GABA B receptors presynaptically modulate excitatory synaptic transmission
in the rat supraoptic nucleus in vitro.
Kombian, Samuel B., Jeffrey A. Zidichouski and Quentin J. Pittman.
Neuroscience Research Group, University of Calgary & 2 Ciba-Geigy Canada
APStracts 3:0051N, 1996.
SUMMARY AND CONCLUSIONS
1. The effect of GABA B receptor activation on excitatory synaptic
transmission in the rat supraoptic nucleus (SON) was examined using the
nystatin perforated-patch whole-cell recording technique in coronal
hypothalamic slices. 2. Stimulation of the hypothalamic region dorso-medial to
the SON elicited glutamate and GABA A receptor-mediated synaptic responses in
electrophysiologically-identified magnocellular neurosecretory cells. 3. Bath
application of the GABA B receptor agonist, [+/-]-baclofen reversibly reduced
pharmacologically-isolated, glutamate-mediated excitatory postsynaptic
currents (EPSCs) in a concentration-dependent manner. At the concentrations
used, baclofen altered neither the postsynaptic conductances of these cells
nor their response to bath applied AMPA. 4. The baclofen-induced synaptic
depression was accompanied by an increase in paired pulse facilitation (PPF).
This increase in PPF, as well as the synaptic depression, was blocked by the
GABA B receptor antagonists CGP36742 and saclofen. 5. In addition to blocking
the actions of baclofen in this nucleus, CGP36742 caused an increase in the
evoked EPSC amplitude without altering postsynaptic cell conductances or
responses induced by bath applied AMPA. Contrary to the action of CGP36742,
saclofen caused a baclofen-like depression of the evoked EPSC suggesting that
it may act as a partial GABA B receptor agonist. 6. These results indicate
that the activation of presynaptic GABA B receptors reduces fast excitatory
synaptic transmission in the SON. They further suggest that presynaptic GABA B
receptors may be tonically activated in vitro . Thus, GABA B receptors may
influence the level of activity and excitation of SON neurons and hence
modulate the secretion of the regulatory neuropeptides vasopressin and
Received 30 November 1995; accepted in final form 4 March 1996.
APS Manuscript Number J809-5.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 27 March 96