Exendin-4剂量依赖性拮抗淀粉样β蛋白所致大鼠突触可塑性损伤  

Exendin-4 dose-dependently prevents against amyloid β-protein induced impairments of synaptic plasticity in rats

作　　者：潘艳芳[1] 应小平[1] 原丽[2] 

机构地区：[1]陕西中医药大学基础医学院病理教研室,陕西咸阳712046 [2]山西医科大学生理学系,山西太原030001

出　　处：《吉林医学》2017年第4期605-608,共4页Jilin Medical Journal

基　　金：陕西省自然科学基础研究计划[项目编号:2015JQ8299]

摘　　要：目的:观察Exendin-4对淀粉样β蛋白(Aβ_(1-42))所致大鼠突触可塑性损伤的影响。方法:SD大鼠(n=60)侧脑室给予Aβ_(1-42)建立AD模型,Exendin-4预处理后,进行在体海马场电位实验记录大鼠海马长时程增强(LTP)。结果:1与对照组相比,Aβ_(1-42)明显压抑了大鼠在体海马CA1区突触传递的LTP效应。2单独给予Exendin-4不影响LTP的诱导与维持,但Exendin-4预处理可有效逆转Aβ_(1-42)引起的LTP压抑,并呈现一定的剂量依赖性。结论:Exendin-4可有效拮抗Aβ_(1-42)所致的大鼠突触可塑性损害,提示其具有一定的神经保护作用。Objective The present study investigated the effects of Exendin-4 pretreatment induced on Aβ（1-42）-induced impairment in synaptic plasticity.Method After intracerebroventricular（ i.c.v.） injection injection of Aβ（1-42） and Exendin-4in rats,A self-made hippocampal local drug delivery catheter and a parallel bound stimulating/recording electrode were used to deliver drugs/stimulation and record field excitatory post-synaptic potentials（ f EPSPs） in the hippocampal CA1 region of rats.High-frequency stimulation（ HFS） was used to induce in vivo LTP in vivo hippocampal long-term potentiation（LTP） of rats were recorded.Results 1 Aβ（1-42） alone inhibited the HFS-induced LTP significantly.2Hippocampal CA1 injection of Exendin-4 alone did not affect the baseline f EPSPs and HFS-induced LTP,but alleviated Aβ（1-42）-induced suppression of LTP in dose-dependent manner,compared with Aβ（1-42） alone group.Conclusion These data indicates that pretreatment with exendin-4 effectively and dose-dependently protected against Aβ（1-42）-induced impairments in synaptic plasticity in rats.

关 键 词：EXENDIN-4 淀粉样Β蛋白 海马长时程增强 阿尔茨海默病 

分 类 号：R749.16[医药卫生—神经病学与精神病学]