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1 Department of Physiology, RCMM, MHCS, University of Debrecen, Debrecen, Hungary
2 INSERM U607/DRDC, Laboratory Canaux Calciques Fonctions et Pathologies, CEA, 17 rue des Martyrs, 38054 Grenoble Cedex 09, France
3 CNRS UMR 6560, Faculté de Médecine Nord, Boulevard Pierre Dramard, 13916 Marseille Cedex 20, France
4 Cell Physiology Research Group of the Hungarian Academy of Sciences, University of Debrecen, Debrecen, Hungary
Maurocalcine (MCa), a 33 amino acid toxin obtained from scorpion venom, has been shown to interact with the isolated skeletal-type ryanodine receptor (RyR1) and to strongly modify its calcium channel gating. In this study, we explored the effects of MCa on RyR1 in situ to establish whether the functional interaction of RyR1 with the voltage-sensing dihydropyridine receptor (DHPR) would modify the ability of MCa to interact with RyR1. In developing skeletal muscle cells the addition of MCa into the external medium induced a calcium transient resulting from RyR1 activation and strongly inhibited the effect of the RyR1 agonist chloro-m-cresol. In contrast, MCa failed to affect the depolarization-induced Ca2+ release. In intact adult fibres MCa did not induce any change in the cytosolic Ca2+ concentration. However, when the surface membrane was permeabilized and calcium release events were readily observable, MCa had a time-dependent dual effect: it first increased event frequency, from 0.060 ± 0.002 to 0.150 ± 0.007 sarcomere–1 s–1, and reduced the amplitude of individual events without modifying their spatial distribution. Later on it induced the appearance of long-lasting events resembling the embers observed in control conditions but having a substantially longer duration. We propose that the functional coupling of DHPRs and RyR1s within a Ca2+ release unit prevents MCa from either reaching its binding site or from being able to modify the gating not only of the RyR1s physically coupled to DHPRs but all RyR1s within the Ca2+ release unit.
(Received 3 March 2005;
accepted after revision 12 April 2005;
first published online 14 April 2005)
Corresponding author M. Ronjat: INSERM U607/DRDC, CEA, 17 rue des Martyrs, 38054 Grenoble Cedex 09, France. Email: mronjat{at}cea.fr
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