CA2-RECEPTOR CHANNEL IN DYSGENIC MYOTUBES( ENTRY THROUGH ACETYLCHOLINE)

Skeletal muscles of mutant mice with ''muscular dysgenesis'' are chara cterized by excitation-contraction uncoupling resulting from the absen ce of dihydropyridine receptors. However contraction of the dysgenic m yotubes can be evoked by afferent nerve stimulation or by ionophoretic application of acetylcholine (ACh) on the muscle. These contractions are elicited by Ca2+ entry through the ionic channel of the ACh recept or at multiple synaptic contacts. In the present paper, the calcium en try through ACh receptors was compared in cultured normal and dysgenic myotubes. At elevated external calcium concentration (110 mM), the el ementatry slope conductance of the ACh-activated ionic channel of dysg enic myotubes did not differ from that found in normal myotubes. We co nclude that dysgenic muscle contraction induced by nerve stimulation d oes not result from an abnormal Ca2+ entry across ACh receptors. We di scuss the possible involvement of sustained high threshold calcium cur rent (I-dys) and of the calcium induced calcium release mechanism in t he contractile response related to synaptic activity of dysgenic myotu bes.