Inflammation alters somatostatin mRNA expression in sensory neurons in the rat.
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.
Abd El-Aleem
Seham A
SA
Department of Physiology, University of Bristol School of Medical Sciences, University Walk, Bristol, UK.
Morales-Aza
Begonia M
BM
McQueen
Daniel S
DS
Donaldson
Lucy F
LF
D000818:Animals; D001168:Arthritis / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D007839:Functional Laterality / Q000502:physiology; D017950:Ganglia, Sensory / Q000166:cytology*; D015870:Gene Expression; D017403:In Situ Hybridization / Q000379:methods; D007249:Inflammation / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism*; D008297:Male; D009474:Neurons / Q000378:metabolism*; D010518:Periodontitis / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism; D011134:Polysaccharides; D018075:RNA, Complementary / Q000096:biosynthesis; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013004:Somatostatin / Q000235:genetics / Q000378:metabolism*; D013997:Time Factors
D011134:Polysaccharides; D018075:RNA, Complementary; D012333:RNA, Messenger; D013004:Somatostatin