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。
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 ability of mice.Alterations of dendritic spines in CA1 region were detected by laser scanning confocal microscopy.Results The learning and memory ability was significantly poorer in I/R group than in sham-operation group（P0.05）.The function was significantly poorer in NVP treatment group than in sham-operation group and I/R group（P0.05）.The number of dendritic spines in CA1 region was significantly less in I/R group than in sham-operation group（P0.01）,indicating that NVP can increase the loss of dendritic spines in CA1 region due to I/R injury（P0.05）.Conclusion NMDA receptor subunit NR2A plays an important role in loss of dendritic spines and cognitive dysfunction in mice due to I/R injury.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2010年第21期2311-2313,共3页
Journal of Third Military Medical University
基金
国家自然科学基金(30721004)~~
