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作 者:王卫东[1] 王津存[2] 程毓华[1] 杨柏林[1] 江文[2] 王洪典[2]
机构地区:[1]武警江西总队医院,南昌330001 [2]第四军医大学西京医院
出 处:《解放军医学杂志》2003年第10期899-901,共3页Medical Journal of Chinese People's Liberation Army
摘 要:通过观察选择性N 甲基 D 天门冬氨酸(NMDA)受体拮抗剂MK 80 1对弥漫性脑损伤后齿状回神经发生的调控作用 ,探讨谷氨酸在神经发生中的作用。将 45只成年雄性SD大鼠制成弥漫性脑损伤模型 ,并随机分为MK 80 1干预组、生理盐水干预组和对照组(n =15 ) ,采用BrdU标记分裂细胞及免疫组织化学方法比较弥漫性脑损伤后 2、4、6、8、12天时大鼠海马齿状回神经前体细胞的增殖速度。结果显示 ,腹腔注射MK 80 1(1mg/kg)后明显抑制了成年大鼠弥漫性脑损伤后 4、6、8、12天时齿状回神经前体细胞的增殖 ,BrdU免疫阳性细胞数目较相应对照组明显减少 (P <0 0 1)。表明弥漫性脑损伤后脑组织NMDA受体的激活促进了海马齿状回神经发生 ,在这一过程中谷氨酸介导的级联生物学事件可能发挥了重要作用。To investigate the effect of selective N-methy-D-aspartate receptor antagonist MK-801 on dentate granule cell neurogenesis after diffuse brain injury in the adult rat, so as to explore the role of glutamic acid on dentate granule cell neurogenesis after diffuse brain injury. 45 adult male SD rats were subjected to diffuse brain injury and randomized into MK-801-treatment group, vehicle-treatment group and control group (n=15 each). By using bromodeoxyuridine ( BrdU ) labelling method and immunohistochemistry to observe dividing cells, the proliferation rates of neural precursor cells in the dentate gyrus(DG) were compared between MK-801-treatment group and corresponding control groups on 2, 4, 6, 8, and 12 days after diffuse brain injury. The results showed that MK-801 (1mg/kg i.p.) significantly reduced the number of BrdU labeled cells in the dentate gyrus on 4, 6, 8 and 12 days after diffuse brain injury (P<0.01), indicating inhibition of the proliferation rate of neural precursor cells in the dentate gyrus. The activation of NMDA receptor after diffuse brain injury might promote the neurogenesis in the dentate gyrus. A cascade of biological events mediated by glutamic acid after diffuse brain injury probably played an important role in neurogenesis after diffuse brain injury.
分 类 号:R742[医药卫生—神经病学与精神病学] R338.2[医药卫生—临床医学]
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