Cadherin activity is required for activity-induced spine remodeling.

神经活动诱导突触前膜和突触后膜的重塑，突触前膜和突触后膜通过细胞粘附分子维持它们的并置。其中，N-钙粘蛋白是重新分布，经历活动依赖性构象变化，并需要突触可塑性。在这里，我们表明，去极化引起的棘头的宽度扩大，而钙粘蛋白的活性是必不可少的突触重排。绿色荧光蛋白显示海马神经元树突棘因AMPA受体激活而扩张，从而扩大了突触并置区。N-cadherin-venus融合蛋白沿着扩张的棘头侧向分散。显性负性形式的N-钙粘蛋白的过度表达导致脊柱扩张的废除。用细胞松弛素D抑制肌动蛋白聚合可消除棘扩张。两者合计，我们的数据表明，钙粘蛋白为基础的粘附机制加上肌动蛋白细胞骨架是至关重要的突触附着区的重塑。

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. Taken together, our data suggest that cadherin-based adhesion machinery coupled with the actin-cytoskeleton is critical for the remodeling of synaptic apposition zone.