The electrophysiological expression of Ca2+ channels and of apamin sensitive Ca2+ activated K+ channels is abolished in skeletal muscle cells from mice with muscular dysgenesis.
Action potentials of myotubes in culture prepared from 18-19 day -old mouse embryos have a contractile activity and action potentials that are followed by a long lasting after hyperpolarization (ahp) which is blocked by apamin. Myotubes prepared from embryos of mice with muscular dysgenesis (mdg/mdg) did not contract and had action potentials which were never followed by a.h.p.'s. Voltage-clamp experiments have shown that Na+ channel activity was identical in mutant and control muscles and that the activity of fast and slow Ca2+ channels was nearly absent in the mutant.
D000200:Action Potentials; D000818:Animals; D001030:Apamin / Q000494:pharmacology*; D001514:Bee Venoms / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism*; D004558:Electric Stimulation; D004594:Electrophysiology; D005260:Female; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology*; D051379:Mice; D009119:Muscle Contraction; D009132:Muscles / Q000503:physiopathology*; D009135:Muscular Diseases / Q000503:physiopathology*; D011188:Potassium / Q000378:metabolism*; D011247:Pregnancy; D012964:Sodium / Q000378:metabolism
D001514:Bee Venoms; D007473:Ion Channels; D001030:Apamin; D012964:Sodium; D011188:Potassium; D002118:Calcium