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Dalton Cardiovascular Research Center, Department of Veterinary Biomedical Sciences, College of Veterinary Medicine, University of Missouri, Columbia, Missouri 65211
The purpose of this study was to evaluate the
use of the fluorescent membrane label FM1-43 as a measure of
synaptic terminal exocytosis during stimulation of labeled aortic
baroreceptor and unlabeled nodose ganglia neurons. Activation of the
nerve terminals with electrical stimulation or depolarization with 90 mM KCl in the presence of 2.0 µM FM1-43 resulted in bright,
punctate staining of synaptic boutons. Additional depolarization in the
absence of dye resulted in destaining with a time course that was
consistent and repeatable in multiple boutons within a given terminal.
Destaining was dependent on calcium influx and was blocked by bath
application of 100 µM CdCl2.
Whole cell patch-clamp studies have reported that
depolarization-induced calcium influx in aortic baroreceptor cell
bodies is predominantly caused by the activation of 
-conotoxin GVIA
(-CgTx)-sensitive N-type calcium channels. In addition, these N-type
channels have been shown to be inhibited by activation of metabotropic
glutamate receptors. In the present study, exocytosis in aortic
baroreceptor terminals was not affected by bath application of 5 µM
nifedipine and only partially inhibited by bath application of 2.0 µM
-CgTx. However, depolarization-induced exocytosis was significantly
inhibited by bath application of 200 µM L-AP4, a type III
metabotropic glutamate receptor agonist. Results from this study
suggest that 1) FM1-43 can be
used to measure synaptic vesicle exocytosis in baroreceptor neurons;
2) the N-type calcium channel may
not be involved in the initial phase of vesicle exocytosis; and
3) activation of L-AP4-sensitive
metabotropic glutamate receptors inhibits 90 mM KCl-induced vesicle
release.
nodose neurons; metabotropic glutamate receptors
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