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机构地区:[1]贵阳医学院附属医院急诊科,贵州贵阳550004 [2]贵阳医学院神经病学教研室 [3]贵阳医学院生理学教研室
出 处:《临床神经电生理学杂志》2009年第4期199-202,共4页Journal of Clinical Electroneurophysiology
摘 要:目的:观察尼莫地平对杏仁核电点燃癫癎鼠模型脑内谷氨酸(glutamate,Glu)表达及海马单位细胞放电(unit cell discharge,UCD)的影响。方法:选择健康雄性Wistar大鼠30只制作动物模型,造模成功后随机分为单纯对照组、癫癎模型组和尼莫地平组,各组10只大鼠,均进行海马UCD的记录,然后分别取脑组织,采用免疫组化的方法检测大鼠脑内Glu的表达并进行方差检验分析。结果:①癫癎模型组Glu灰度值在杏仁核、海马、颞叶分别为(92.5582±13.9345)、(94.0579±12.8117)和(100.5922±16.1048),与对照组的相应值(113,1562±36.7147)、(124.4130±29.6738)和(126.5704±35.8527)比较有明显降低(注:灰度值越高Glu的表达越少;灰度值越低Glu的表达越多)(P〈0.05);尼莫地平组中,Glu灰度值与模型组的比较无明显差异(P〉0.05),②海马UCD频率癫癎模型组(164.55±74.708)较单纯对照组(70.925±44.125)明显增快,尼莫地平组(82.175±35.046)与模型组比较,海马UCD频率明显降低。差异有显著意义(P〈0.05)。结论:尼莫地平不能抑制Glu的表达,但可抑制海马UCD频率。Objective:To observe the influence of nimodipine on the expression of glutamate (Glu) in brain tissues and unit cell discharge(UCD) of hippocampal neurons in amygdaloid kindling rat model. Methods: Thirty healthy Wistar male rats were selected to make the amygdaloid kindling models. All Wistar rats were randomly divided into 3 groups ; the control,epileptic model and nimodipine groups,The UCD was recorded in each group, The expressions of Glu were examined by immunohistochemical method and the analysis of linear correlation was performed. Results: ①The frequency of hippocampal neuron UCD increased significantly in the epileptic group as compared with the control group. The frequency of UCD decreasedre markablly in the nimodipine group as compared with the epileptic model group. ②The average grey value of Glu in the amygdala, hippocampus and temporal lobe in the epileptic model group significantly increased as campared.with the control group. No significant difference in the average grey value was noted between the nimodipine group and the epileptic model group(P〉0. 05). Conclusion. Nimodipine might significantly inhibit the frequency of hippocampal neuron UCD, but might not restrain the expression of Glu in the amygdaloid kindling rat model.
关 键 词:点燃模型 尼莫地平 谷氨酸(Glu) 单位细胞放电(UCD)
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