Analgesia after lesions of nucleus reticularis magnocellularis: differential effect on supraspinal versus spinal pain reflexes

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Abstract
The effect of bilateral electrolytic lesions of descending fibers arising from nucleus reticularis magnocellularis (NMC) on responding to noxious peripheral thermal or mechanical stimulation and on spinal cord monoamine levels was examined in rats. The lesion effects were quantified by examining 2 supraspinally organized pain responses, the hot plate latency and vocalization threshold and 2 spinally organized nociceptive reflexes, tail flick latency and hind limb flexion threshold. Following interruption of descending NMC fibers, a profound analgesia was observed on supraspinally organized pain responses. Assay of spinal cord serotonin [5-hydroxytryptamine] (5-HT) indicated that the NMC lesions also destroyed appreciable numbers of descending 5-HT fibers of passage originating in nucleus raphe magnus (RM). A modest hypersensitivity to pain occurred after control lesions in RM suggesting that the analgesia observed after NMC lesions would have been even more pronounced if RM fibers of passage had not been concomitantly destoryed. To assess whether the analgesia observed after NMC lesions was due to nonspecific destruction of a given volume of reticular tissue, control lesions were placed in nucleus subcoeruleus (NSC). NSC lesions resulted in a hypersensitivity to pain and significant depletion of spinal cord noradrenaline [norepinephrine] (NA). The analgesia observed after NMC lesions was not due to nonspecific destruction of the reticular formation, and descending NSC NA fibers tonically suppress pain. There analgesic effects were observed exclusively on supraspinally organized pain responses, not spinally organized nociceptive reflexes. This supports previous studies demonstrating differential descending control of nociception in the spinal vs. intact preparations. Descending NMC fibers tonically suppress ascending pain transmission.