Yu Xiang, Malenka Robert C
Nancy Friend Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, California 94304, USA.
Nat Neurosci. 2003 Nov;6(11):1169-77. doi: 10.1038/nn1132. Epub 2003 Oct 5.
Regulated growth and arborization of dendritic processes are critical to the formation of functional neuronal networks. Here we identify beta-catenin as a critical mediator of dendritic morphogenesis. We found that increasing the intracellular levels of beta-catenin and other members of the cadherin/catenin complex, namely N-cadherin and alphaN-catenin, enhances dendritic arborization in rat hippocampal neurons, an effect that does not require Wnt/beta-catenin-dependent transcription. Conversely, proteins that sequester beta-catenin decreased dendritic branch tip number and total dendritic branch length. Enhancement of dendritic growth elicited by depolarization requires beta-catenin and increased Wnt release. These results identify Wnt/beta-catenin signaling as an important mediator of dendritic development and suggest that the intracellular level of the cadherin/catenin complex is a limiting factor during critical stages of dendritic morphogenesis.
树突状突起的生长调控和分支形成对于功能性神经网络的形成至关重要。在此,我们确定β-连环蛋白是树突形态发生的关键调节因子。我们发现,增加β-连环蛋白以及钙黏蛋白/连环蛋白复合物的其他成员(即N-钙黏蛋白和αN-连环蛋白)的细胞内水平,可增强大鼠海马神经元的树突分支,这种效应并不需要Wnt/β-连环蛋白依赖性转录。相反,隔离β-连环蛋白的蛋白质会减少树突分支尖端数量和总树突分支长度。去极化引发的树突生长增强需要β-连环蛋白和增加的Wnt释放。这些结果确定Wnt/β-连环蛋白信号传导是树突发育的重要调节因子,并表明钙黏蛋白/连环蛋白复合物的细胞内水平是树突形态发生关键阶段的限制因素。