Course and mode of action of descending system conveying nucleus raphe magnus induced inhibition of flexion reflex in rats.

In lightly anaesthetized rats, the latencies and magnitudes of heat-evoked withdrawal reflexes from the hindlimb were measured electromyographically. Low-intensity (20-50 microA) stimulation of the nucleus raphe magnus (NRM) resulted in an inhibition of the flexion reflex (commonly referred to as analgesia) as evidenced by increased latency and decreased amplitude. The effect lasted for several minutes after the stimulation was terminated. Following lesions of the dorsolateral funiculus (DLF) at the neural thoracic levels 7-8, baseline latencies were reduced and the effect of the NRM stimulation was abolished. Lesions of the DLF at lumbar level 1 resulted in unaltered baseline latencies with persistence of the inhibitory effect of NRM stimulation. The results of the present experiment show that pathways exerting a tonic inhibition of the withdrawal reflex, and mediating the effect of electrical stimulation from the NRM, descend in the DLF at the thoracic level of the spinal cord. At the lumbar level, there is a shift away from the DLF. The antinociceptive effect of 20 microA NRM stimulation was partly reduced by pretreatment with the serotonin synthesis inhibitor para-chlorophenylalanine (PCPA) or the opiate naloxone (1 mg kg-1 i.v.). In animals pretreated with PCPA, naloxone (1 mg kg-1 i.v.) completely abolished the analgesic effect of the stimulation. Thus, both serotonergic and opioid systems may be implicated in mediating the analgesia. With 50 microA stimulation the same treatment only partly attenuated the NRM-induced analgesia, indicating an additional non-serotonergic and non-opioid mechanism which requires a higher current intensity for its activation.