A cytoskeletal mechanism for Ca2+ channel metabolic dependence and inactivation by intracellular Ca2+.
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.
Johnson
B D
BD
Department of Biological Sciences, University of Southern California, Los Angeles 90089-2520.
Byerly
L
L
D000199:Actins / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001464:Barium / Q000378:metabolism; D002118:Calcium / Q000494:pharmacology*; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism*; D003078:Colchicine / Q000494:pharmacology; D003571:Cytochalasin B / Q000494:pharmacology; D003599:Cytoskeleton / Q000187:drug effects / Q000502:physiology*; D004553:Electric Conductivity; D008195:Lymnaea; D017239:Paclitaxel / Q000494:pharmacology; D010590:Phalloidine / Q000494:pharmacology; D010766:Phosphorylation; D014404:Tubulin / Q000494:pharmacology
D000199:Actins; D015220:Calcium Channels; D014404:Tubulin; D010590:Phalloidine; D001464:Barium; D003571:Cytochalasin B; D000255:Adenosine Triphosphate; D017239:Paclitaxel; D003078:Colchicine; D002118:Calcium