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Joint work with David Gall.
The glucose-stimulated secretion of insulin from -cells
in pancreatic islets is induced by bursting electrical activity,
consisting of a periodic alternation of active and silent phases.
The modulation of the plateau fraction (fraction of time spent
in the active phase) is an essential factor in the regulation
of insulin release (Meissner, H.P. and H. Schmelz, 1974).
The Na+/Ca2+ exchanger
is a Ca2+-activated electrogenic Ca2+-transporter
of the plasma membrane of the pancreatic -cells
(Gall, D. et al., 1999). We have incorporated the Na+/Ca2+
exchange in different single-cell models (Sherman, A., 1996)
to investigate its role on electrical bursting behavior and
insulin secretion. We show that the depolarizing influence of
the Na+/Ca2+ exchange current
is able to prolong the burst duration and increase the plateau
fraction. In addition, the Na+/Ca2+
exchange can provide a physiological mechanism, among others
like K(ATP) channels, to increase the plateau fraction as the
glucose concentration is raised.
Gall, D., J. Gromada, I. Susa, A. Herchuelz, P. Rorsman, and
K. Bokvist. Significance of Na/Ca-exchange for Ca2+-buffering
and electrical activity in mouse pancreatic -cells.
{\it Biophysical. J.}, in press.
\noindent Meissner, H.P. and H. Schmelz. Membrane potential
of -cells in pancreatic islets.
{\it Pfl\"ugers Arch.}, 351:195-206, 1974.
Sherman, A. Contributions of modeling to understanding stimulus-secretion
coupling in pancreatic -cells. {\it Am. J. of Phys.}, 271: E362-E372, 1996.
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