Peripheral injury produces long term changes in peptide content in dorsal r
oot ganglion (DRG) cells that contribute to the inflammatory process in the
periphery and neuronal plasticity in the spinal cord. We report here the p
roportion of colonic afferents labeled for calcitonin gene-related peptide
(CGRP), substance P (SP) or somatostatin (Som) in the T13-L2 and L6-S2 DRG
and changes in the percentage of SP or CGRP labeled afferents 6, 24, and 72
h following induction of experimental colitis. Following injection of fluo
rogold (FG) into the descending colon, significantly more FG labeled DRG ce
lls were observed in the T13-L2 than L6-S2 DRG. In noninflamed rats, in bot
h spinal regions, 60-70% of the colonic afferents that were labeled with FG
were double labeled for SP. Similar results were obtained when double labe
ling for CGRP. Only 20-30% of the FG labeled afferents were double labeled
for Som. Following experimental colitis induced by intracolonic zymosan, th
ere was a significant decrease in the percentage of cells double labeled fo
r SP in the T13-L2 and L6-S2 DRG at 6, 24, and 72 h. The percentage of CGRP
double labeled cells was decreased in the T13-L2 DRG at all time points, b
ut only at 24 h in the L6-S2 DRG. The cell bodies of CGRP labeled colonic a
fferents were significantly larger than SP or Som in control rats. Inflamma
tion did not affect the mean size of the double labeled cells. These result
s suggest that colonic inflammation increases SP and CORP release in the sp
inal cord and the colon that is manifest as a decrease in peptide content i
n the cell bodies of the colonic afferents during the first 72 h following
injury. (C) 1999 Elsevier Science Inc. All rights reserved.