title: Regulation of galanin and neuropeptide Y in dorsal root ganglia and dorsal horn in rat mononeuropathic models: possible relation to tactile hypersensitivity.
abstract: The expression of galanin and neuropeptide Y in rat lumbar 5 (L5) dorsal root ganglia and dorsal horn (L4-5) was studied after four types of peripheral nerve injury using immunohistochemistry and in situ hybridization. The possible correlation between these two peptides and tactile allodynia-like behaviour was analysed as well. The models employed were the Gazelius (photochemical lesion) and Seltzer and Bennett (constriction lesions) models, as well as complete sciatic nerve transection (axotomy). Two weeks after surgery, the Gazelius model rats more frequently displayed a greater tactile allodynia 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 number of galanin-immunoreactive and galanin messenger RNA-positive neuron profiles was observed in ipsilateral dorsal root ganglia in all types of models. The increase in allodynic rats (Gazelius, Seltzer and Bennett models) was less pronounced than that after axotomy. In addition, in the Bennett model the number of galanin-immunoreactive neurons was significantly lower in allodynic rats as compared to non-allodynic rats, and the same tendency, but less obvious was found in the Seltzer model. Furthermore, an increase in galanin-immunoreactive fibres was found in the superficial laminae of the ipsilateral dorsal horn in all lesion models, especially in lamina II. A dramatic 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.
authors.affiliation: Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
authors.forename: T J
authors.initials: TJ
authors.lastname: Shi
authors.forename: J G
authors.initials: JG
authors.lastname: Cui
authors.forename: B A
authors.initials: BA
authors.lastname: Meyerson
authors.forename: B
authors.initials: B
authors.lastname: Linderoth
authors.forename: T
authors.initials: T
authors.lastname: Hökfelt
mesh_terms: D000818:Animals; D019771:Axotomy; D001522:Behavior, Animal / Q000187:drug effects; D048429:Cell Size; D015342:DNA Probes; D019004:Galanin / Q000378:metabolism*; D005727:Ganglia, Spinal / Q000378:metabolism* / Q000473:pathology; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D008297:Male; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D009478:Neuropeptide Y / Q000378:metabolism*; D010146:Pain / Q000378:metabolism* / Q000473:pathology; D010523:Peripheral Nervous System Diseases / Q000378:metabolism* / Q000473:pathology; D010812:Physical Stimulation; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000378:metabolism* / Q000473:pathology
chemical_list: D015342:DNA Probes; D009478:Neuropeptide Y; D012333:RNA, Messenger; D019004:Galanin