title: The Dmca1D channel mediates Ca(2+) inward currents in Drosophila embryonic muscles.
abstract: 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.
authors.affiliation: a Division of Neurogenetics, Tohoku University Graduate School of Life Sciences , Sendai, Miyagi , Japan.
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Hara
authors.affiliation: a Division of Neurogenetics, Tohoku University Graduate School of Life Sciences , Sendai, Miyagi , Japan.
authors.forename: Masayuki
authors.initials: M
authors.lastname: Koganezawa
authors.affiliation: a Division of Neurogenetics, Tohoku University Graduate School of Life Sciences , Sendai, Miyagi , Japan.
authors.forename: Daisuke
authors.initials: D
authors.lastname: Yamamoto
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000235:genetics / Q000378:metabolism*; D029721:Drosophila Proteins / Q000235:genetics / Q000378:metabolism*; D004331:Drosophila melanogaster / Q000196:embryology / Q000378:metabolism; D015640:Ion Channel Gating / Q000502:physiology; D008564:Membrane Potentials / Q000502:physiology; D018482:Muscle, Skeletal / Q000196:embryology / Q000378:metabolism*
chemical_list: C112195:Ca-alpha1D protein, Drosophila; D015220:Calcium Channels; D029721:Drosophila Proteins; D002118:Calcium
keywords: Ca2+ channel gating; Ca2+ permeability; mutants; skeletal muscle; whole-cell patch clamp