OGD后突触后膜GluRs含量变化及神经元延迟性死亡研究  

Changes of GluRs on postsynaptic membrane and delayed neuron death after OGD

作　　者：刘宝松[1] 曾琳[1] 陈恒胜[1] 龙在云[1] John G Mielke Michael G Fehlings 万芪[2] 

机构地区：[1]第三军医大学大坪医院野战外科研究所,重庆400042 [2]多伦多大学生理系多伦多西区研究所

出　　处：《中华神经医学杂志》2004年第5期321-323,共3页Chinese Journal of Neuromedicine

基　　金：重庆市科技计划项目(8107);第三军医大学回国启动基金(XG200355)

摘　　要：目的 探时OGD损伤后神经元突触后膜GluR1～3含量变化及其在神经元延迟性细胞死亡中的作用。方法 采用PI染色、细胞比色分析和双重免疫荧光技术定量观察神经元死亡、膜表面及灾触GluR1～3含量变化。结果 OGD后神经元死亡数量明显增加;膜表面GluR2含量、含GluR2的突触数目以及突触部位GluR2含量都明显降低(P<0.05),膜表面GluR2含量下降以突触部位为主,而膜表面GluR1和GluR3却明显增加。结论 OGD损伤可致突触后膜表面GluR2含量降低,GluR1和GluR3增加并可形成缺乏GluR2的AMPA受体通道,从而介导了Ca^(2-)的快速内流,引起神经元的延迟性死亡。Objective To explore the changes of glutamate receptor (GluR)1～3 in the postsynaptic membrane and the effects on the delayed neuron death after oxygen-glucose deprivation (OGD). Methods The neuron death was quantitated with P1 staining, while the quantities of GluR 1～3 in the neuron membrane and the postsynaptic membrane were quantitatively measured with colorimetric assay and double immuno-fluorescence labeling. Results The number of delayed death neurons increased significantly after OGD. The total surface GluR2, the number of synapse with GluR2, and the quantity of GluR2 in synapse were marked lower than that of the control (P<0.05). OGD-induced reduction of GluR2 mainly occurred at synapses. GluR1 and GluR3, however, highly increased. Conclusion OGD s able to induce the reduction of GluR2 at postsynaptic membrane. The increase of GluR1 and GluR3 may further result in the formation of GluR2-1acking amino-3-hydroxy-5 methylisoxazole-4-propionic acid (AMPA) receptors, which mediates the influx of Ca^(2+) and cause the delayed neuron death.

关 键 词：OGD 突触 延迟性 含量变化 神经元死亡 部位 损伤 细胞死亡 数目 CA^2+ 

分 类 号：R741[医药卫生—神经病学与精神病学]