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Peptides in the parabrachial nucleus modulate visceral input to the thalamus
Ist Teil von
American journal of physiology. Regulatory, integrative and comparative physiology, 1993-04, Vol.264 (4), p.668-R675
Ort / Verlag
United States
Erscheinungsjahr
1993
Link zum Volltext
Quelle
MEDLINE
Beschreibungen/Notizen
T. M. Saleh and D. F. Cechetto
Robarts Research Institute, University of Western Ontario, London, Canada.
The role of neuropeptides in ascending visceral pathways was investigated
by recording the changes in the response of thalamic neuronal activity
evoked by vagal stimulation before and after peptide injection in the
parabrachial nucleus (PB). Male Wistar rats (n = 25) were anesthetized with
chloral hydrate and ventilated, and 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 in the parvocellular visceral relay nuclei in the ventral basal
thalamus. Peristimulustime histograms of thalamic activity were made before
and after 200-nl injections of peptides or artificial cerebrospinal fluid
(CSF) controls in the PB. Injection of calcitonin gene-related peptide
(CGRP) at 5 mM or substance P (SP) at 2 mM into the PB significantly
attenuated the evoked response of thalamic neuronal activity by 87-100% and
85-100%, respectively. Injections of somatostatin (SOM; 1 mM) did not
significantly alter the response evoked by vagal stimulation but
significantly inhibited the spontaneous firing of thalamic units, resulting
in a 10-fold increase in the response-to-background ratio. This suggests
that SOM in the PB inhibits cells in a parallel pathway that terminates on
thalamic visceral neurons but that are not part of the ascending visceral
sensory pathway. Spontaneous thalamic neuronal activity and vagally evoked
responses were significantly enhanced (278-508%) by injection of 1 mM
neurotensin (NT) in the PB. Cholecystokinin (CCK) at low doses (0.0002-0.2
mM) attenuated while the highest dose, 2 mM, briefly excited the
spontaneous activity of thalamic units before inhibiting their
activity.