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J Biol Chem, Vol. 273, Issue 22, 13905-13911, May 29, 1998
From the Departments of Neuroscience and Physiology, and
§ Division of Endocrinology, Tufts University School of
Medicine, Boston, Massachusetts 02111
The initiation of insulin release from rat islet
Class A Calcium Channel Variants in Pancreatic Islets and
Their Role in Insulin Secretion
cells relies, in large part, on calcium influx through
dihydropyridine-sensitive (
1D) voltage-gated
calcium channels. Components of calcium-dependent insulin
secretion and whole cell calcium current, however, are resistant to
L-type channel blockade, as well as to 
-conotoxin GVIA,
a potent inhibitor of 1B channels, suggesting the
expression of additional exocytotic calcium channels in the islet. We
used a reverse transcription-polymerase chain reaction-based strategy to ascertain at the molecular level whether the 1A
calcium channel isoform was also present. Results revealed two new
variants of the rat brain 1A channel in the islet with
divergence in a putative extracellular domain and in the carboxyl
terminus. Using antibodies and cRNA probes specific for
1A channels, we found that the majority of cells in rat
pancreatic islets were labeled, indicating expression of the
1A channels in cells, the predominant islet cell
type. Electrophysiologic recording from isolated islet cells
demonstrated that the dihydropyridine-resistant current was sensitive
to the 1A channel blocker, -agatoxin IVA. This toxin
also inhibited the dihydropyridine-resistant component of
glucose-stimulated insulin secretion, suggesting functional overlap
among calcium channel classes. These findings confirm the presence of
multiple high voltage-activated calcium channels in the rat islet and
implicate a physiologic role for 1A channels in
excitation-secretion coupling in cells.
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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