A CYTOSKELETAL MECHANISM FOR CA2+ CHANNEL METABOLIC DEPENDENCE AND INACTIVATION BY INTRACELLULAR CA2+

被引:207
作者
JOHNSON, BD
BYERLY, L
机构
[1] Section of Neurobiology Department, Biological Sciences University of Southern California, Los Angeles
关键词
D O I
10.1016/0896-6273(93)90196-X
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Many different types of voltage-dependent Ca2+ channels inactivate when intracellular ATP declines or intracellular Ca2+ rises. An inside-out, patch-clamp technique was applied to the Ca2+ channels of Lymnaea neurons to determine the mechanism(s) underlying these two phenomena. Although no evidence was found for a phosphorylation mechanism, agents that act on the cytoskeleton were found to alter Ca2+ channel activity. The cytoskeletal disrupters colchicine and cytochalasin B were found to speed Ca2+ channel decline in ATP, whereas the cytoskeletal stabilizers taxol and phalloidin were found to prolong Ca2+ channel activity without ATP. In addition, cytoskeletal stabilizers reduced Ca2+-dependent channel inactivation, suggesting that both channel metabolic dependence and Ca2+-dependent inactivation result from a cytoskeletal interaction.
引用
收藏
页码:797 / 804
页数:8
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