Proinflammatory
neuropeptides, such as
substance P and
calcitonin gene-related peptide, are up-regulated in primary afferent neurons in acute and chronic
inflammation. While these
neuropeptides have been intensively studied, potentially anti-inflammatory and/or anti-nociceptive
neuropeptides such as
somatostatin (SS) have been less widely investigated. Endogenous
somatostatin is thought to exert a tonic antinociceptive effect. Exogenous SS is anti-inflammatory and antinociceptive and is thought to exert these actions through inhibition of proinflammatory
neuropeptide release. In this study we have compared the expression of
somatostatin in two inflammatory models:
arthritis, a condition associated with increased nociception, and
periodontitis, in which there is little evidence of altered nociceptive thresholds. In acute
arthritis (< 24 h) SS
mRNA was down-regulated in ipsilateral dorsal root ganglia (DRG; 52 +/- 7% of control, P < 0.05), and up-regulated in contralateral DRG (134 +/- 10% of control; P < 0.05). In chronic
arthritis (14 days) this pattern of
mRNA regulation was reversed, with SS being up-regulated ipsilaterally and down-regulated contralaterally. In chronic mandibular
periodontitis (7-10 days), SS
mRNA was up-regulated in only the mandibular division of the ipsilateral trigeminal ganglion (TG) (day 7, 219 +/- 9% and day 10, 217 +/- 12% of control; P < 0.02) but showed no change in other divisions of the trigeminal ganglion or in the mesencephalic nucleus. These data show that antinociceptive and anti-inflammatory
neuropeptides are also regulated in
inflammation. It is possible that the degree of
inflammation and nociception seen may depend on the balance of pro- and anti-inflammatory and nociceptive
peptide expression in a particular condition.