Irie Fumitoshi, Yamaguchi Yu
The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA.
Front Biosci. 2004 May 1;9:1365-73. doi: 10.2741/1325.
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.
树突棘是树突表面的小的球状突起，是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。在一些神经疾病如智力迟钝和精神分裂症中观察到棘突的形态异常（4）。因此，对树突棘形态调节的研究可能与我们对高等脑功能的分子机制和神经疾病病理生理学的理解密切相关。在这里，我们综述了细胞表面硫酸乙酰肝素蛋白聚糖syndecan-2和ephrin-Eph信号在树突棘发育中的作用的最新进展。这些新进展的信息提示了一个模型，其中细胞表面ephrin-Eph信号诱导syndecan-2的聚集和细胞质分子的募集，这通过Rho家族GTP酶、N-WASP和Arp2/3复合物导致局部肌动蛋白聚合。
