Simpson R K, Gondo M, Robertson C S, Goodman J C
Department of Neurosurgery, Baylor College of Medicine, Houston, Texas 77030, USA.
Neurochem Res. 1996 Oct;21(10):1221-6. doi: 10.1007/BF02532399.
We have previously reported that enhanced glycine release is produced by epidural spinal cord stimulation, a clinical method for treating neuropathic pain. Our current hypothesis is that glycine administered intrathecally reduces neuropathic pain as measured by the Randall-Selitto method. Neuropathic rats created by unilateral partial ligation of the sciatic nerve were treated with intrathecal infusion of glycine, strychnine, MK-801, or 5,7-DKA at 0.1 mumol, or artificial CSF for 2 hours at a rate of 10 microliters/min. Force required to produce the pain response was significantly increased after glycine administration and reduced using strychnine, a specific glycine receptor (Gly l) antagonist. Strychnine blocked the response to glycine when infused together. Administration of the non-specific NMDA receptor MK-801 antagonist and 5,7-DKA, a specific glycine-NMDA receptor (Gly 2) antagonist, however, failed to block the response to glycine. Our results provide evidence for the use of glycine and related compounds to treat neuropathic pain.
我们之前曾报道,硬膜外脊髓刺激可增强甘氨酸释放,这是一种治疗神经性疼痛的临床方法。我们目前的假设是,鞘内注射甘氨酸可减轻用兰德尔-塞利托法测量的神经性疼痛。通过坐骨神经单侧部分结扎制造的神经性大鼠,以10微升/分钟的速率接受鞘内输注0.1微摩尔的甘氨酸、士的宁、MK-801或5,7-DKA,或人工脑脊液,持续2小时。给予甘氨酸后,产生疼痛反应所需的力显著增加,而使用特异性甘氨酸受体(Gly 1)拮抗剂士的宁则降低。当一起输注时,士的宁阻断了对甘氨酸的反应。然而,给予非特异性NMDA受体拮抗剂MK-801和特异性甘氨酸-NMDA受体(Gly 2)拮抗剂5,7-DKA未能阻断对甘氨酸的反应。我们的结果为使用甘氨酸及相关化合物治疗神经性疼痛提供了证据。