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机构地区:[1]重庆医科大学附属第一医院,重庆市神经病学重点实验室,重庆400016
出 处:《临床神经电生理学杂志》2006年第5期287-291,共5页Journal of Clinical Electroneurophysiology
基 金:重庆市教委应用基础研究基金和重庆市医学科技基金2001~2004资助[批准编号:渝教科(2001)12-29和(01-1-013)]
摘 要:目的:观察液氮损伤诱导局灶性皮质发育障碍(FCD)大鼠脑皮质和海马中γ-氨基丁酸(GABA)和),γ-氨基丁酸A受体α1亚型(GABAARα1)的表达,探讨其与癫癎发生的关系。方法:实验随机分为正常对照组、假手术组和液氮损伤组,建立FCD大鼠模型,喂养至16~18周处死取脑,经病理学HE、Nissl染色,免疫组织化学方法用SABC法,肉眼观察,光镜下观察小脑回及周围结构和海马CA1~CA4、齿状回中GABA和GABAARα1阳性细胞表达情况,免疫组化图像仪分析。结果:大鼠脑嘴尾方向形成了一微脑回。在液氮冻损伤组,微脑回及前额和海马CA1、齿状回的GABA和GABAARα1阳性着色神经元的表达均较正常对照组或假手术组的表达减少,经统计学分析差异有显著意义(P<0.05),但在其他脑皮质和海马结构区的表达则无明显改变。结论:微脑回及周围和同侧海马结构中CA1及齿状回的GABA和GABAARα1下调和抑制功能的降低可能在癫癎发病机制中起到了重要作用。Objective:To obsevre the situ focal cortical dysplasia (microgyria) epileptogenicity and the expression of GABA and GABAARα1. Methods: Three groups were performed in the experiment including freeze-lesioned,sham-operated and normal groups. Newborn Wistar rats (〈24 hr old; n= 12) was cooled with liquid nitrogen on the exposed calvaium above the primary parietal cortex (par1) in freeze-lesioned groups. All rats were allowed to survive for 16-18 weeks before HE,Nissl Stain and SABC methods were Performed in the brains. The structure of mierogyrus and expression of GABA and GABAARα1 subunit in the animal model were obsrved. Results: All freeseqesioned animals displayed typical cortical malformations consisting of a longitudinal microgyrus. There are chances of GABA and GABAARα1 subunit in cortical dyspiasia,CAland dentate gyru. Only the optical densities of GABA-immunoreactive neurons and GABAARα1 -immunoreactive neurons located Fr,microgyria,CA1 of hippocampus and dentate gyru of the lesion was significant(P〈0.05) between the experimental groups and the two control groups. Conclusion: Decreased expression of GABA and GABAARα1 subunit surrounding microgyrus ,microgyrus,CA1 and dentate gyru could be important mechanism in an intrinsic epileptogenicity of cortical dysplasias.
关 键 词:液氮损伤 皮质发育障碍 局灶性 Γ-氨基丁酸 γ-氨基丁酸A受体α1亚型
分 类 号:Q95-33[生物学—动物学] R742.1[医药卫生—神经病学与精神病学]
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