RISC (Repolarization-induced stop of caffeine-contracture) is not due to store depletion in cultured murine skeletal muscle |
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Authors: | N Suda C Heinemann |
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Institution: | 1. Department of Molecular biology of Neuronal signaling, Max-Planck-Institut für Experimentelle Medizin, Hermann-Rein-Strasse 3, D-37075, G?ttingen, Germany 3. Department of Membrane Biophysics, Max-Planck-Institut für biophysikalische Chemie, Am Fassberg, D-37077, G?ttingen, Germany
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Abstract: | 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.
Received: 23 April 1996 / Accepted: 12 July 1996 |
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Keywords: | Skeletal muscle E-C coupling Ryanodine receptors Calcium-induced calcium release Caffeine Cardiac muscle |
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