Facilitating effect of cholecystokinin on nicotinic
neurotransmission in cat pancreatic ganglion.
Ma, R. C., and J. H. Szurszewski.
Department of Physiology and Biophysics, Mayo Clinic and Mayo
Foundation, Rochester, MN 55905, U.S.A.
APStracts 2:0193G, 1995.
Previous studies have demonstrated the presence of CCK-like peptides
in nerve terminals surrounding ganglion neurons of the cat pancreas.
The present?study was undertaken to determine the effect of CCK8 on
ganglionic transmission. Recordings were made intracellularly in
vitro from ganglion neurons in isolated pieces of the pancreas. S
-CCK8 and NS-CCK8 initiated or increased ongoing F-EPSP activity, an
effect antagonized by hexamethonium. Superfusion of S-CCK8 in
concentrations ranging from 10-11 to 10-8 M signifi cantly augmented
the amplitude of nerve evoked subthreshold F-EPSPs without a
significant change in either membrane potential or membrane input
resistance. S-CCK8 (10-8 M) also increased the quantal content and
quantal size of nerve-evoked F-EPSPs, and increased the response to
exogenously applied ACh. Concentrations of S-CCK8 higher than 10-8 M
caused depolarization and an increase in membrane input resistance,
an effect unaltered by a low Ca2+-high Mg2+ solution. It was
concluded that S-CCK8 potentiated nicotinic transmis sion by
facilitating release of ACh from preganglionic nerve terminals and by
increasing the postsynaptic membrane sensitivity to acetylcholine.
Received 3 March 1995; accepted in final form 11 September 1995.
APS Manuscript Number G97-5.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95