Dopamine (DA) is thought to have a neurotransmitter role in the spinal cord of the rat. Intrathecal administration of the DA receptor agonist apomorphine has previously been shown to reduce nocifensive responses. The present experiments investigated the site of action of apomorphine, and the mechanisms by which DA agonists apparently produce antinociception. Small doses of apomorphine (40-80 micrograms/kg) increased the tail flick latency (TFL) in lightly anaesthetised rats when given intrathecally and intravenously but not intracerebroventricularly. This effect is probably mediated via D2 receptors since the D2 agonist LY171555 had a similar effect whereas the D1 agonist SK&F 38393 was inactive. Furthermore the D2 antagonist sulpiride blocked the effects of apomorphine and LY171555. The spinal monosynaptic reflex was not modified by 150 micrograms/kg apomorphine suggesting that sensory rather than motor processes are being influenced. Pretreatment with the serotonin receptor antagonist methysergide prevented the apomorphine induced increase in TFL. It is concluded that exogenously applied DA agonist can result in antinociception in the spinal cord and that this effect may be dependent upon activity in the spinal 5-hydroxytryptaminergic and noradrenergic systems.