RISC (Repolarization-induced stop of caffeine-contracture) is not due to store depletion in cultured murine skeletal muscle.
We have combined the patch-clamp technique with Fura-2 measurements to investigate whether RISC (repolarization-induced stop of caffeine-contracture) is a consequence of store depletion in cultured skeletal muscles of rats and mice. Weak depolarizations (-45 to -40 mV) of long duration induced a barely detectable Ca2+ transient. Even under these conditions, caffeine-activated Ca2+transients (CafTs) were terminated upon membrane repolarization (-70 mV) at all stages of CafT. Following the peak of the CafT, massive Ca2+ release was elicited by either flash-photolysis of caged Ca2+ or further depolarization to 0 mV, demonstrating the lack of store depletion. Thus, RISC is not due primarily to store depletion but to closure of the Ca2+ release channels possibly through a mechanical interaction with voltage sensors. RISC was not present in rat heart muscle, further supporting a role of direct interaction in skeletal muscle.
Suda
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N
Department of Molecular Biology of Neuronal signaling, Max-Planck-Institut für Experimentelle Medizin, Hermann-Rein-Strasse 3, D-37075 Göttingen, Germany.
Heinemann
C
C
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002110:Caffeine / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism; D002478:Cells, Cultured; D051379:Mice; D009119:Muscle Contraction / Q000187:drug effects*; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000378:metabolism; D051381:Rats; D012519:Sarcoplasmic Reticulum / Q000187:drug effects / Q000378:metabolism
D002110:Caffeine; D002118:Calcium