| 阻断NR2A可增强脑缺血小鼠海马神经元树突棘丢失和认知功能障碍 |
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| 引用本文： | 陈远寿,陈旻,张弛.阻断NR2A可增强脑缺血小鼠海马神经元树突棘丢失和认知功能障碍[J].第三军医大学学报,2010,32(21). |
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| 作者姓名： | 陈远寿 陈旻 张弛 |
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| 作者单位： | 遵义医学院生理学教研室;中国科学院神经科学研究所神经科学国家重点实验室; |
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| 摘 要： | 目的 探讨N-甲基-D-天门冬氨酸受体(N-methyl-D-aspartate receptor, NMDAR or NR)亚基NR2A在脑缺血再灌注引起的海马CA1区神经元树突棘丢失和认知功能障碍中的作用.方法 制作三动脉阻断(3-VO)GFP转基因小鼠全脑缺血模型,小鼠随机分为假手术组、脑缺血再灌注(I/R)组和NVP-AAM077(NVP)干预组;应用跳台试验测试小鼠学习记忆能力,激光共聚焦和Neurolucida软件分析检测海马CA1区神经元形态及树突棘的变化.结果 学习记忆能力测试发现,I/R组明显差于sham组(P<0.05),NVP干预组差于sham组和I/R组(P<0.05);I/R组CA1区神经元树突棘的数量明显少于假手术组(P<0.01),NVP干预能进一步增加缺血/再灌注所致的CA1区神经元树突棘的丢失(P<0.05).结论 NMDA受体亚基NR2A在小鼠脑缺血再灌注所致树突棘丢失和脑认知功能损害中具有重要作用.
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| 关 键 词： | NVP-AAM077 NMDA受体 树突棘 学习记忆 脑缺血 |
Blocking NR2A enhances loss of neuronal dendritic spines and cognitive dysfunction in mice after cerebral ischemia |
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| Chen Yuanshou,Chen Min,Zhang Chi.Blocking NR2A enhances loss of neuronal dendritic spines and cognitive dysfunction in mice after cerebral ischemia[J].Acta Academiae Medicinae Militaris Tertiae,2010,32(21). |
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| Authors: | Chen Yuanshou Chen Min Zhang Chi |
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| Institution: | Chen Yuanshou1,Chen Min2,Zhang Chi2(1Department of Physiology,Zunyi Medical College,Zunyi,Guizhou Province,563003,2State Key Laboratory of Neuroscience,Institute of Neuroscience,Chinese Academy of Sciences,Shanghai,200031,China) |
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| Abstract: | Objective To study the role of N-methyl-D-aspartate(NMDA)receptor subunit NR2A in loss of dendritic spines in CA1 region and cognitive dysfunction due to reperfusion of cerebral ischemia.Methods A global cerebral ischemia model of male C57BL/6 GFP transgenic mice was established using the three-Vessel occlusion(3-VO)method.The mice were randomly divided into sham-operation group,ischemia/reperfusion(I/R)group and NVP-AAM077 treatment group(NVP).Step-down test was used to evaluate the learning and memory abi... |
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| Keywords: | NVP-AAM077 NMDA receptor dendritic spine learning and memory global cerebral ischemia |
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