Raigorodsky G, Urca G
Department of Physiology and Pharmacology, Tel Aviv University Medical School, Ramat Aviv, Israel.
Brain Res. 1987 Sep 29;422(1):158-62. doi: 10.1016/0006-8993(87)90551-8.
Injection of the excitatory amino acid N-methyl-D-aspartate (NMDA) into the spinal subarachnoid space of rats produces both hyperalgesic and analgesic effects. At lower concentrations (0.5 mM) little behavioral effect is elicited by the drug. However, brief hyperalgesia followed by several minutes of analgesia can be detected in these animals. Higher concentrations of the drug produce vocalization, caudally directed scratching and biting and hyper-responsiveness to light touch. The NMDA antagonist, arginine vasopressin, produces analgesia when injected by itself and completely reverses all effects of NMDA. NMDA-induced analgesia, but not hyperalgesia, is reversed by intrathecal administration of naloxone, methysergide and phentolamine. The analgesic effects of both agonist and antagonist are markedly potentiated by spinalization. These results suggest the involvement of NMDA receptors in both the transmission of pain and the mediation of spinal segmental pain inhibitory mechanism.
将兴奋性氨基酸N-甲基-D-天冬氨酸（NMDA）注射到大鼠脊髓蛛网膜下腔会产生痛觉过敏和镇痛两种效应。在较低浓度（0.5 mM）时，该药物几乎不会引起行为效应。然而，在这些动物中可以检测到短暂的痛觉过敏，随后是几分钟的镇痛。较高浓度的药物会引起发声、尾部搔抓和咬以及对轻触的高反应性。NMDA拮抗剂精氨酸加压素单独注射时会产生镇痛作用，并完全逆转NMDA的所有效应。鞘内注射纳洛酮、甲基麦角新碱和酚妥拉明可逆转NMDA诱导的镇痛作用，但不能逆转痛觉过敏。脊髓横断显著增强了激动剂和拮抗剂的镇痛作用。这些结果表明NMDA受体参与了疼痛的传递和脊髓节段性疼痛抑制机制的介导。
