首页 | 本学科首页   官方微博 | 高级检索  
检索        

双(7)-他克林对慢性脑缺血老龄鼠海马胶质细胞可塑性及学习记忆功能的干预作用
引用本文:舒细记,柳威,杨荣,沙佩林,刘宇炜,陈莹,陈晓青,艾永循.双(7)-他克林对慢性脑缺血老龄鼠海马胶质细胞可塑性及学习记忆功能的干预作用[J].中华老年心脑血管病杂志,2012,14(1).
作者姓名:舒细记  柳威  杨荣  沙佩林  刘宇炜  陈莹  陈晓青  艾永循
作者单位:江汉大学医学院病理学与病理生理学教研室, 武汉,430056
摘    要:目的探讨双(7)-他克林(B7T)对持续性低血流灌注脑缺血老年大鼠学习记忆损害及海马胶质细胞可塑性的干预作用。方法雄性SD大鼠30只,随机分为缺血组、对照组和干预组,每组10只。Morris水迷宫实验评估大鼠学习记忆功能,免疫组织化学染色及图像分析技术检测海马CA1区胶质细胞的数量、胞质突起长度等可塑性变化。结果缺血组海马CA1区锥体细胞排列稀疏紊乱,凋亡多见;对照组和干预组锥体细胞排列整齐而密集,凋亡细胞少见。缺血组海马CA1区胶质细胞酸性蛋白(GFAP)阳性细胞和胞质突起长度明显少于对照组和干预组。缺血组逃逸时间明显多于对照组和干预组;缺血组在平台象限停留时间和跨越平台区域的次数明显少于对照组和干预组(P<0.05.P<0.01)。缺血组、对照组及干预组海马CA1区GFAP阳性细胞的数量、胞质突起长度与空间记忆改善呈正相关。结论 B7T可通过促进海马胶质细胞的可塑性改变,改善慢性脑缺血所致的学习记忆认知障碍。胶质细胞的可塑性变化是学习记忆功能改善的重要病理修复机制。

关 键 词:脑缺血  海马  记忆  受体  N-甲基-D-天冬氨酸  认知障碍  神经胶质  干预性研究

Intervention effect of B7T on hippocampal gliacyte plasticity and cognitive handicap in aged rats with chronic cerebral hypoperfusion
SHU Xi-ji , LIU Wei , YANG Rong , SHA Pei-lin , LIU Yu-wei , CHEN Ying , CHEN Xiao-qing , AI Yong-xun.Intervention effect of B7T on hippocampal gliacyte plasticity and cognitive handicap in aged rats with chronic cerebral hypoperfusion[J].Chinese Journal of Geriatric Cardiovascular and Cerebrovascular Diseases,2012,14(1).
Authors:SHU Xi-ji  LIU Wei  YANG Rong  SHA Pei-lin  LIU Yu-wei  CHEN Ying  CHEN Xiao-qing  AI Yong-xun
Abstract:Objective To explore the treatment effects of bis(7)-tactrine(B7T) on hippocampal gliacyte plasticity and cognitive handicap in aged rats with chronic cerebral hypoperfusion.Methods Thirty male SD rats were randomly divided into ischemic model,control and B7T-treated groups,each group had 10 rats.Spatial learning and memory were assessed by Morris water maze test,immunohistochemistry and image analysis were employed to detect the number and cytoplasmic process length of GFAP positive cells in hippocampal CAl region.Results The pyramidal cells in hippocampal CAl region of ischemic model group arranged sparser and more indiscriminate, compared with control group and B7T-treated group.More apoptotic cells were observed in the rats of ischemic model group.GFAP positive cells were significantly less and their cytoplasmic process length was shorter in ischemic model group than in control group and B7T-treated group. Escape latency of rats in ischemic model group was longer than that in control group and B7T-treated group.Ischemic model group spent less time in the platform quadrant than control group and B7T-treated group.The number of crossing the platform area in rats of ischemic model group was less than that in control group and B7T-treated group(P<0.05,P<0.01).Number and the cytoplasmic process length of glia cells were positively correlated to spatial learning in ischemic model group,control group and B7T-treated group.Conclusion Chronic cerebral hypoperfusion impaired the spatial learning and memory in aged rats,B7T can enhance the congnitive function by promoting gliacyte plasticity.
Keywords:brain ischemia  hippocampus  memory  receptors  N-methyl-D-aspartate  cognition disorders  neuroglia  intervention studies
本文献已被 万方数据 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号