NEUROPEPTIDE CHANGES PERSIST IN SPINAL-CORD DESPITE RESOLVING HYPERALGESIA IN A RAT MODEL OF MONONEUROPATHY

Citation
R. Munglani et al., NEUROPEPTIDE CHANGES PERSIST IN SPINAL-CORD DESPITE RESOLVING HYPERALGESIA IN A RAT MODEL OF MONONEUROPATHY, Brain research, 743(1-2), 1996, pp. 102-108
Citations number
40
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Neurosciences
Journal title
Brain research → ACNP
ISSN journal
0006-8993
Volume
743
Issue
1-2
Year of publication
1996
Pages
102 - 108
Database
ISI
SICI code
0006-8993(1996)743:1-2<102:NCPISD>2.0.ZU;2-T
Abstract
We have previously described the changes in spinal cord neuropeptides in the unilateral sciatic chronic constriction injury (CCI) model of B ennett and Xie [Pain, 33 (1988) 87-108] at 28 days, a time of maximum mechanical hyperalgesia. In this study we examine the same model 100-1 20 days post injury by which time resolution of the hyperalgesia and p eripheral nerve injury has occurred according to previous studies. Rat s underwent either CCI of the sciatic nerve (n = 12) or else sham oper ation (n = 8) which involved exposure but no Ligation of the nerve. Me chanical hyperalgesia was assessed with a Ugo-Basile analgesymeter and immunohistochemistry performed on the spinal cord sections of the ani mals and quantified using a confocal microscope. At this late time poi nt CCI rats were no longer significantly mechanically hyperalgesic com pared to the sham animals (P greater than or equal to 0.09). However, examination of the lumbar spinal cord revealed the following changes. (i) The neuropeptides substance P (SP) (P < 0.0001) and galanin (P < 0 .003) both showed decreases of about 30% ipsilaterally in immunoreacti vity in laminae 1 and 2 of the dorsal horn compared to the sham operat ed animals. (ii) Calcitonin gene-related peptide (CGRP) and neuropepti de Y (NPY) in laminae 1 and 2 showed no significant changes compared t o sham animals. (iii) NPY levels in laminae 3 and 4 of the spinal cord showed a 15% increase in immunoreactivity compared to sham animals (P = 0.008). These results indicate that changes in neuronal markers in the spinal cord can persist after apparent resolution of a peripheral nerve injury. We suggest that these changes may form a substrate for s ubsequent development of abnormal pain states.