The thermal cutaneous evoked tail flick and hot plate nociceptive responses as well as the chemical visceral elicited acetic acid writhing response were determined in rats following lumbar intrathecal administration of the dopamine (DA) agonist apomorphine. Apomorphine failed to influence tail flick latency even at high doses (660 nmol). In contrast, intrathecal apomorphine (33-330 nmol) produced a dose-dependent increase of the hot plate and acetic acid writhing responses, which was antagonized by the prior intrathecal administration of cis-flupenthixol (a DA receptor antagonist). Intrathecal pretreatment with either trans-flupenthixol (the inactive stereoisomer of cis-flupenthixol), methysergide, phentolamine or naloxone did not antagonize the apomorphine-induced increase of hot plate response latency. Intrathecal apomorphine did produce an increase of tail flick latency following pretreatment with methysergide and phentolamine, however. Intraventricular administration of apomorphine (82.5-165 nmol) had no influence on either tail flick or hot plate response latencies. The present data provide evidence for the modulatory role of apomorphine on spinal afferent sensory functions. It is suggested that a spinal DA receptor population has an inhibitory effect on noxious input to the spinal cord.