Receptor‐triggered polyphosphoinositide turnover produces less cytosolic free calcium in cultured dysgenic myotubes than in normal myotubes

Myotubes prepared from mice with muscular dysgenesis (mdg) were used to further elucidate the putative role of inositol triphosphate (InsP3) in excitation-contraction (E-C) coupling of skeletal muscle. The mdg mutation is characterized by an uncoupling of the E-C coupling. InsP3 production in normal and mdg/mdg myotube cultures and its relation to the levels of cytosolic free calcium were analyzed. Basal and ATP-stimulated levels of InsP3 were equal in normal and mdg/mdg myotube cultures. In contrast, the transient increases of cytosolic free calcium in mdg/mdg myotubes in culture were generally much lower than those in normal ones. This suggests that the defect in dysgenic myotubes does not rest on the InsP3 formation but on the InsP3-triggered transduction of excitation and/or the induction of calcium release from internal stores.