Rats were used to study the effect of unilateral stimulation of the substantia nigra on the reflex discharge of alpha-motoneurones and on the reaction time of the tail-flick response. In preparations with prenigral decerebration, nigral stimulation facilitated monosynaptic alpha-reflex activity, whilst gamma-reflex activity remained unchanged. The facilitation of monosynaptic alpha-reflex activity was reduced by naloxone (1 mg/kg); morphine (2 mg/kg) did not change the number of alpha-reflex discharges, but it reduced the alpha-reflex latency, enhanced the effect of nigral stimulation on the latency and abolished the effect of naloxone on nigral facilitation. Nigral stimulation prolonged the reaction time of the tail-flick response in rats with an intact brain and after prenigral decerbration. Naloxone did not influence the anti-nociceptive effect of nigral stimulation, whilst morphine enhanced it in rats with an intact brain. The anti-nociceptive effect exerted by morphine in animals with an intact brain was abolished by prenigral decerbration, and an additional spinalization restored it. Inactivating the nigral neurones by unilateral microinjections of procaine or GABA into the substantia nigra depressed the nociceptive reflex. It is concluded that (1) activation of nigral neurones influenced mono- and polysynaptic reflexes in a reciprocal fashion by a pathway descending via brain stem relays to the spinal cord, (2) inactivation of nigral neurones produced similar changes in reflex activity by altering the function of the nigro-striatal feedback system, the outlet from the system to the spinal cord not being the substantia nigra, (3) morphine influenced the nociceptive reflex by an action at different levels of the central nervous system.