中文摘要：

目的研究可溶性邮寡聚体在海马神经元中对突触蛋白表达的影响。方法用免疫细胞化学方法检测在NMDA拮抗剂与激动剂作用下，Aβ25-35。对突触后密度蛋白（PSD-95）表达的影响。结果Aβ25-35引起的PSD-95减少具有时间、剂量依赖性。PSD-95的减少可被非特异性NMDA受体拮抗剂（MK801）缓解；突触外NMDA受体被阻断时，也可显著缓解；而在突触内NMDA受体被阻断时，无显著性改变。结论邮引起的PSD-95减少依赖NMDA受体活性，突触外NMDA受体可能参与Aβ诱导突触蛋白降解。

英文摘要：

Objective To investigate the mechanism of the soluble Aβ oligomers-induced alteration of synaptic proteins. Methods This study applied immunocytochemistry technique to investigate the changes of the expression of postsynaptic density- 95（PSD-95） in primary hippoeampal neurons, which was exposed to Aβ25-35 after NMDAR antagonist or agonist treatment. Results The results showed that Aβ25-35 downregnlated PSD-95 protein in a dose- and time-dependent manner. Treatment of cells with MK801 （a general NMDA receptor antagonist） prevented Aβ-induced PSD-95 degradation. Moreover, when extrasynaptic NMDA receptors were blocked by ifenprodil （a NR2B subunit specific antagonist）, the Aβ-induced downregulation of PSD-95 was significantly attenuated. Whereas, when synaptic NMDA receptors were blocked by bicuculline （a GABA receptor antagonist） in combination with MK801, the PSD-95 degradation did not change significantly. Conclusion The results suggest that Aβ-induced downregulation of PSD-95 depends on NMDAR activity, and extrasynaptic NMDA receptors may be involved in Aβ-indueed synaptic protein degradation.