EPHB receptor signaling in dendritic spine development.
EPHB receptor signaling in dendritic spine development.
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DOI：
10.2741/1325
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发表时间：
2004-05
期刊：
影响因子：
--
通讯作者：
F. Irie;Yu Yamaguchi
中科院分区：
文献类型：
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作者：
F. Irie;Yu Yamaguchi
树突棘是树突表面的小球状突起，作为兴奋性突触的主要突触后靶点（1-3）。树突棘的结构修饰被认为是学习和记忆的细胞基础。在一些神经系统疾病中观察到脊柱的形态异常，如精神发育迟滞和精神分裂症（4）。因此，树突棘的形态调控的研究可能有很强的相关性，我们的理解更高的脑功能和神经系统疾病的病理生理学的分子机制。本文综述了细胞表面硫酸乙酰肝素蛋白聚糖syndecan-2和ephrin-Eph信号通路在树突棘发育中的作用。来自这些新发展的信息表明了一种模型，其中细胞表面肝配蛋白-Eph信号传导诱导多配体蛋白聚糖-2的聚集和细胞质分子的募集，这导致通过Rho家族GTP酶、N-WASP和Arp 2/3复合物的局部肌动蛋白聚合。
Dendritic spines are small bulbous protrusions on the surface of dendrites that serve as principle postsynaptic targets for excitatory synapses (1-3). Structural modifications of dendritic spines have been implicated as a cellular basis for learning and memory. Morphological abnormalities of spines are observed in some neurological diseases such as mental retardation and schizophrenia (4). Thus, studies on the morphological regulation of dendritic spines could have strong relevance to our understanding of the molecular mechanisms of the higher brain function and the pathophysiology of neurological disorders. Here we review recent progress on the role of the cell surface heparan sulfate proteoglycan syndecan-2 and ephrin-Eph signaling in dendritic spine development. Information from these new developments suggests a model in which cell surface ephrin-Eph signaling induces clustering of syndecan-2 and recruitment of cytoplasmic molecules, which leads to localized actin polymerization via Rho family GTPases, N-WASP, and the Arp2/3 complex.