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机构地区:[1]大连大学附属中山医院,大连116001 [2]大连医科大学实验动物中心,大连116001 [3]大连医科大学第二临床医院,大连116027
出 处:《中国比较医学杂志》2010年第6期26-28,38,89,共5页Chinese Journal of Comparative Medicine
基 金:辽宁省科技计划项目(20054080020);大连市科技计划项目(2005E11SF006)
摘 要:目的探讨BDNF(Brain derived neurotrophic factor)改善痴呆老龄鼠记忆障碍的机制。方法利用Morris迷宫试验观察脑内微量注射BDNF对痴呆小鼠自发活动和记忆巩固过程的影响,应用透射电镜和形态计量学分析痴呆老龄鼠海马GrayⅠ型突触的突出结构参数的变化。结果BDNF使痴呆小鼠在新异环境中的自发活动和探究行为明显增多;并显著延长电击后24 h的步入潜伏期(STL);BDNF使痴呆老龄鼠海马CA1区GrayⅠ型突触的体积密度、面积密度、比表面和面数密度较治疗前增大,突触平均面积增大;突出界面曲率、突出间隙宽度、突出后致密物质均较治疗前增大,而较正常对照组减小。结论突触结构的变化和突出数量的减少是痴呆发病的病理机制之一;BDNF能够促进突触重建,改善痴呆老龄鼠的学习记忆。Objective To explore the mechanism of the BDNF on senile dementia mice.Method The senile dementia mice were tested by Morris water maze.The changes of the hippocampus synaptic structural parameters and Gray typeⅠwere studied with transmission electron microscope and morph metric analysis.Result The spontaneous activity and exploratory behavior in the new and abnormal environment were obviously increased.The step-through latency(STL) was prolonged significantly after electrical stimulation.After treatment by BDNF the volume density on area of Gray type Ⅰ synapses in CA1 sector of hippocampus were increased significantly,the parameters were decreased compared with the normal mice.Especially,the curvature of synaptic interface,the width of synaptic cleft and the thickness of postsynaptic density were increased compared with the control group,while the parameters were decreased compared with the normal mice.Conclusion The change of the synaptic structure and decrease in the synaptic number is one of the reasons on dementia pathological mechanism.BDNF can promote synaptic reconstruction and improve the memory of senile dementia mice.
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