突触后膜GluR2含量变化及脑继发性损害的实验研究

目的　探讨缺血损伤后神经元突触后膜谷氨酸α 氨基羟甲基异恶唑丙酸 (AMPA)受体第二亚单位 (GluR2 )的含量、受体离子通透功能变化及其在延迟性细胞死亡中的作用。方法　采用PI染色和双重免疫荧光技术定量观察神经元死亡和突触GluR2含量变化 ,以膜片钳技术检测自发兴奋性突触后电流(mEPSCs)的变化。结果　缺氧后神经元死亡数量明显增加 ;膜表面GluR2总量、含GluR2的突触数目以及突触部位GluR2含量都明显降低 (P <0 .0 5 ) ,膜表面GluR2含量下降以突触部位为主 ;缺乏GluR2的受体通道功能明显增强。结论　缺氧损伤可致突触后膜表面GluR2含量降低 ,形成缺乏GluR2的新的AMPA受体通道 ,介导了Ca2 的快速内流 ,引起神经元的延迟性死亡

Experimental study on the changes of GluR2 on post-synaptic membrane and its related brain secondary injury

Objective To explore the changes of GluR2 on the post synaptic membrane,ion permeable function of AMPA receptor and the effects on the delayed death of neuron.Methods The neuron death and the quantity of GluR2 on post synaptic membrane was quantitated with PI staining and double immuno fluorescence labeling. The mEPSCs (miniature excitatory postsynaptic currents) was measured with patch clamp.Results The number of delayed death neuron increased significantly after OGD (oxygen glucose deprivation). The total surface GluR2,the number of synapse with GluR2,and the quantity of GluR2 in synapse were marked lower than that of control group. OGD induced reduction of GluR2 mainly occurred at synapses. OGD also resulted in the increased expression of functional GluR2 lacking AMPA receptors at postsynaptic membrane.Conclusion OGD induced the reduction of GluR2 at postsynaptic membrane and the formation of GluR2 lacking AMPA receptors,which mediated the influx of Ca 2 and resulted the delayed neuron death.