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首页> 外文期刊>The European Journal of Neuroscience >Characterization of physiological phenotypes of dentate gyrus synapses of PDZ1/2 domain-deficient PSD-95-knockin mice
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Characterization of physiological phenotypes of dentate gyrus synapses of PDZ1/2 domain-deficient PSD-95-knockin mice

机译：PDZ1 / 2域缺陷型PSD-95基因敲除小鼠的齿状回突触的生理表型表征

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摘要

The hippocampal formation is involved in several important brain functions of animals, such as memory formation and pattern separation, and the synapses in the dentate gyrus (DG) play critical roles as the first step in the hippocampal circuit. Previous studies have reported that mice with genetic modifications of the PDZ1/2 domains of postsynaptic density (PSD)-95 exhibit altered synaptic properties in the DG and impaired hippocampus-dependent behaviors. Based on the involvement of the DG in the regulation of behaviors, these data suggest that the abnormal behavior of these knockin (KI) mice is due partly to altered DG function. Precise understanding of the phenotypes of these mutant mice requires characterization of the synaptic properties of the DG, and here we provide detailed studies of DG synapses. We have demonstrated global changes in the PSD membrane-associated guanylate kinase expression pattern in the DG of mutant mice, and DG synapses in these mice exhibited increased long-term potentiation under a wide range of stimulus intensities, although the N-methyl-d-aspartic acid receptor dependence of the long-term potentiation was unchanged. Furthermore, our data also indicate increased silent synapses in the DG of the KI mice. These findings suggest that abnormal protein expression and physiological properties disrupt the function of DG neurons in these KI mice.
机译：海马的形成与动物的几个重要脑功能有关，例如记忆形成和模式分离，而齿状回（DG）中的突触是海马回路的第一步，起着至关重要的作用。先前的研究报道，对突触后密度（PSD）-95的PDZ1 / 2结构域进行遗传修饰的小鼠在DG中显示出改变的突触特性，并损害了海马依赖性行为。基于DG在行为调节中的参与，这些数据表明这些敲入（KI）小鼠的异常行为部分是由于DG功能改变所致。准确了解这些突变小鼠的表型需要表征DG的突触特性，在这里我们提供DG突触的详细研究。我们已经证明了突变小鼠DG中PSD膜相关鸟苷酸激酶表达模式的全球变化，尽管这些小鼠的DG突触在N甲基-d-天冬氨酸受体的长期增强依赖性没有改变。此外，我们的数据还表明，KI小鼠的DG中的沉默突触增加。这些发现表明异常的蛋白质表达和生理特性破坏了这些KI小鼠中DG神经元的功能。

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