APP/PS1转基因AD鼠海马CA1区神经元突触超微结构

Ultrastructure of neuronal synapse in area CA1 of the hippocampus of APP/PS1 transgenic mouse with Alzheimer's disease

目的:探讨携带5个家族性基因突变的APP/PS1转基因阿尔茨海默病(AD)(5×FAD)模型小鼠海马CA1区神经元突触超微结构改变。方法:应用透射电镜观察和形态计量学分析5×FAD转基因AD鼠海马CA1区GrayⅠ型突触界面结构参数,包括突触间隙长度、突触间隙面积、突触后致密物浓度和突触界面曲率的变化。结果:5×FAD转基因AD鼠海马CA1区神经元突触活性区长度显著小于对照组,差异有统计学意义;突触后致密物厚度、突触界面曲率及宽度与对照组差异无统计学意义。结论:5个家族性突变基因导致小鼠海马CA1区神经元突触可塑性的改变,这可能是该突变基因导致的发病机制之一。

Objective： To analyze ultrastructure changes of neuronal synapse in area CA1 of the hippocampus of five familiar APP/PS1 tramsgenic mouse with Alzheimer＇s disease （5×FAD）. Methods.. The length of synaptic cleft, area of synaptic cleft, thickness of postsynaptic density, and curvature of synapse active zone were measured in the interface of synapse by morphometry analysis. Results： The length of synaptic cleft in 5 X FAD mice group was significantly shorter than that in control group. There were no significant differences between 5 N FAD mice group and control group in the area of synaptic cleft, thickness of postsynaptic density and curvature of synapse active zone. Conclusion： The gene of 5×FAD can induce the change of synaptic plasticity in area CA1 of the hippocampus, which may be one of the mechanisms for these genes to induce Alzheimer＇s disease.