Wu Cuiying, Niu Lijun, Yan Zhongjie, Wang Chong, Liu Ning, Dai Yiwu, Zhang Peng, Xu Ruxiang
Affiliated Bayi Brain Hospital, The Military General Hospital of Beijing PLA, Beijing, China.
Department of Neurosurgery, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
J Mol Neurosci. 2015 Aug;56(4):822-828. doi: 10.1007/s12031-015-0515-8. Epub 2015 Feb 17.
Proper formation of neuronal dendritic branching is crucial for correct brain function. The number and distribution of receptive synaptic contacts are defined by the size and shape of dendritic arbors. Our previous research found that protocadherin 11 X-linked protein (Pcdh11x) is predominantly expressed in neurons and has an influence on dendritic branching. In this study, gain-of-function and loss-of-function experiments revealed that Pcdh11x acts as a negative regulator of dendritic branching in cultured cortical neurons derived from embryonic day 16 mice. Overexpression of wild-type Pcdh11x (Pcdh11x-GFP) reduced dendritic complexity, whereas knockdown of Pcdh11x increased dendritic branching. It was further demonstrated that Pcdh11x activates PI3K/AKT signaling to negatively regulate dendritic branching.
神经元树突分支的正确形成对于大脑的正常功能至关重要。感受性突触接触的数量和分布由树突分支的大小和形状决定。我们之前的研究发现，X连锁原钙黏蛋白11（Pcdh11x）主要在神经元中表达，并对树突分支有影响。在本研究中，功能获得和功能丧失实验表明，Pcdh11x在源自胚胎第16天小鼠的培养皮质神经元中作为树突分支的负调节因子发挥作用。野生型Pcdh11x（Pcdh11x-GFP）的过表达降低了树突复杂性，而Pcdh11x的敲低增加了树突分支。进一步证明，Pcdh11x激活PI3K/AKT信号通路以负调节树突分支。
