Evidence for an inflammation-induced change in the local glutamatergic regulation of postganglionic sympathetic efferents

Citation
Re. Coggeshall et Sm. Carlton, Evidence for an inflammation-induced change in the local glutamatergic regulation of postganglionic sympathetic efferents, PAIN, 83(2), 1999, pp. 163-168
Citations number
42
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
PAIN
ISSN journal
03043959 → ACNP
Volume
83
Issue
2
Year of publication
1999
Pages
163 - 168
Database
ISI
SICI code
0304-3959(199911)83:2<163:EFAICI>2.0.ZU;2-R
Abstract
Sympathetic efferents are involved in the pain of inflammation. Thus the co ntrol of these fibers is a matter of considerable importance, in this regar d, postganglionic sympathetic fibers in normal rats express ionotropic glut amate receptors. The present study tests the hypothesis that inflammation l eads to a significant increase in numbers of sympathetic efferents that exp ress these receptors.;In normal rats, the percentage of fibers in the L4 an d L5 sympathetic gray rami immunostained with antibodies against subunits o f NMDA (NMDARI), AMPA (GluR1), or kainate (GluR5,6,7) receptors are 29, 5 a nd 5%, respectively. Forty-eight hours following injection of complete Freu nd's adjuvant into one hindpaw, the percentages of fibers in the ipsilatera l gray rami immunostained for NMDA, AMPA or kainate are 57, 52 and 48% resp ectively. Thus, following inflammation there is a two-fold increase in axon s expressing NMDA receptors and a ten-fold increase in axons expressing AMP A or kainate receptors. These data suggest that postganglionic activity may be enhanced by glutamate receptor activation during inflammation. Increase d activity in postganglionic fibers could lead to an increased release of N E and other substances in postganglionic efferents such as prostaglandins w hich in turn could enhance nociceptor activity. This change in glutamate re ceptor organization offers a possible site of pharmacological intervention for the maladaptive symptoms that often arise following peripheral inflamma tion. (C) 1999 International Association for the Study of Pain. Published b y Elsevier Science B.V.