Premium
Inflammation alters somatostatin mRNA expression in sensory neurons in the rat
Author(s) -
ElAleem Seham A. Abd,
MoralesAza Begonia M.,
McQueen Daniel S.,
Donaldson Lucy F.
Publication year - 2005
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2004.03854.x
Subject(s) - somatostatin , nociception , neuropeptide , substance p , calcitonin gene related peptide , proinflammatory cytokine , trigeminal ganglion , medicine , endocrinology , inflammation , arthritis , bradykinin , neurogenic inflammation , neuroscience , sensory system , biology , receptor
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.