Abstract
R-Apomorphine (0.02–1.75 μmol/kg), administered by intrathecal infusion to spinalized rats, caused a dose-dependent increase in tail-flick latency. The effect of R-apomorphine was counteracted significantly by the dopaminergic receptor antagonists cis-flupenthixol (0.20–3.94 μmol/kg) and (+)-butaclamol (0.78 μmol/kg), but not by their enantiomers nor by phenoxybenzamine (29.40 μmol/kg) or methysergide (28.40 μmol/kg). The findings suggest that dopaminergic mechanisms play a role in the modulation of nociception in the spinal cord.
Published Version
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