Intrathecal @entity1772 and @entity6341 , but not XXXX , are antinociceptive using the rat-formalin model.

@entity6341 @entity1246 @entity1027 @entity7233 @entity406 @entity1245 @entity12761 @entity1772 @entity1363
Both @entity1246 ( @entity1246 )A and GABAB receptor subtypes have been implicated in spinally mediated antinociception in @entity12761 models. In the current study, the @entity406 test was used as a model of protracted nociception to examine the effect of intrathecally (i.t.) administered @entity1772 (GABAB agonist), @entity6341 (GABAA agonist) or @entity1363 (a @entity1245 ) on antinociception. At doses that did not affect motor function, @entity1772 (0.3 and 1.0 micrograms, i.t.) decreased the flinch response in a dose-dependent manner during Phase 1 and Phase 2. This effect was reversible by the GABAB-specific antagonist, @entity7233 ( @entity7233 ). @entity6341 (0.3 and 1.0 microgram i.t.) evoked a dose-dependent, @entity1027 -reversible decrease in flinching during Phase 1 and Phase 2, but @entity1363 had no effect on either phase. No attenuation of the quiescent period between Phase 1 and Phase 2 was seen upon administration of @entity1772 , @entity6341 or @entity1363 . Additionally, no increase in nocifensive behavior was observed upon administration of either GABAA or GABAB antagonists alone. Therefore, our conclusions are that both GABAA and GABAB agonists are antinociceptive at the spinal cord level and that endogenous spinal @entity1246 levels are insufficient for a @entity1246 potentiator to act alone in an antinociceptive manner.
