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中华神经创伤外科电子杂志 ›› 2016, Vol. 02 ›› Issue (02) : 89 -93. doi: 10.3877/cma.j.issn.2095-9141.2016.02.007

所属专题: 文献

基础研究

Pcdh11x蛋白对体外培养皮层神经元树突发育的影响
吴翠莹1, 张鹏1, 牛力军1, 陶庆霞1, 刘宁1, 王翀1, 徐如祥1,()   
  1. 1. 100700 北京,北京军区总医院附属八一脑科医院
  • 收稿日期:2016-02-04 出版日期:2016-04-15
  • 通信作者: 徐如祥
  • 基金资助:
    国家自然科学基金青年项目(81401031)

Effects of Pcdh11x on the development of cortical neuronal dendritic branching

Cuiying Wu1, Peng Zhang1, Lijun Niu1, Qingxia Tao1, Ning Liu1, Chong Wang1, Ruxiang Xu1,()   

  1. 1. Affiliated Bayi Brain Hospital, The Military General Hospital of Beijing PLA, Beijing 100700, China
  • Received:2016-02-04 Published:2016-04-15
  • Corresponding author: Ruxiang Xu
  • About author:
    Corresponding author: Xu Ruxiang, Email:
引用本文:

吴翠莹, 张鹏, 牛力军, 陶庆霞, 刘宁, 王翀, 徐如祥. Pcdh11x蛋白对体外培养皮层神经元树突发育的影响[J]. 中华神经创伤外科电子杂志, 2016, 02(02): 89-93.

Cuiying Wu, Peng Zhang, Lijun Niu, Qingxia Tao, Ning Liu, Chong Wang, Ruxiang Xu. Effects of Pcdh11x on the development of cortical neuronal dendritic branching[J]. Chinese Journal of Neurotraumatic Surgery(Electronic Edition), 2016, 02(02): 89-93.

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。

Objective

To discuss the effects of Protocadherin 11 X-linked protein (Pcdh11x) on formation of neuronal dendritic branching.

Methods

In 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.

Results

Compared 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.

Conclusions

Pcdh11x Negatively Regulates Dendritic Branching, including primary dendrites, secondary dendrites, dendritic tips and crossing number.

图1 皮层神经元发育过程中Pcdh11x蛋白的表达水平
图2 Pcdh11x蛋白对皮层神经元树突分支的影响(×63)
[1]
Hattori D,Millard SS,Wojtowicz WM, et al. Dscam-mediated cell recognition regulates neural circuit formation[J]. Annu Rev Cell Dev Biol, 2008, 24, 597-620.
[2]
RW Sperry. Chemoaffinity In The Orderly Growth Of Nerve Fiber Patterns And Connections[J]. Proc Natl Acad Sci U S A, 1963, 50, 703-710.
[3]
Zipursky JR,Sanes JR. Chemoaffinity revisited: dscams, protocadherins, and neural circuit assembly[J]. Cell, 2010, 143(3): 343-353.
[4]
Jan YN,Jan LY. Branching out: mechanisms of dendritic arborization[J]. Nat Rev Neurosci, 2010, 11(5): 316-328.
[5]
Branco T,Clark BA,Hausser M. Dendritic discrimination of temporal input sequences in cortical neurons[J]. Science, 2010, 329(5999): 1671-1675.
[6]
Branco T,Hausser M. Synaptic integration gradients in single cortical pyramidal cell dendrites[J]. Neuron, 2011, 69(5): 885-892.
[7]
Gidon A,Segev I. Principles governing the operation of synaptic inhibition in dendrites[J]. Neuron, 2012, 75(2): 330-341.
[8]
Hausser M,Spruston N,Stuart GJ. Diversity and dynamics of dendritic signaling[J]. Science, 2000, 290(5492): 739-744.
[9]
Lavzin M,Rapoport S,Polsky A, et al. Nonlinear dendritic processing determines angular tuning of barrel cortex neurons in vivo[J]. Nature, 2012, 490(7420): 397-401.
[10]
Parrish JZ,Emoto K,Kim MD, et al. Mechanisms that regulate establishment, maintenance, and remodeling of dendritic fields[J]. Annu Rev Neurosci, 2007, 30, 399-423.
[11]
Lin YC,Koleske AJ. Mechanisms of synapse and dendrite maintenance and their disruption in psychiatric and neurodegenerative disorders[J]. Annu Rev Neurosci, 2010, 33, 349-378.
[12]
Takeichi M. The cadherin superfamily in neuronal connections and interactions[J]. Nat Rev Neurosci, 2007, 8(1): 11-20.
[13]
Ye B,Jan YN. The cadherin superfamily and dendrite development[J]. Trends Cell Biol, 2005, 15(2): 64-67.
[14]
Yu X,Malenka RC. Beta-catenin is critical for dendritic morphogenesis[J]. Nat Neurosci, 2003, 6(11): 1169-1177.
[15]
Morishita H,Yagi T. Protocadherin family: diversity, structure, and function[J]. Curr Opin Cell Biol, 2007, 19(5): 584-592.
[16]
Suo L,Lu H,Ying G, et al. Protocadherin clusters and cell adhesion kinase regulate dendrite complexity through Rho GTPase[J]. J Mol Cell Biol, 2012, 4(6): 362-376.
[17]
Toyoda S,Kawaguchi M,Kobayashi T, et al. Developmental epigenetic modification regulates stochastic expression of clustered protocadherin genes, generating single neuron diversity[J]. Neuron, 2014, 82(1): 94-108.
[18]
Zhang P,Wu C,Liu N, et al. Protocadherin 11 x regulates differentiation and proliferation of neural stem cell in vitro and in vivo[J]. J Mol Neurosci, 2014, 54(2): 199-210.
[19]
Jaworski SJ,Spangler S,Seeburg DP, et al. Control of dendritic arborization by the phosphoinositide-3′-kinase-Akt-mammalian target of rapamycin pathway[J]. J Neurosci, 2005, 25(49): 11300-11312.
[20]
Sholl DA. Dendritic organization in the neurons of the visual and motor cortices of the cat[J]. J Anat, 1953, 87(4): 387-406.
[21]
Srinivasan Y,Elmer L,Davis J, et al. Ankyrin and spectrin associate with voltage-dependent sodium channels in brain[J]. Nature, 1988, 333(6169):177-180.
[22]
Zhou D. Lambert S, Malen PL. AnkyrinG is required for clustering of voltage-gated Na channels at axon initial segments and for normal action potential firing[J]. J Cell Biol, 1998, 143(5): 1295-1304.
[23]
A Ghysen. Dendritic arbors: a tale of living tiles[J]. Curr Biol, 2003, 13(11): R427-429.
[24]
T Yagi. Genetic basis of neuronal individuality in the mammalian brain[J]. J Neurogenet, 2013, 27(3): 97-105.
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