Pcdh11x蛋白对体外培养皮层神经元树突发育的影响

目的探讨Pcdh11x蛋白对神经元树突分支的影响。 方法通过增加与敲低Pcdh11x的表达水平，评价Pcdh11x蛋白对神经元树突的影响。应用SPSS13.0软件使用单因素方差分析的方法对树突分支数量进行统计分析。 结果培养3 d时，与对照质粒组(2.60±0.22)相比，pcdh11x-shRNA转染组可明显增加一级(5.80±0.39)和二级(9.80±0.81)树突的数目，而pCAG-Pcdh11x-GFP转染组可减少一级(1.40±0.16)和二级树突(2.90±0.46)的数目。同时发现，过表达Pcdh11x时则会减少树突点的数目(3.11±0.51)，而敲低Pcdh11x会增加树突点的数目(14.44±0.56)。通过Sholl分析发现过表达Pcdh11x时可减少树突终末分支的数目，而敲低Pcdh11x时可增加树突终末分支的数目。培养六天时，亦有相似结果。由此可见，过表达Pcdh11x可降低树突的复杂度，而抑制Pcdh11x的表达可增加树突的分支数量，增加其复杂度，因此，Pcdh11x蛋白负性调控小鼠体外培养的发育16 d胎脑源皮层神经元的的树突发育。 结论Pcdh11x蛋白抑制培养的皮层神经元一级、二级树突、树突点以及树突终末分支的发育。

Effects of Pcdh11x on the development of cortical neuronal dendritic branching

ObjectiveTo discuss the effects of Protocadherin 11 X-linked protein (Pcdh11x) on formation of neuronal dendritic branching. MethodsIn this study, using gain-of-function and loss-of-function studies, we count the number of neural dendritic branching, and analyzed the data with SPSS 13.0 software by one way ANOVA. ResultsCompared with the control GFP vector, Pcdh11x-shRNA increased, whereas pCAG-Pcdh11x-GFP decreased the number of primary and secondary dendrites. The number of dendritic tips was reduced in neurons overexpressing pCAG-Pcdh11x-GFP, whereas it was increased when Pcdh11x activity was inhibited by overexpression of Pcdh11x-shRNA. The effects of Pcdh11x-shRNA and pCAG-Pcdh11x-GFP on dendritic branching were confirmed by Sholl analysis. Therefore pcdh11x acts as a negtive regulator of dendritic branching in cultured cortical neurons from embryonic day 16 mouse embryos. ConclusionsPcdh11x Negatively Regulates Dendritic Branching, including primary dendrites, secondary dendrites, dendritic tips and crossing number.