Cadherin activity is required for activity-induced spine remodeling
Cadherin activity is required for activity-induced spine remodeling
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DOI：
10.1083/jcb.200406030
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发表时间：
2004-12-06
影响因子：
7.8
通讯作者：
Miki, N
中科院分区：
文献类型：
--
作者：
Okamura, K;Tanaka, H;Miki, N
神经活动诱导突触前膜和突触后膜的重塑，并通过细胞粘附分子维持其并置。其中，N-钙粘蛋白被重新分布，经历活动依赖性构象变化，并且是突触可塑性所必需的。在这里，我们发现去极化会导致脊柱头部宽度增大，而钙粘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显示的树突棘显示出由于 AMPA 受体的激活而扩张，因此突触并置区可能扩大。 N-钙粘蛋白-金星融合蛋白沿着扩张的脊柱头部横向分散。 N-钙粘蛋白显性失活形式的过度表达导致脊柱扩张的终止。用细胞松弛素 D 抑制肌动蛋白聚合，消除了脊柱的扩张。总之，我们的数据表明，基于钙粘蛋白的粘附机制与肌动蛋白细胞骨架相结合对于突触附着区的重塑至关重要。
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.