机构地区:[1]哈尔滨医科大学生理学教研室,黑龙江省哈尔滨市150086 [2]哈尔滨医科大学附属第二医院神经科,黑龙江省哈尔滨市150086
出 处:《中国临床康复》2006年第6期76-79,共4页Chinese Journal of Clinical Rehabilitation
基 金:国家自然科学基金(30240058);黑龙江省教育厅科技研究项目(10551141)~~
摘 要:目的:探讨γ-氨基丁酸、荷包牡丹碱对正常大鼠伏核内痛反应神经元电活动的影响。方法:实验于2004-05/2005-05在哈尔滨医科大学神经痛觉电生理研究室完成。选用健康、成年Wistar系大鼠50只。随机分γ-氨基丁酸组(20只)和生理盐水对照组(5只);γ-氨基丁酸+荷包牡丹碱组(20只)和生理盐水对照组(5只)。大鼠麻醉后,实施常规手术。将不锈钢套管插入侧脑室供注药用。①γ-氨基丁酸组内匀速注入γ-氨基丁酸(50g/L,10μL);②γ-氨基丁酸+荷包牡丹碱组在注入γ-氨基丁酸后2min,向侧脑室内再注入荷包牡丹碱(1g/L,10μL),用等体积生理盐水作为对照实验。实验采用电生理学的方法,以电脉冲刺激坐骨神经作为伤害性痛刺激。用玻璃微电极记录痛反应神经元放电的变化,并连续观察和记录痛反应神经元的电变化30min。结果:Wistar大鼠50只在实验过程中无脱失值,全部进入结果分析。侧脑室注入γ-氨基丁酸能使正常大鼠伏核中痛兴奋神经元痛诱发放电频率的净增值由注药前的(8.59±1.17)Hz减少至(-1.38±0.51)Hz、潜伏期由(0.17±0.04)s延长至(0.69±0.08)s,而痛抑制神经元的净增值由注药前的(-4.34±0.37)Hz增加至(5.12±1.58)Hz、完全抑制时程由(0.72±0.08)s缩短至(0.27±0.03)s。②侧脑室注入γ-氨基丁酸A受体拮抗剂荷包牡丹碱可对抗γ-氨基丁酸的作用,即痛兴奋神经元的净增值增加到(6.61±1.23)Hz,潜伏期缩短至(0.18±0.08)s;痛抑制神经元的净增值减少为(-1.33±0.21)Hz,抑制时程延长至(0.69±0.06)s。痛兴奋神经元和痛抑制神经元两者相互配合活动。结论:①外源性γ-氨基丁酸可使正常大鼠伏核中痛兴奋神经元和痛抑制神经元对伤害性刺激的反应均减弱,表现出镇痛效应。②γ-氨基丁酸的镇痛作用主要是通过γ-氨基丁酸A受体介导的。γ-氨基丁酸和伏核在痛觉调制中具有重要的作用。③荷包牡丹碱可对抗γ-氨基丁AIM: To study the effects of γ-aminobutyric acid and bieueulline on the electrical activities of pain-related neuron in nucleus accumbens of normal rats. METHODS: The experiment was conducted in the electrophysiological laboratory for painful sense, Harbin Medical University from May 2004 to May 2005. Fifty healthy adult Wistar rats were divided into the γ- aminobutyric acid group (n=20) and physiological saline group (n=5); γ- aminobutyric acid + bicuculline group (n=20) and physiological saline group (n=5). The rats were anesthetized and actualized general operation. A stainless steel cannula was inserted into the lateral veniricle for injected drug. ①γ-aminobutyric acid groups: γ-aminobutyric acid (50 g/L, 10μL) was injected uniformly into the lateral ventricle. ②γ-aminobutyric acid + bicuculline groups: 2 minutes after injection of γ-aminobutyric acid, bicuculline (1 g/L, 10 μL) was injected into the lateral ventricle again. The control groups: the drugs were replaced by physiological saline of the same volumes. The electrophysiological method was used in the experiment. The trains of electrical impulses applied to the sciatic nerve were used as noxious stimulation. The electrical changes of pain-related neuron in nucleus accumbens were recorded by the glass microelectrode. The electrical changes of pain-related neuron were continually observed and recorded for 30 minutes. RESULTS: All the 50 Wistar rats were involved in the analysis of resuits without deletion. ① After the injection of γ-aminobutyric acid in the lateral ventricle, the net-increased value of the pain-evoked discharge frequency of pain-excitation neuron in nucleus accumbens of the normal rats was reduced from (8.59±1.17) Hz of before injecting drug to (-1.38 ±0.51) Hz, the latency was prolonged from (0.17±0.04) s to (0.69±0.08) s, while the net-increased value of pain-inhibition neurons was increased from (-4.34±0.37) Hz of before injecting drug to (5.12±1.58�
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