Davar G, Hama A, Deykin A, Vos B, Maciewicz R
Pain Physiology Laboratory, Massachusetts General Hospital, Charlestown 02129.
Brain Res. 1991 Jul 12;553(2):327-30. doi: 10.1016/0006-8993(91)90844-l.
Loose ligation of the sciatic nerve in the rat can produce behavioral signs of hyperalgesia in the hindpaw. This study examined the effect of an NMDA (N-methyl-D-aspartate) receptor antagonist (MK-801) on the development of hyperalgesia in this model. Rats received i.p. injections of saline or MK-801 (1.0 mg/kg) prior to and then for 7 days after a unilateral sciatic nerve ligation. Testing of each hindpaw for latency to withdrawal from a standardized thermal stimulus was performed prior to ligation and then at 10, 12, 17, 27, and 37 days postoperatively. Hyperalgesia of the operated hindpaw developed in saline-treated animals as measured by a decrease in withdrawal latency. Hyperalgesia did not develop in animals treated with MK-801. MK-801 may therefore prevent the development of hyperalgesia following experimental nerve injury, possibly through an NMDA receptor-mediated effect.
在大鼠中对坐骨神经进行松弛结扎可导致后爪出现痛觉过敏的行为迹象。本研究检测了N-甲基-D-天冬氨酸（NMDA）受体拮抗剂（MK-801）对该模型中痛觉过敏发展的影响。大鼠在单侧坐骨神经结扎前及结扎后7天接受腹腔注射生理盐水或MK-801（1.0毫克/千克）。在结扎前以及术后第10、12、17、27和37天，对每只后爪进行从标准化热刺激中撤回的潜伏期测试。通过撤回潜伏期的缩短来衡量，在接受生理盐水治疗的动物中，手术侧后爪出现了痛觉过敏。接受MK-801治疗的动物未出现痛觉过敏。因此，MK-801可能通过NMDA受体介导的效应预防实验性神经损伤后痛觉过敏的发展。
