BACKGROUND: Glutamic acid is an excitatory transmitter in the sensory afferent fibers, and its receptors widely exist in central and peripheral nerve system, which has specific distribution in spinal dorsal neuron to mediate peripheral traumatic information transmission.OBJECTIVE: To observe the impact of injecting glutamicacid into cerebral ventricle on the electrophysiology of pain-excited neuron (PEN) in parafascicular nucleus (PF) of thalamencephalon in central nerve system of rat.DESIGN: A grouping case controlled study was conducted.SETTINGS and PARTICIPANTES: The study was completed in the Department of Physiology, Harbin Medical University. Subjects were 30 Wistar rats in either gender with a body mass from 240 g to 280 g obtained from Department of Experimental Animals of the Second Affiliated Hospital of Harbin Medical University.INTERVENTION: Animals were allocated into 4 groups for our study,which were control group ( n =8), glutamicacid group ( n = 18), glutamicacid + NS group ( n = 18), and glutamicacid + MK-801 group ( n = 10).Corresponding liquids were injected into cerebral ventricles. Traumatic pain stimulation was stimulated by electrical pulse in stimulating right sciatic nerve. The variety of the electric activity in central neuron was recorded at extracellular by glass microelectrode.MAIN OUTCOME MEASURES: The impact of traumatic stimulation on PEN electric activity, the impact of glutamicacid on the PEN electric activity in the PF of thalamencephalon, the enhancement of PEN electric discharge through the interdiction on the reaction of glutamicacid by MK-801 injection.discharge of PEN in the PF of thalamencephalon. The frequency of electric discharge before stimulation in control group was (2.45 ± 0, 89)Hz, which was significantly different from the frequency of (20. 34 + 3.25) Hz after stimulacerebral ventricle enhanced the electric activity of PEN by increasing the net increment of the frequency of electric discharge of PEN and shortening the latency. The comparisons of every index 8 to 20 minutes after the injection of glutamicacid between glutamicacid group and control group in the same time glutamicacid could be interdicted by MK-801 (340 mg/L), an antagonist of N-methyl-D-asparaginic acid(NMDA) receptor of glutamicacid. The comparisons of every index at 8 to 20 minutes after the injection of glutamicacid between glutamicacid group and glutamicacid + NS group in the same time period had significances( t =4. 31 -5.68, P ＜ 0.01).%背景:谷氨酸是感觉传人纤维的兴奋性递质,其受体广泛存在于中枢和外周神经系统,在脊髓背角神经元上有特异性分布,介导外周伤害性信息的传递.目的:观察脑室注射谷氨酸对大鼠中枢神经系统丘脑束旁核(PF)痛兴奋神经元(PEN)电生理学的影响.设计:分组对照实验研究.地点和对象:哈尔滨医科大学生理教研室完成,对象为Wistar大鼠30只,体质量240～280 g,雌雄不限,由哈尔滨医科大学附属第二医院动物学部提供.干预:实验分4组:①对照组(n=8).②谷氨酸组(n=18).③谷氨酸+生理盐水组(n=8).④谷氨酸+MK-801组(n=10).分别于脑室注射相应液体.以电脉冲刺激右侧坐骨神经作为伤害性疼痛刺激,用玻璃微电极细胞外记录中枢神经元电活动的变化.主要观察指标:伤害性刺激对PEN电活动的影响,谷氨酸对丘脑PF的PEN电活动的影响,核团注射MK-801阻断谷氨酸对PEN放电的加强作用.结果:①伤害性刺激使大鼠丘脑PF的PEN诱发放电频率增加,刺激前(对照组)放电频率为(2.45±0.89)Hz,刺激后放电频率为(20.34±3.25)Hz,差异有非常显著性意义(t=8.12,P＜0.01).②脑室注射谷氨酸(150 mg/L)加强PEN的电活动,使PEN放电频率的净增值增加,潜伏期缩短,注射谷氨酸后8～20 min的各项指标分别与对照组同期数据相比,差异有非常显著性意义(t=5.05～7.72,P＜0.01).③这种作用可被谷氨酸的N-甲基-D-天冬氨酸(NMDA)受体拮抗剂MK-801(340 mg/L)所阻断,注射谷氨酸后8～20 min的各项指标分别与谷氨酸+生理盐水组同期数据相比,差异有非常显著性意义(t=4.31～5.68,P＜0.01).结论:谷氨酸在中枢痛觉调制中可能起兴奋作用,而NMDA受体参与介导中枢伤害性信息的传递过程.
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