title: Membrane repolarization stops caffeine-induced Ca2+ release in skeletal muscle cells.
abstract: We have combined the patch-clamp technique with fura-2 measurements to investigate whether the Ca(2+)-induced Ca(2+)-release channel is under the control of membrane potential in rat skeletal myoballs. We report that Ca2+ release induced by 10 mM caffeine is turned off by membrane repolarization, a phenomenon that we term RISC (repolarization-induced stop of Ca2+ release). The RISC phenomenon is voltage- and time-dependent. It is evident only when the release channels are first transferred into a functionally "voltage-activated" state through membrane depolarization. The results demonstrate that membrane repolarization actively closes the caffeine-activated release channels and suggest that the ryanodine receptor is actually the physiological depolarization-induced Ca(2+)-release channel. Thus, our data provide compelling evidence for a bidirectional voltage control (depolarization and repolarization) of the Ca(2+)-release channel in the sarcoplasmic reticulum by a voltage sensor in the transverse tubule membrane.
authors.affiliation: Max-Planck-Institut für biophysikalische Chemie, Göttingen, Germany.
authors.forename: N
authors.initials: N
authors.lastname: Suda
authors.forename: R
authors.initials: R
authors.lastname: Penner
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D002110:Caffeine / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000502:physiology; D002478:Cells, Cultured; D066298:In Vitro Techniques; D015640:Ion Channel Gating / Q000187:drug effects; D008564:Membrane Potentials; D009124:Muscle Proteins / Q000502:physiology; D009132:Muscles / Q000378:metabolism*; D051381:Rats; D019837:Ryanodine Receptor Calcium Release Channel; D012519:Sarcoplasmic Reticulum / Q000502:physiology; D013997:Time Factors
chemical_list: D015220:Calcium Channels; D009124:Muscle Proteins; D019837:Ryanodine Receptor Calcium Release Channel; D002110:Caffeine; D002118:Calcium