In precollicularly decerebrated cats immobilized with Flaxedil (2 mg/kg, i.v.), a dopamine mechanism played a role in the inhibition produced by brain stem stimulation of nociceptive activated cells in the spinal cord. Lamina V cell activity evoked by natural stimulation (pinch not touch) to the left hind limb or electrical stimulation (0.1 msec pulses at 1/sec) to the left sural nerve exposed at the popliteal fossa was recorded at levels L6 and L7. Brain stimulation consisted of 100 msec trains of either single rectangular pulses or 3 pulses/sec for 1 min. The stimulation was delivered to substantia nigra, periaqueductal gray (PAG) and dorsal raphe nucleus via concentric bipolar electrodes. Descending inhibition of the late burst of lamina V cell discharge elicited by mechanical pinch or sural shock could be demonstrated following individual stimulation of the 3 brain stem sites. Nigral-induced inhibition was abolished by injecting tetrabenazine (40 mg/kg, i.v.) or bulbocapnine (20 mg/kg, i.v.); the inhibition was re-established by L-DOPA (20 mg/kg, i.v.) or apomorphine (20 mg/kg, i.v.) indicating that a dopaminergic link has access to the descending inhibitory action on segmental transmission of “pain” impulses. Both nigral and PAG actions were sensitive to methysergide (1 mg/kg, i.v.), while the serotonergic blockade could be overcome by 5-hydroxytryptamine (70 mg/kg, i.v.). We proposed that nigral and PAG actions were relayed in part through the descending raphe system. Through this relay, they exhibit their antinociceptive effects.