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本文引用的文献

1
Extracellular matrix and perineuronal nets in CNS repair.细胞外基质与中枢神经系统修复中的神经周细胞网络
Dev Neurobiol. 2011 Nov;71(11):1073-89. doi: 10.1002/dneu.20974.
2
Influence of matrix metalloproteinase MMP-9 on dendritic spine morphology.基质金属蛋白酶 MMP-9 对树突棘形态的影响。
J Cell Sci. 2011 Oct 1;124(Pt 19):3369-80. doi: 10.1242/jcs.090852. Epub 2011 Sep 6.
3
Extracellular matrix molecules, their receptors, and secreted proteases in synaptic plasticity.细胞外基质分子、其受体和分泌的蛋白酶在突触可塑性中的作用。
Dev Neurobiol. 2011 Nov;71(11):1040-53. doi: 10.1002/dneu.20958.
4
Role of extracellular matrix proteins and their receptors in the development of the vertebrate neuromuscular junction.细胞外基质蛋白及其受体在脊椎动物神经肌肉接头发育中的作用。
Dev Neurobiol. 2011 Nov;71(11):982-1005. doi: 10.1002/dneu.20953.
5
Glutamate induces de novo growth of functional spines in developing cortex.谷氨酸诱导发育皮层中的新功能性棘突生长。
Nature. 2011 Jun 2;474(7349):100-4. doi: 10.1038/nature09986. Epub 2011 May 8.
6
Reduced spine density in specific regions of CA1 pyramidal neurons in two transgenic mouse models of Alzheimer's disease.阿尔茨海默病两种转基因小鼠模型中海马 CA1 锥体神经元特定区域的脊柱密度降低。
J Neurosci. 2011 Mar 9;31(10):3926-34. doi: 10.1523/JNEUROSCI.6142-10.2011.
7
Differential interactions of cerebellin precursor protein (Cbln) subtypes and neurexin variants for synapse formation of cortical neurons.小脑蛋白前体(Cbln)亚型与神经连接蛋白变异体在皮质神经元突触形成中的差异相互作用。
Biochem Biophys Res Commun. 2011 Mar 25;406(4):627-32. doi: 10.1016/j.bbrc.2011.02.108. Epub 2011 Feb 26.
8
A role for thrombospondin-1 deficits in astrocyte-mediated spine and synaptic pathology in Down's syndrome.唐氏综合征中天冬酰胺酶-1 缺陷在星形胶质细胞介导的脊柱和突触病变中的作用。
PLoS One. 2010 Dec 2;5(12):e14200. doi: 10.1371/journal.pone.0014200.
9
Multiple events lead to dendritic spine loss in triple transgenic Alzheimer's disease mice.多种事件导致三转基因阿尔茨海默病小鼠树突棘丢失。
PLoS One. 2010 Nov 16;5(11):e15477. doi: 10.1371/journal.pone.0015477.
10
The dual role of the extracellular matrix in synaptic plasticity and homeostasis.细胞外基质在突触可塑性和动态平衡中的双重作用。
Nat Rev Neurosci. 2010 Nov;11(11):735-46. doi: 10.1038/nrn2898. Epub 2010 Oct 14.

在树突棘上撒网:细胞外基质及其受体。

Casting a net on dendritic spines: the extracellular matrix and its receptors.

机构信息

Division of Biomedical Sciences, Biochemistry and Molecular Biology Program, University of California Riverside, Riverside, California 92521, USA.

出版信息

Dev Neurobiol. 2011 Nov;71(11):956-81. doi: 10.1002/dneu.20963.

DOI:10.1002/dneu.20963
PMID:21834084
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3192312/
Abstract

Dendritic spines are dynamic structures that accommodate the majority of excitatory synapses in the brain and are influenced by extracellular signals from presynaptic neurons, glial cells, and the extracellular matrix (ECM). The ECM surrounds dendritic spines and extends into the synaptic cleft, maintaining synapse integrity as well as mediating trans-synaptic communications between neurons. Several scaffolding proteins and glycans that compose the ECM form a lattice-like network, which serves as an attractive ground for various secreted glycoproteins, lectins, growth factors, and enzymes. ECM components can control dendritic spines through the interactions with their specific receptors or by influencing the functions of other synaptic proteins. In this review, we focus on ECM components and their receptors that regulate dendritic spine development and plasticity in the normal and diseased brain.

摘要

树突棘是大脑中容纳大多数兴奋性突触的动态结构,受来自突触前神经元、神经胶质细胞和细胞外基质(ECM)的细胞外信号的影响。ECM 环绕树突棘并延伸到突触间隙,维持突触的完整性,并介导神经元之间的突触间通讯。构成 ECM 的几种支架蛋白和聚糖形成晶格状网络,为各种分泌糖蛋白、凝集素、生长因子和酶提供了一个有吸引力的基础。ECM 成分可以通过与特定受体的相互作用或通过影响其他突触蛋白的功能来控制树突棘。在这篇综述中,我们重点介绍 ECM 成分及其受体,它们调节正常和患病大脑中的树突棘发育和可塑性。