High permeation of l-type calcium channels at physiological calcium
concentrations: homogeneity and dependence on the [alpha]1
subunit.
Gollasch, Maik, Christian Ried, Michael Liebold, Hermann Haller, Franz
Hofmann, and Friedrich C. Luft.
Franz Volhard Clinic and Max Delbr[umlaut]uck Center for Molecular
Medicine, Virchow Klinikum, Humboldt University of Berlin, and the
Institute for Pharmacology, Technical University of Munich, Munich,
Germany
APStracts 3:0108C, 1996.
Molecular cloning has identified multiple isoforms of dihydropyridine
-sensitive C class L-type Ca2+ channels. We tested the hypotheses that
L-type (C class) channels exhibit homogeneous high permeation
properties at physiological calcium concentrations and membrane
potentials. We measured unitary currents through single
dihydropyridine-sensitive, w-conotoxin-insensitive endocrine and
smooth muscle L-type Ca2+ channels in rat pituitary GH3 and rat
aortic A7r5 cell lines. We also measured unitary currents through
smooth muscle (Cb) Ca2+ channel [alpha]1-subunits in CHO cells. Our
results show that single-channel conductances of all three (C class)
L-type channels are uniform with high barium concentrations; e.g. 23
pS with 110 mM Ba2+. The single-channel conductances were reduced to
similar values when the [Ba2+] was lowered to near-physiological
values; 11.1 pS, 9.3 pS and 8.4 pS in GH3 cells, A7r5 cells and CHO
cells at 2 mM Ba2+, respectively. The single-channel conductances
were not significantly different with near-physiological calcium
concentrations. The conductances were 5.5 pS, 5.9 pS and 4.9 pS in
GH3 cells, A7r5 cells, and CHO cells at 2 mM Ca2+, respectively. The
data suggest that (C class) L-type channels are homogeneous in terms
of Ca2+ permeation at physiological charge carrier concentrations and
membrane potentials. Furthermore, the data indicate that the
relatively high Ca2+ permeation under physiological conditions is
determined by the intrinsic properties of the pore-forming Ca2+
channel [alpha]1-subunit.
Received 26 December 1995; accepted in final form 25 March 1996.
APS Manuscript Number C764-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 16 April 96