Glutamate receptor subtypes mediate excitatory synaptic responses
of rat lateral parabrachial neurons.
Zidichouski, Jeffrey A., Jacob C. Easaw, and Jack H. Jhamandas.
Department of Medicine (Neurology) and Division of Neuroscience,
University of Alberta, Edmonton, Alberta, Canada
APStracts 2:0425H, 1995.
The lateral parabrachial nucleus (LPBN) is a major recipient of
cardiovascular-related information from the periphery. Previous
studies have provided anatomical and electrophysiological evidence
for the presence of excitatory amino acid receptors on LPBN neurons.
In the present study we examined the role of specific excitatory
amino acid receptors in synaptic transmission within this nucleus.
Whole-cell patch recordings were made from coronal brainstem slices
of the LPBN and biophysical and pharmacological studies of excitatory
postsynaptic responses were conducted on 156 LPBN neurons. Two types
of pharmacologically distinct excitatory postsynaptic responses were
observed upon intra-LPBN stimulation. The first involved the
contribution of non-NMDA receptors, which mediated the fast component
of the excitatory postsynaptic current (EPSC), and N-methyl-D
-aspartate (NMDA) receptors which governed the late component of the
EPSC. The second type of postsynaptic response was mediated solely by
non-NMDA receptors. EPSC responses reversed near 0mV regardless of
whether a late NMDA component was evident. In neurons displaying a
first type of EPSC, the non-selective EAA receptor blocker kynurenic
acid reduced both the fast and late components. The fast component
was selectively and reversibly attenuated by a series of non-NMDA
antagonists (CNQX, DNQX and NBQX). The late component was reduced by
application of APV (10 [mu]M) and was augmented by the elimination of
Mg2+ from the external medium. In neurons which displayed the second
type of synaptic response, the EPSC was completely blocked by the
non-NMDA antagonists CNQX (20[mu]M) and NBQX (1[mu]M). In addition,
the late component of these EPSCs could not be augmented by removing
Mg2+ from the external medium nor did APV affect the slow component
at -60mV or at -80mV (in the absence of Mg2+). EPSCs were markedly
attenuated (to about 50% of control) by the application of the
metabotropic receptor agonist, trans-ACPD (10[mu]M). The effect
appears to restricted to a presynaptic site as we did not observe any
postsynaptic effects in the 9 cells tested. We conclude that intra
-LPBN stimulation causes the synaptic release of excitatory
transmitter, presumably glutamate, which depolarizes LBPN neurons via
activation of non-NMDA and NMDA receptors. In addition, we also
provide evidence that synaptically-released glutamate can negatively
influence its own release via action on presynaptically-located
metabotropic receptors.
Received 10 May 1995; accepted in final form 6 September 1995.
APS Manuscript Number H446-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 31 October 95