We studied, in a genetic model organism, Drosophila melanogaster, the channel mechanisms underlying membrane excitation in the embryonic body wall muscle whose biophysical properties have been poorly characterized. The inward current underlying the action potential was solely mediated by a high-threshold class of voltage-gated Ca(2+) channels, which exhibited slow inactivation, Ca(2+) permeability with saturation at high [Ca(2+)]OUT, and sensitivity to a Ca(2+) channel blocker, Cd(2+). The Ca(2+) current in the embryonic muscle was completely eliminated in Dmca1D mutants, indicating that the Dmca1D-encoded Ca(2+) channel is the major mediator of inward currents in the body wall muscles throughout the embryonic and larval stages.
Keywords: Ca2+ channel gating; Ca2+ permeability; mutants; skeletal muscle; whole-cell patch clamp.