Guy Raymond

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During in vitro development of rat skeletal muscle cells, contraction and calcium currents progressively appear after fusion of myoblasts. To investigate whether muscle-specific functions are expressed in the absence of myoblast fusion, rat neonatal muscle cells were cultured in a differentiation medium under conditions that are well known to inhibit(More)
Calcium mishandling in Duchenne dystrophic muscle suggested that dystrophin, a membrane-associated cytoskeleton protein, might regulate calcium signaling cascade such as calcium influx pathway. It was previously shown that abnormal calcium entries involve uncontrolled stretch-activated currents and store-operated Ca2+ currents supported by TRPC1 channels.(More)
The whole-cell patch-clamp technique coupled with intracellular [Ca2+] measurements was used to investigate the sodium-calcium exchange mechanism in rat skeletal muscle cells in primary culture. Replacing external Na+ ions with Li+ or N-methyl-D-glucamine (NMDG+) ions generated outward currents which were correlated with significant increases of free(More)
Primary cultures from enzymatically dissociated satellite cells of newborn rat skeletal muscles enabled developmental in vitro studies of mechanical and electrical properties during the first steps of myogenesis. The present work focused on the appearance, evolution and roles of two types of calcium currents (ICa,T and ICa,L) and of depolarization-induced(More)
The transient outward current was studied, using the whole-cell patch-clamp technique, in isolated ventricular cells from the ferret heart. In the presence of 4-aminopyridine and cadmium chloride which respectively blocked the Ca-insensitive and the Ca-dependent outward currents, a residual transient outward current was observed in about 30% of the cells(More)
We present here evidence for the enhancement of an inositol 1,4,5-trisphosphate (IP3) mediated calcium signaling pathway in myotubes from dystrophin-deficient cell lines (SolC1(-)) as compared to a cell line from the same origin but transfected with mini-dystrophin (SolD(+)). With confocal microscopy, we demonstrated that calcium rise, induced by the(More)
We present here evidence for the enhancement, at rest, of an inositol 1,4,5-trisphosphate (IP3)-mediated calcium signaling pathway in myotubes from dystrophin-deficient cell lines (SolC1(-)) as compared to a cell line from the same origin but transfected with mini-dystrophin (SolD(+)). With confocal microscopy, the number of sites discharging calcium(More)
Resting intracellular calcium levels and intracellular calcium transients induced by three types of stimulus (acetylcholine, high potassium and caffeine) were recorded, during in vitro myogenesis, by means of a ratiometric fluorescence method using the calcium probe Indo-1 under laser illumination. Resting levels seemed to decrease with the age of cultured(More)
Many studies of in vitro skeletal myogenesis have demonstrated that fusion of myoblasts into multinucleated myotubes is regulated by calcium-dependent processes. Calcium ions appear to be necessary at the outer face of the membrane, and an additional internal calcium increase seems required to promote fusion of aligned myoblasts. It has been proposed that a(More)
Defective expression of dystrophin in muscle cells is the primary feature of Duchenne muscular dystrophy (DMD), which is accompanied by fiber necrosis and intracellular calcium mishandling. These features led to the hypothesis that dystrophin could control calcium movements. Calcium mishandling in human DMD myotubes is dependent on contraction and/or(More)