Johnson B D, Byerly L
Department of Biological Sciences, University of Southern California, Los Angeles 90089-2520.
Neuron. 1993 May;10(5):797-804. doi: 10.1016/0896-6273(93)90196-x.
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 Ca(2+)-dependent channel inactivation, suggesting that both channel metabolic dependence and Ca(2+)-dependent inactivation result from a cytoskeletal interaction.
当细胞内三磷酸腺苷（ATP）含量下降或细胞内钙离子（Ca2+）浓度升高时，许多不同类型的电压依赖性Ca2+通道会失活。采用内面向外式膜片钳技术研究椎实螺神经元的Ca2+通道，以确定这两种现象背后的机制。虽然未发现磷酸化机制的证据，但发现作用于细胞骨架的试剂会改变Ca2+通道活性。发现细胞骨架破坏剂秋水仙碱和细胞松弛素B会加速ATP存在时Ca2+通道的失活，而细胞骨架稳定剂紫杉醇和鬼笔环肽则能在无ATP的情况下延长Ca2+通道的活性。此外，细胞骨架稳定剂可降低Ca(2+)依赖性通道失活，这表明通道的代谢依赖性和Ca(2+)依赖性失活均源于细胞骨架相互作用。
