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Intrathecal pertussis toxin but not cyclic AMP blocks kappa opioid-induced antinociception in rat.

The role of inhibitory G-proteins and cyclic AMP in spinal mechanisms of kappa opioid receptor-mediated antinociception was assayed by recording the withdrawal response latency of the rat tail following immersion into a water bath of 49 degrees C. Intrathecal administration of pertussis toxin (1 microgram/rat, five days before the behavioral evaluation) prevented the antinociceptive effect of the kappa receptor agonist U-50,488H, while administration of dibutyryl cyclic AMP (10 micrograms/rat, 17 min. after U-50,488H) did not antagonize the antinociceptive action of the kappa ligand. Results suggest that in the spinal cord the signal transduction mechanism subserving the antinociceptive effect of U-50,488H involves a Gi or Go protein, but also that cyclic AMP is not implicated in coupling Gi/Go proteins to the effector system.