下丘脑弓状核内微量注射谷氨酸提高大鼠痛阈及其受体机制

目的观察下丘脑弓状核（ARC）内微量注射谷氨酸（Glu）对大鼠痛阈的影响,初步探讨Glu参与ARC痛觉调制作用的受体机制。方法ARC内分别微量注射Glu或NMDA受体激动剂N-甲基-D-天门冬氨酸（NMDA）和拮抗剂5-甲基-二氢-丙环庚烯-亚胺马来酸（MK-801）以及非NMDA受体拮抗剂6-氰基-7-硝基喹喔啉-2,3-二酮（CNQX）,用电刺激鼠尾-嘶叫法测定痛阈。结果ARC内微量注射Glu（3.0,5.0,10.0 nmol）能剂量依赖性地提高大鼠的痛阈,出现镇痛效应。ARC内微量注射NMDA受体激动剂NMDA（0.1,0.5,1.0 nmol）能模拟Glu的作用,也能剂量依赖性地提高痛阈,出现镇痛效应。NMDA受体拮抗剂NK-801可翻转Glu和NMDA的镇痛效应,而非NMDA受体拮抗剂CNQX不能翻转这种效应。结论ARC内微量注射Glu能参与ARC对痛觉的调制,产生镇痛效应,且这种调制是由NMDA受体介导的。

Mechanism of Increase of the Pain Threshold in the Rat and Its Receptor after Microinjection of Glutamie Acid into Hypothalamic Areuate Nucleus

Objective To observe the effect of glutamic acid （Glu） microinjection into hypothalamic areuate nucleus （ARC） on pain threshold and to explore the role played by the receptor. Methods Glu, its NMDA receptor antagonist N-methyl-D-aspartate （NMDA）, NMDA receptor antagonist MK-801 and non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2, 3-dione （CNQX） were microinjeeted into ARC. The pain threshold was measured by tail stimulation-vocalization test. Results Microiniection of GLU （3.0,5.0,10.0 nmol） into ARC could dose-dependently increase the pain threshold and produce analgesic effect. This analgesic effect could be mimicked by NMDA receptor antagonist NMDA （0.1,0.5,1.0 nmol）, which were also dose-dependently increased the pain threshold, and reversed by NMDE receptor antagonist MK-801, but not by non-NMDA receptor antagonist CNQX. Conclusion Glu mieroiniected into ARC play a role in the pain modulation and produces analgesic effect which is mediated by NMDA receptor.