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脑缺血后大脑皮质神经元NT-3的表达变化

The Change on the Expression of NT-3 in Neurons of Cerebral Cortex of Adult Rat Following Local Ischemia

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【作者】 高礼王廷华曾兢张晓米兰兰

【Author】 GAO Li, WANG Ting-hua, ZENG Jing, ZHANG Xiao, MI Lang-lang (Institute of Neuroscience, Kunming Medical College, Kunming 650031)$$$$

【机构】 昆明医学院神经科学研究所昆明医学院神经科学研究所 昆明650031第三军医大学成都军医学院中心实验室昆明650031昆明650031第三军医大学成都军医学院中心实验室昆明650031第三军医大学?

【摘要】 为探讨NT - 3与局灶性脑缺血后大脑皮质神经元损伤修复的关系 ,采用免疫组织化学ABC法观察了脑缺血 1h后大鼠大脑皮质NT - 3的变化 .结果 :NT - 3样免疫阳性反应物主要分布于大脑皮质第 3,5层的神经元 .脑缺血 1h后 ,NT - 3在皮质神经元的表达明显减少 (P <0 0 5 ) .提示NT - 3可能通过不同于其它生长因子的调节方式参与脑缺血后大脑皮层神经细胞的损伤修复

【Abstract】 In order to explore the relation between NT-3 and neuronal injury in cerebra cortex following ischemia, ten adult SD rats were performed unilateral local ischemia operation. After 1 hour following ischemia, the cerebral cortex on both operated side and un-operated side was taken respectively and the tissue was made into frozen sections(20?μm on thickness). The sections were stained using specific antiserum of NT-3 by immunohistochemical ABC method. The level of NT-3 in neuron was estimated according to the average degree by computer analysis system. The results were as following: NT-3 like immunoreactive products distributed mainly in neurons of the third and the fifth layers in cerebral cortex. On 1 hour following local ischemia, the average degree of NT-3 in neurons of cerebral cortex increased more greatly on operated side than on un-operated side(P<0 05). This demonstrated that the level of NT-3 in neurons of cerebral cortex following ischamia was downregulated apparently. It indicated that not only NT-3 plays an important role in the process of neuron reaction induced by ischemia in cerebral cortex but also the modulation mechanism of NT-3 is different from other neurotrophic factor such as nerve growth factor and brain derived neurotrophic factor.

【关键词】 神经营养因子3大脑皮质脑缺血
【Key words】 NT-3Cerebral cortexIschemia
【基金】 国家自然科学基金资助项目 (30 0 0 0 2 2 7)
  • 【文献出处】 昆明医学院学报 ,Academic Journal of Kunming Medical College , 编辑部邮箱 ,2002年01期
  • 【分类号】R364
  • 【被引频次】2
  • 【下载频次】59
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