A Cytoskeletal Mechanism for Ca 2+ Channel Metabolic Dependence and Inactivation by Intracellular Ca 2

Many different types of voltage-dependent Ca 2+ channels inactivate when intracellular ATP declines or intracellular Ca 2+ rises. An inside-out, patch-clamp technique was applied to the Ca 2+ channels of Lymnaea neurons to determine the mechanism(s) underlying these two phenomena. Although no eviden...

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Bibliographic Details
Published inNeuron (Cambridge, Mass.) Vol. 10; no. 5; pp. 797 - 804
Main Authors Johnson, Barry D., Byerly, Lou
Format Journal Article
LanguageEnglish
Published Elsevier Inc 1993
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Summary:Many different types of voltage-dependent Ca 2+ channels inactivate when intracellular ATP declines or intracellular Ca 2+ rises. An inside-out, patch-clamp technique was applied to the Ca 2+ 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 Ca 2+ channel activity. The cytoskeletal disrupters colchicine and cytochalasin B were found to speed Ca 2+ channel decline in ATP, whereas the cytoskeletal stabilizers taxol and phalloidin were found to prolong Ca 2+ 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.
ISSN:0896-6273
1097-4199
DOI:10.1016/0896-6273(93)90196-X