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Cadherin activity is required for activity-induced spine remodeling

机译:钙黏蛋白活性是活动诱导的脊柱重塑所必需的

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摘要

Neural activity induces the remodeling of pre- and postsynaptic membranes, which maintain their apposition through cell adhesion molecules. Among them, N-cadherin is redistributed, undergoes activity-dependent conformational changes, and is required for synaptic plasticity. Here, we show that depolarization induces the enlargement of the width of spine head, and that cadherin activity is essential for this synaptic rearrangement. Dendritic spines visualized with green fluorescent protein in hippocampal neurons showed an expansion by the activation of AMPA receptor, so that the synaptic apposition zone may be expanded. N-cadherin-venus fusion protein laterally dispersed along the expanding spine head. Overexpression of dominant-negative forms of N-cadherin resulted in the abrogation of the spine expansion. Inhibition of actin polymerization with cytochalasin D abolished the spine expansion. Together, our data suggest that cadherin-based adhesion machinery coupled with the actin-cytoskeleton is critical for the remodeling of synaptic apposition zone.
机译:神经活动诱导突触前和突触后膜的重塑,该膜通过细胞粘附分子维持其并置。其中,N-钙粘着蛋白被重新分布,经历依赖于活性的构象变化,并且是突触可塑性所必需的。在这里,我们显示去极化诱导脊柱头部宽度的扩大,而钙粘着蛋白活性对于这种突触重排至关重要。海马神经元中绿色荧光蛋白可视化的树突棘通过AMPA受体的激活而扩张,因此突触并置区可能会扩张。 N-钙粘着蛋白-金星融合蛋白沿不断扩展的脊柱头部横向分散。 N-钙粘着蛋白的显性阴性形式的过度表达导致脊柱扩张的消失。用细胞松弛素D抑制肌动蛋白的聚合消除了脊柱的扩张。在一起,我们的数据表明,基于钙黏着蛋白的粘附机制与肌动蛋白的细胞骨架相结合对于突触并置区的重塑至关重要。

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