CALCITONIN-GENE-RELATED PEPTIDE CONTENT, BASAL OUTFLOW AND ELECTRICALLY-EVOKED RELEASE FROM MONOARTHRITIC RAT SPINAL-CORD IN-VITRO

In this study, Freund's adjuvant-induced monoarthritis in the rat hind paw was used to induce chronic pain and inflammation. In order to com pare the basal outflow, electrically-evoked release and total content of calcitonin gene-related peptide like immunoreactivity (CGRP-LI) wit h previously reported changes in substance P (SP-LI), the lumbar enlar gement of monoarthitic (complete Freund's adjuvant-treated, CFA rat) a nd control (incomplete Freund's adjuvant-treated, IFA rat) spinal cord s were used. During the 4-wk period after injection, neither the basal nor the evoked release of CGRP-LI from CFA cords differed from contro ls. By contrast, we have previously reported that SP-LI release from C FA rat spinal cords was significantly higher than from controls, 21 da ys after inoculation with Freund's adjuvant. Electrically-evoked CGRP- LI release from 21-day CFA rat spinal cord slices was not modified by superfusion with a GABA(B) antagonist, CGP 36742 (100 mu M) which coul d greatly increase SP-LI release. However, the release of both peptide s was significantly increased to the same extent in IFA and normal tis sue but to a lesser extent in CFA cords, by superfusion with the opioi d antagonist naloxone (1 mu M). In conclusion, CGRP-LI, unlike SP-LI, did not appear to be susceptible to any changes in the lumbar enlargem ent of the rat spinal cord during inflammation of the hind paw. In add ition, CGRP-LI release was increased by antagonism of opiate but not G ABA(B) receptors, suggesting that during chronic inflammation of one h ind paw, the GABA(B)ergic system, unlike the opioid system, might be a ctivated to selectively inhibit the enhanced SP-LI release but not CGR P-LI release which is not changed.