中科院神经所于翔课题组近期的工作表明，Wnt信号的传导分子β-catenin 蛋白，及由 cadherin，β-catenin 和 α-catenin 组成的细胞粘附复合物，是调节树突形态的重要介导物。在分离的海马神经元中增加细胞内 cadherin/catenin 复合物的含量可以增强树突的树状分支程度；相反，过表达 Ncad(intra)，一种可隔离阻断 β-catenin 功能的分子，则导致树突分支末端数目的减少，并且阻止模拟神经活动或激活 Wnt 信号传递所引起的树突形态发生的增强。实验结果还显示，模拟神经活动的增强(增加细胞外液钾离子的浓度，从而使神经元去极化)可以提高细胞培养液中的 Wnt 活性，显示神经活动可能调节 Wnt 的基因表达。
而这篇文章则主要针对形态学与功能学的相互关系，神经环路发育需要形态学方面和功能上的改变，研究人员发现了提高神经活性之后，树突形态学和mEPSC (miniature excitatory post-synaptic current，微小兴奋性突触后电流)变化之间的相对应关系。并且发现β-catenin分子的过量表达，与通过降低mEPSC变化幅度一样，都能达到增加神经活性的作用。
更加重要的是，研究人员还发现β-catenin体内过表达能促进树突生长，减少mEPSC变化幅度，从而研究人员提出，这些数据证明树突形态学和单一刺激突触强度的同样变化也许都是避免神经元在神经环路发育过程中过于兴奋的一种重要机制。
这项研究通过体内和体外研究，结合分子生物学、光学成像、电生理学等手段阐述树突形态发生的分子机制及其对突触功能和神经环路形成的影响，将更清晰地阐明树突发育和神经环路形成的分子机制，并将有助于对发育性神经疾病的理解。（生物谷Bioon.com）
生物谷推荐原始出处：
Neuron, Volume 61,15 January 2009 doi:10.1016/j.neuron.2008.11.015
Coordinated Changes in Dendritic Arborization and Synaptic Strength during Neural Circuit Development
Yi-Rong Peng1,2,Shan He1,2,Helene Marie3,4,Si-Yu Zeng1,2,Jun Ma1,Zhu-Jun Tan1,2,Soo Yeun Lee3,Robert C. Malenka3,,andXiang Yu1,5,,
1 Institute of Neuroscience and State Key Laboratory of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China
2 Graduate School of the Chinese Academy of Sciences, Shanghai 200031, China
3 Nancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94304-5485, USA
4 Present address: European Brain Research Institute, Rome 00143, Italy
5 Previous address: Nancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94304-5485, USA
Neural circuit development requires concurrent morphological and functional changes. Here, we identify coordinated and inversely correlated changes in dendritic morphology and mEPSC amplitude following increased neural activity. We show that overexpression of -catenin, a molecule that increases total dendritic length, mimics the effects of increased neuronal activity by scaling down mEPSC amplitudes, while postsynaptic expression of a protein that sequesters -catenin reverses the effects of activity on reducing mEPSC amplitudes. These results were confirmed immunocytochemically as changes in the size and density of surface synaptic AMPA receptor clusters. In individual neurons there was an inverse linear relationship between total dendritic length and average mEPSC amplitude. Importantly, -catenin overexpression invivo promoted dendritic growth and reduced mEPSC amplitudes. Together, these results demonstrate that coordinated changes in dendritic morphology and unitary excitatory synaptic strength may serve as an important intrinsic mechanism that helps prevent neurons from overexcitation during neural circuit development.
