AJP - Regulatory, Integrative and Comparative Physiology, Vol 268, Issue 3 786-R795, Copyright © 1995 by American Physiological Society
Neurochemical interactions in the parabrachial nucleus mediating visceral inputs to visceral thalamic neurons
T. M. Saleh and D. F. Cechetto
Robarts Research Institute, University of Western Ontario, London, Canada.
Previously we demonstrated that glutamatergic and noradrenergic receptors
mediate the relay of visceral information through the parabrachial nucleus
(PBN) and that calcitonin gene-related peptide (CGRP), substance P (SP),
somatostatin (SOM), neurotensin (NT), and cholecystokinin (CCK) may
modulate these responses. The interactions of these neurotransmitters and
neuropeptides were examined in male Wistar rats (17) that were anesthetized
with chloral hydrate and ventilated and in which blood pressure and heart
rate were continuously monitored. The left cervical vagus nerve was
stimulated at submaximal current intensities to elicit changes in single
and multiunit activity of visceral thalamic neurons (VTNs).
Peristimulus-time and continuous-time histograms of VTN activity were made
before and after 200-nl injections of peptides, neurotransmitter agonists
or antagonists, or artificial cerebrospinal fluid into the PBN. Combined
injection of CGRP and SP into the PBN produced a synergistic inhibition of
spontaneous VTN activity and the vagally evoked VTN response. Combined
injection of NT and phenylephrine (PE) into the PBN produced only an
additive increase in the spontaneous activity of VTNs. Prior administration
of SOM in the PBN blocked the excitatory action of an alpha-adrenergic
agonist (phenylephrine) injection on the spontaneous activity of VTNs,
whereas CGRP, SP, or CCK had no effect on the alpha-agonist-induced
response. Prior injection of an alpha-adrenergic antagonist (phentolamine)
prevented the excitatory effect of NT in the PBN. Injection of CGRP, SP,
NT, or CCK into the PBN did not change the response of VTNs to application
of glutamate. These results suggest mechanisms for peptide interaction with
primary neurotransmitters in the PBN and indicate whether the neuropeptides
are acting before the primary neurotransmitter synapse or postsynaptically.
