Dolan S, Nolan A M
Department of Veterinary Preclinical Studies, University of Glasgow Veterinary School, UK.
Neuroreport. 1999 Feb 25;10(3):449-52. doi: 10.1097/00001756-199902250-00002.
The role of spinal NMDA receptors in mechanical nociceptive processing was assessed in sheep. Intrathecal NMDA (2 nmol-1 micromol) produced a significant reduction in mechanical withdrawal thresholds. This effect was attenuated by pretreatment with the NMDA receptor antagonist MK801 (100 nmol), the cyclooxygenase-2 (COX-2) inhibitor 5,5-dimethyl-3-(3-flourophenyl)-4-(4-methylsulphonyl)phenyl-2(5H) furanone DFU; 200 nmol) and the nitric oxide synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME; 2 micromol), but not by the metabotropic glutamate receptor antagonist (S)-alpha-methyl-4-carboxyphenylglycine (MCPG; 200 nmol-2 micromol) or the non-NMDA receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX; 200 nmol-1 micromol). This first report of NMDA-induced mechanical allodynia suggests that spinal NMDA receptors are involved in mediating acute mechanical nociceptive processing through activation of NOS and COX-2 enzymes.
在绵羊中评估了脊髓N-甲基-D-天冬氨酸（NMDA）受体在机械性伤害感受处理中的作用。鞘内注射NMDA（2纳摩尔至1微摩尔）可使机械性撤腿阈值显著降低。这种效应可被NMDA受体拮抗剂MK801（100纳摩尔）、环氧化酶-2（COX-2）抑制剂5,5-二甲基-3-（3-氟苯基）-4-（4-甲基磺酰基）苯基-2（5H）呋喃酮DFU（200纳摩尔）以及一氧化氮合酶（NOS）抑制剂N（G）-硝基-L-精氨酸甲酯（L-NAME；2微摩尔）预处理所减弱，但代谢型谷氨酸受体拮抗剂（S）-α-甲基-4-羧基苯基甘氨酸（MCPG；200纳摩尔至2微摩尔）或非NMDA受体拮抗剂6,7-二硝基喹喔啉-2,3-二酮（DNQX；200纳摩尔至1微摩尔）预处理则无此作用。这篇关于NMDA诱导的机械性异常性疼痛的首次报告表明，脊髓NMDA受体通过激活NOS和COX-2酶参与介导急性机械性伤害感受处理。
