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目的研究皮下注射吗啡、静脉注射N-甲基-D-天冬氨酸(N-methyl-D-aspartate,NMDA)受体拮抗剂5-甲基二氢丙环庚烯马来酸(MK-801)对电刺激隐神经(saphenous nerve,SN)引起大鼠扣带回前部(anterior cingulate gyrus,ACG)多巴胺含量增高的影响,以及MK-801对吗啡作用的影响。方法应用高效液相色谱-电化学检测技术进行实验研究。结果电刺激SN引起ACG多巴胺含量显著增高;皮下注射吗啡抑制电刺激SN引起的ACG多巴胺含量的显著增高;静脉注射MK-801能够拮抗电刺激SN引起的ACG多巴胺含量的显著增高,并且能够增强吗啡抑制电刺激SN引起的ACG多巴胺含量的显著增高。结论 SN传导的伤害性信息能够到达ACG,激活ACG多巴胺能神经元,释放多巴胺,谷氨酸NMDA受体参与此过程;吗啡抑制ACG多巴胺能神经元的活动;MK-801增强吗啡的抑制作用。
Objective To study the effects of morphine and morphine on morphine-induced morphine withdrawal induced by hypoxia in rats.Methods Morphine was injected subcutaneously into the mice and received intravenous injection of 5-methyl-D-aspartate (NMDA) receptor antagonist MK- 801) on the dopamine content of anterior cingulate gyrus (ACG) induced by electrical stimulation of the saphenous nerve (SN) in rats and the effect of MK-801 on the morphine function. Methods High performance liquid chromatography - electrochemical detection technique was used to carry out experimental study. RESULTS: Electrical stimulation of SN caused a significant increase in the dopamine content of ACG. Subcutaneous injection of morphine inhibited the SNP-induced increase of ACG dopamine concentration. Intravenous injection of MK-801 antagonized the SNP-induced ACG dopamine upregulation and enhanced morphine Inhibit the electrical stimulation of SN caused by ACG dopamine increased significantly. Conclusion SN-mediated nociceptive information can reach ACG, activate ACG dopaminergic neurons and release dopamine and glutamate NMDA receptors. Morphine can inhibit the activity of ACG dopaminergic neurons. MK-801 enhances the inhibitory effect of morphine.