β-淀粉样蛋白25-35和31-35片段对大鼠在体海马长持续长时程增强抑制作用的研究

Suppressive action of amyloid β-protein fragments 31-35 and 25-35 on the late phase of long-term potentiation in rat hippocampus in vivo

目的在体条件下观察β-淀粉样蛋白25-35和31-35片段对大鼠海马CA1区长持续长时程增强(L-LTP)的影响。方法在体海马CA1区L-LTP记录技术;侧脑室给药技术。结果25nmol浓度的Aβ31-35或Aβ25-35不影响基础突触传递(n=5,P>0.05);Aβ25-35对L-LTP的抑制具有一定的剂量依赖性效应:6.25nmol,12.5nmol和25nmolAβ25-35组和对照组相比,显著抑制了L-LTP的维持(在高频刺激后3h:均P<0.05);12.5nmolAβ31-35同Aβ25-35,抑制L-LTP的维持(高频刺激后3h,P<0.05)。结论Aβ25-35和Aβ31-35可显著抑制在体海马L-LTP的维持,从而损害突触可塑性。

Objective To detect the effect of Aβ-protein（25-35 and 31-35）on the maintenance of hippocampal late phase of long-term potentiation（L-LTP）in vivo.MethodsMultiple HFSs was used to record hippocampal L-LTP and Aβ was given by intracerebroventricular（i.c.v.）injection.Results25 nmol Aβ25-35 or 31-35 did not affect the basic synaptic transmission（n=5,P〉0.05）.Aβ25-35 showed a dose-dependent suppression on L-LTP：compared with control group,6.25,12.5 and 25 nmol Aβ25-35 obviously suppressed the maintenance of L-LTP（post-HFSs 3 h,all P〈0.05）.12.5 nmol Aβ31-35 also significantly suppressed L-LTP at 3 h post-HFSs compared to control group（P〈0.05）,which was the same as 12.5 nmol Aβ25-35.ConclusionsBoth Aβ25-35 and 31-35 can strongly suppress the maintenance of L-LTP in vivo and thereby impair hippocampal synaptic plasticity.