Peptide changes in the parabrachial nucleus ...

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Title Peptide changes in the parabrachial nucleus following cervical vagal stimulation
Author(s) Tarek M. Saleh, D. F. Cechetto
Journal The Journal of Comparative Neurology
Date 1996
Volume 366
Issue 3
Start page 390
End page 405
Abstract Previous studies in our laboratory have shown that the peptides, neurotensin (NT), cholecystokinin (CCK), substance P (SP), somatostatin (SOM), and calcitonin gene-related peptide (CGRP), have a role in modulating ascending visceral sensory information from the nucleus of the solitary tract to the thalamus via a mandatory synapse in the parabrachial nucleus (PB). In this investigation, we examined the changes in the levels of these peptides detected by immunohistochemistry in response to cervical vagal stimulation in the inactin-anesthetized male Wistar rat. Paired control and experimental animals were instrumented to monitor blood pressure and heart rate. The vagus nerve was stimulated for 0.5, 2, or 4 hours, after which time the animals were perfused and the brains processed immunohistochemically for the Fos protein and the peptides NT, CCK, SP, SOM, and CGRP. Vagal stimulation for 1 hour produced large numbers of Fos-positive cells in the external lateral (el), external medial (em), and central lateral (cl) subnuclei of the PB (N = 3). Vagal stimulation produced a reduction in the level of immunolabeling for NT, SOM, and CCK in the el and em subnuclei of the PB. This depletion was present at 0.5 hour and increased in magnitude with the length of vagal stimulation, reaching a maximum after 4 hours. In contrast, the immunolabeling for SP and CGRP increased after 0.5 hour, reaching a maximum after 2 hours of vagal stimulation in the el and em subnuclei of the PB. After 4 hours of vagal stimulation, the immunolabeling for SP and CGRP was depleted in the two PB subnuclei. Thus, the neuropeptides NT, CCK, SP, SOM, and CGRP, which modulate the visceral sensory information in the PB, are influenced somewhat differentially by the level of activity in the vagus nerve.
DOI 10.1002/(SICI)1096-9861(19960311)366:3<390::AID-CNE2>3.0.CO,10.1002/(SICI)1096-9861(19960311)366:3<390::AID-CNE2>3.0.CO,2-#

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