Institute of Clinical Neuroanatomy, Neuroscience Center, Goethe-University, Frankfurt am Main, Germany.
Exp Brain Res. 2012 Apr;217(3-4):441-7. doi: 10.1007/s00221-011-2911-9. Epub 2011 Nov 11.
The amyloid precursor protein (APP) plays a crucial role in the pathogenesis of Alzheimer's disease. Here, we studied whether the lack of APP affects the synaptic properties in the dentate gyrus by measuring granule cell field potentials evoked by perforant path stimulation in anesthetized 9-11-month-old APP-deficient mice in vivo. We found decreased paired-pulse facilitation, indicating altered presynaptic short-term plasticity in the APP-deficient dentate gyrus. In contrast, excitatory synaptic strength and granule cell firing were unchanged in APP knockout mice. Likewise, long-term potentiation (LTP) induced by a theta-burst stimulation protocol was not impaired in the absence of APP. These findings suggest that the deletion of APP may affect presynaptic plasticity of synaptic transmission at the perforant path-granule cell synapse but leaves synaptic efficacy intact and LTP preserved, possibly due to functional redundancy within the APP gene family.
淀粉样前体蛋白（APP）在阿尔茨海默病的发病机制中起着至关重要的作用。在这里，我们通过测量麻醉 9-11 个月大的 APP 缺陷型小鼠体内海马齿状回颗粒细胞场电位，研究了 APP 的缺乏是否会影响颗粒细胞层的突触特性。我们发现，APP 缺陷型齿状回的成对脉冲易化作用降低，提示突触前短期可塑性发生改变。相比之下，APP 敲除小鼠的兴奋性突触强度和颗粒细胞放电没有变化。同样，在没有 APP 的情况下，由 theta 爆发刺激方案诱导的长时程增强（LTP）也没有受损。这些发现表明，APP 的缺失可能会影响到海马齿状回颗粒细胞突触的突触传递的突触前可塑性，但突触效能完整且 LTP 保留，这可能是由于 APP 基因家族内的功能冗余。
