摘要
目的:研究不同神经元退行性变动物模型中单胺氧化酶B(MAO B)活性变化,并探讨其意义。方法:NIH雄性小鼠,分别建立脑缺血再灌注、铝过负荷及一氧化碳中毒神经元退行性变模型。采用Morris水迷宫和跳台实验进行学习记忆能力测试,HE切片染色光镜下观察海马病理变化和以市售标准试剂盒测定脑匀浆MAO B活性。结果:各模型组小鼠较相应对照组学习记忆能力显著降低,海马切片可见神经元核固缩和细胞丢失等退行性改变。脑缺血再灌注模型组MAO B活性与对照组相比无显著变化,但铝中毒和一氧化碳中毒模型小鼠MAO B活性较对照组显著升高。结论:MAO B活性异常升高在各种神经元退行性变动物模型中不具有普遍性意义。脑缺血再灌注模型可能适用于痴呆研究,而一氧化碳中毒和铝过负荷模型可能适用于痴呆和锥体外系疾病研究。
Objective:To investigate the changes of monoamine oxidase B ( MAO B ) activity in variety of neurodegenerative animal models and to discuss their significance. Methods: The neurodegenerative models were built with NIH male mice by means of the cerebral ischemia-reperfusion, aluminum overloading and carbon monoxide intoxication, respectively.The learning and memory ability of mice, MAO B activity of brain homogenates, and pathomorphological changes of hippocampal slices were determined using Morris maze and Step-down tests, MAO B kit, as well as microscopic observation with HE stain.Result:Although the significantly decreasing learning and memory ability and loss and karyopyknosis of hippocampal neurons were observed in three groups of animal models, compared with control group, the changes of MAO B activity were quite different. There was no significant change in cerebral ischemia-reperfusion model, but the unusual elevation was found in both aluminum overloading model and carbon monoxide intoxication model.Conclusion:The abnormal increase of MAO B does not occur in a variety of neurodegenerative animal models,which may indicate that the cerebral ischemia-reperfusion model can be used in the research of dementia and aluminum overloading model and carbon monoxide intoxication model can be used in the research of both dementia and extrapyramidal disease.
出处
《重庆医科大学学报》
CAS
CSCD
2006年第5期681-683,714,共4页
Journal of Chongqing Medical University