论文部分内容阅读
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。
Objective To investigate the effect of glutamate (Glu) on the pain threshold of hypothalamic arcuate nucleus (ARC) in rats and to explore the mechanism of Glu ’s involvement in the pain modulation of ARC. Methods Micro-injection of Glu or NMDA receptor agonist N-methyl-D-aspartate (NMDA) and antagonist 5-methyl-dihydropropycloheptene-imine maleic acid -801) and non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Results Microinjection of Glu (3.0, 5.0 and 10.0 nmol) into ARC can increase the pain threshold of rats in a dose-dependent manner and produce analgesic effect. Microinjection of NMDA receptor agonist NMDA (0.1, 0.5, 1.0 nmol) into ARC can simulate the action of Glu and also increase the pain threshold in a dose-dependent manner with analgesic effect. The NMDA receptor antagonist NK-801 reversed the analgesic effects of Glu and NMDA, whereas the non-NMDA receptor antagonist CNQX failed to reverse this effect. Conclusion Microinjection of Glu into ARC can participate in the modulation of pain induced by ARC and produce analgesic effect, and this modulation is mediated by NMDA receptors.