Involvement of Mg2+ in terminating Ca2+ release in cultured rat skeletal muscle.
Combined patch-clamp and fura-2 measurements were performed to investigate the mechanism that terminates Ca2+ release in rat skeletal myoballs. When cells were intracellularly perfused with solution containing 1 mM free Mg2+, the caffeine (10 mM)-induced Ca2+ transient was abruptly terminated by membrane repolarization (-70 mV). With low intracellular Mg2+ (e.g. 50 microM) perfusion, however, repolarization failed to terminate the caffeine transient. The results show that intracellular Mg2+ is necessary for repolarization-induced closing of the Ca2+ release channel.
Suda
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Max-Planck-Institut für Biophysikalische Chemie, Göttingen, Germany.
D000818:Animals; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism; D002478:Cells, Cultured; D008274:Magnesium / Q000378:metabolism*; D008564:Membrane Potentials; D009124:Muscle Proteins / Q000378:metabolism; D018482:Muscle, Skeletal / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D018408:Patch-Clamp Techniques; D051381:Rats; D019837:Ryanodine Receptor Calcium Release Channel
D015220:Calcium Channels; D009124:Muscle Proteins; D019837:Ryanodine Receptor Calcium Release Channel; D002110:Caffeine; D008274:Magnesium; D002118:Calcium