Zemlan Frank P, Kow Lee-Ming, Pfaff Donald W
The Rockefeller University, 1230 York Avenue, New York, NY 10021 U.S.A. Laboratory of Psychobiology, Departments of Psychiatry and Physiology, University of Cincinnati School of Medicine, Cincinnati, OH 45202 U.S.A.
Pain. 1984 Mar;18(3):221-237. doi: 10.1016/0304-3959(84)90818-2.
The present studies examine 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. The lesion effects were quantified by examining two supraspinally organized pain responses, the hot plate latency and vocalization threshold and two 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-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 destroyed. To assess whether the analgesia observed after NMC lesions was due to non-specific 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 (NA). These data suggest both that the analgesia observed after NMC lesions was not due to non-specific destruction of the reticular formation, and that descending NSC NA fibers tonically suppress pain. The above analgesic effects were observed exclusively on supraspinally organized pain responses, not spinally organized nociceptive reflexes. This supported previous studies demonstrating differential descending control of nociception in the spinal versus intact preparations. In summary, the present data suggest that descending NMC fibers tonically suppress ascending pain transmission.
本研究探讨了源自巨细胞网状核(NMC)的下行纤维双侧电解损伤对有害外周热刺激或机械刺激反应以及脊髓单胺水平的影响。通过检测两种脊髓上组织的疼痛反应(热板潜伏期和发声阈值)以及两种脊髓组织的伤害性反射(甩尾潜伏期和后肢屈曲阈值)来量化损伤效应。在中断NMC下行纤维后,观察到脊髓上组织的疼痛反应出现深度镇痛。脊髓5-羟色胺(5-HT)测定表明,NMC损伤也破坏了相当数量起源于中缝大核(RM)的下行5-HT传导纤维。在RM进行对照损伤后出现了对疼痛的适度超敏反应,这表明如果RM传导纤维没有同时被破坏,NMC损伤后观察到的镇痛作用会更加明显。为了评估NMC损伤后观察到的镇痛是否是由于一定体积的网状组织非特异性破坏所致,在蓝斑下核(NSC)进行了对照损伤。NSC损伤导致对疼痛超敏以及脊髓去甲肾上腺素(NA)显著耗竭。这些数据表明,NMC损伤后观察到的镇痛并非由于网状结构的非特异性破坏,并且下行NSC NA纤维对疼痛具有紧张性抑制作用。上述镇痛作用仅在脊髓上组织的疼痛反应中观察到,而在脊髓组织的伤害性反射中未观察到。这支持了先前的研究,即证明在脊髓与完整制剂中伤害感受的下行控制存在差异。总之,目前的数据表明,下行NMC纤维对上行疼痛传递具有紧张性抑制作用。