Abstract

The effects on spinal reflex activity of morphine and conditioning stimulation of the substantia nigra (SN) or the periaqueductal gray matter (PAG) were compared. Reflex activity was evoked by stimulation of various afferents in the sural nerve. In spinal rats. morphine (2 mg/kg, i.v.) did not significantly affect the ventral root short-latency reflex response to sural nerve stimulation but depressed the long-latency reflex response. Naloxone (0.2 mg/kg, i.v.) abolished this depressant effect of morphine. In rats with prenigral decerebration, trains of conditioning stimuli delivered to the SN or PAG (1) enhanced the short-latency reflex response to sural nerve stimulation, (2) depressed the long-latency reflex response to stimulation of the skin nerve and (3) evoked potentials in ventral and dorsal roots. The effects of stimulation of the SN or PAG were markedly reduced by lesioning of the dorsolateral funiculi. Morphine enhanced the potentials evoked in ventral and dorsal roots by brainstem stimulation with short trains of impulses, not those evoked by stimulation with long trains of impulses. Neither morphine nor naloxone exerted an effect on the unconditioned ventral root long-latency reflex response or on the conditioned long-latency reflex response in rats with prenigral decerebration and an intact spinal cord. Since, in rats with prenigral decerebration, SN stimulation depressed the C fibre evoked long-latency reflex response as well as did conditioning stimulation of the PAG, or as did morphine in spinal rats, it is concluded that the SN inhibits transmission of nociceptive impulses in the rat spinal cord.

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