Meynert核注射β-淀粉样蛋白对大鼠脑突触生长素表达的影响及尼莫地平的保护作用

Expression of Synaptophysin and Protective Function of Nimodipine after Amyloid-beta Protein Injected into Meynert Nucleus in Rats

目的 :探讨Meynert核注射 β 淀粉样蛋白 (amyloid betaprotein ,Aβ)对大鼠脑突触生长素表达的影响及尼莫地平的保护作用。方法 :将Aβ1 40 10 μg·μL-1注入右侧Meynert核建立大鼠AD模型 ,测定其学习记忆能力和脑组织突触生长素的表达变化及尼莫地平的影响作用。结果 :Aβ注射后出现较持久的学习记忆障碍 ,Aβ组呈渐进性加重 ,治疗组有一定改善。Aβ组Meynert核、海马区和皮质区突触生长素免疫反应阳性产物较对照组明显减少 ;治疗组较对照组减少 ,但较Aβ组有明显增加。 结论 :Meynert核、海马和皮质区突触数量的减少及其功能异常可能是AD学习记忆障碍和痴呆形成的重要因素之一。

Aim:To investigate whether amyloid beta protein injected into Meynert nucleus might affect memory ability and expression of synaptophysin immunoreactive positive products in rats, and the protection of nimodipine.Methods:The AD rat model was established by injection of amyloid beta protein (Aβ 1 40 ,10 μg) into right Meynert nucleus in rats. Learning and memory ability, synaptophysin immunoreactive positive products were studied. Possible protective effects of nimodipine were also observed. Results:Learning and memory disorder aggravatd progressively in experimental group and ameliorated obviously in nimodipine administrated group at the 4th week. Synaptophysin immunoreactive positive products in Meynert nucleus, hippocampus and cortex fields decreased remarkablely in experimental group, and those in nimodipine administrated group reduced obviously than in control group, but more than in experimental group. Conclusion:Decreased synapes and its dysfunction induced by Aβ might play an important role in memory defects and AD formation. Administration of nimodipine induces certain protective effects.