Abstract

The present study explored the role of central dopaminergic transmission in a model of carrageenan-induced inflammatory pain by examining the effects of selective agonists and antagonists of dopamine receptors. The results were as follow: (1) LY171555 ( trans-(−)-4a R-4,4a,5,6,7,8,8a,9-Octahydro-5-propyl-1 H-pyrazolo[3,4-g]quinoline hydrochloride), dopamine D 2 receptor agonist, produced anti-hyperalgesia or hypoalgesia in the inflamed hindpaws and non-inflamed hindpaws, respectively; spiperone hydrochloride (8-[4-(4-Fluorophenyl)-4-oxobutyl]-1-phenyl-1,3,8-triazaspiro[4,5]decan-4-one hydrochloride), dopamine D 2 receptor antagonist, decreased the pain threshold of the non-inflamed hindpaws. (2) (±)-SKF38393 hydrochloride ((±)-1-Phenyl-2,3,4,5-tetrahydro-(1 H)-3-benzazepine-7,8-diol hydrochloride), dopamine D 1 receptor agonist, produced anti-hyperalgesia or hypoalgesia when administered in a high dose (600 nmol), and decreased the pain threshold of non-inflamed hindpaws when administered in a low dose (150 nmol); R(+)-SCH23390 hydrochloride ( R(+)-7-Chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1 H-3-benzazepine hydrochloride), dopamine D 1 receptor antagonist, induced anti-hyperalgesia or hypoalgesia, respectively. The present study suggests that the dopaminergic system is involved in the central modulation of inflammatory hyperalgesia, and that the different effects are probably induced by the different receptors.

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