Regulation of galanin and neuropeptide Y in dorsal root ganglia and dorsalhorn in rat mononeuropathic models: Possible relation to tactile hypersensitivity

The expression of galanin and neuropeptide Y in rat lumbar 5 (L5) dorsal ro ot ganglia and dorsal horn (L4-5) was studied after four types of periphera l nerve injury using immunohistochemistry and in situ hybridization. The po ssible correlation between these two peptides and tactile allodynia-like be haviour was analysed as well. The models employed were the Gazelius (photoc hemical lesion) and Seltzer and Bennett (constriction lesions) models, as w ell as complete sciatic nerve transection (axotomy). Two weeks after surger y, the Gazelius model rats more frequently displayed a greater tactile allo dynia than the rats from the Seltzer and Bennett models. Tactile allodynia was not observed in any of the axotomized rats. A marked increase in the nu mber of galanin-immunoreactive and galanin messenger RNA-positive neuron pr ofiles was observed in ipsilateral dorsal root ganglia in all types of mode ls. The increase in allodynic rats (Gazelius, Seltzer and Bennett models) w as less pronounced than that after axotomy. In addition, in the Bennett mod el the number of galanin-immunoreactive neurons was significantly lower in allodynic rats as compared to non-allodynic rats, and the same tendency, bu t less obvious was found in the Seltzer model. Furthermore, an increase in galanin-immunoreactive fibres was found in the superficial laminae of the i psilateral dorsal horn in all lesion models, especially in lamina II. A dra matic increase in the number of neuropeptide Y and neuropeptide Y messenger RNA-positive neuron profiles was also found in the ipsilateral dorsal root ganglia in all models, but no significant difference was found in peptide levels between allodynic and non-allodynic rats in any of the models. The present results suggest that the levels of endogenous galanin may play a role in whether or not allodynia develops in the Bennett model. (C) 1999 IBRO. Published by Elsevier Science Ltd.