摘要
目的探讨缺血缺氧后大鼠海马神经元突触后膜谷氨酸受体-2(GluR2)含量变化情况。方法体外培养胚胎大鼠海马神经元,模拟临床缺血过程致神经元缺氧损伤,运用双重免疫荧光技术标记和共聚焦检测技术观察缺血缺氧后不同时间点海马神经元突触后膜GluR2含量变化情况。结果体外培养海马神经元进行模拟缺血处理后,膜表面的GluR2总含量、含有GluR2突触的相对含量以及含有突触部位GluR2的相对含量均明显降低,而且上述变化随着模拟缺血时间的延长而增加,各组间均存在显著性差异(P<0.05)。结论缺血缺氧损伤可致突触后膜表面GluR2含量降低并随着缺血时间的延长而增加,形成缺乏GluR2的新的AMPA受体通道,介导Ca2+的快速内流,引起神经元的延迟性死亡。
Objective To explore the changes of GluR2 on the post-synaptic membrane of cultured rat hippocampal neurons induced by oxygen and glucose deprivation (OGD). Methods The rat hippocampal neurons cultured in vitro were used to simulate the ischemia and reperfusion injury. The GluR2 at different post-ischemia time points on post-synaptic membrane was quantitated with double immuno-fluorescence labelling and confocal microscopy. Results After OGD, the total surface GluR2, the number of synapse with GluR2 and the quantity of GluR2 in synapse were significantly lower than those of the control group. Furthermore, all of the above-mentioned decreases were increased with the prolongation of the ischemia time. Significant differences could be observed between the experimental groups (P<0.05). Conclusion OGD-induced decreases of GluR2 at post-synaptic membrane were increased with the prolongation of ischemia time, and resulted in the formation of GluR2-lacking AMPA receptors. The increased expression of functional GluR2-lacking AMPA receptors at postsynaptic membrane mediated the influx of Ca2+ and resulted in the delayed neuron death.
出处
《中华神经医学杂志》
CAS
CSCD
2005年第3期235-237,共3页
Chinese Journal of Neuromedicine
基金
广东省科技计划项目(2003A3020304)
军队九五军事医学研究课题(98M067)
