytoskeleton in regulating voltage-gated ion channels in retinal ganglion cells. (C) 2004 IBRO. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:583 / 590
页数:8
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