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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Role of actin cytoskeleton in dendritic spine morphogenesis.
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Role of actin cytoskeleton in dendritic spine morphogenesis.

机译：肌动蛋白细胞骨架在树突棘形态发生中的作用。

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Dendritic spines are the postsynaptic receptive regions of most excitatory synapses, and their morphological plasticity play a pivotal role in higher brain functions, such as learning and memory. The dynamics of spine morphology is due to the actin cytoskeleton concentrated highly in spines. Filopodia, which are thin and headless protrusions, are thought to be precursors of dendritic spines. Drebrin, a spine-resident side-binding protein of filamentous actin (F-actin), is responsible for recruiting F-actin and PSD-95 into filopodia, and is suggested to govern spine morphogenesis. Interestingly, some recent studies on neurological disorders accompanied by cognitive deficits suggested that the loss of drebrin from dendritic spines is a common pathognomonic feature of synaptic dysfunction. In this review, to understand the importance of actin-binding proteins in spine morphogenesis, we first outline the well-established knowledge pertaining to the actin cytoskeleton in non-neuronal cells, such as the mechanism of regulation by small GTPases, the equilibrium between globular actin (G-actin) and F-actin, and the distinct roles of various actin-binding proteins. Then, we review the dynamic changes in the localization of drebrin during synaptogenesis and in response to glutamate receptor activation. Because side-binding proteins are located upstream of the regulatory pathway for actin organization via other actin-binding proteins, we discuss the significance of drebrin in the regulatory mechanism of spine morphology through the reorganization of the actin cytoskeleton. In addition, we discuss the possible involvement of an actin-myosin interaction in the morphological plasticity of spines.
机译：树突棘是大多数兴奋性突触的突触后受体区域，它们的形态可塑性在较高的大脑功能（如学习和记忆）中起关键作用。脊柱形态的动态是由于肌动蛋白细胞骨架高度集中在脊柱中。细足的细小和无头的突起被认为是树突棘的前体。 Drebrin是丝状肌动蛋白（F-actin）的脊柱驻留侧结合蛋白，负责将F-actin和PSD-95募集到丝状伪足中，并建议用于控制脊柱形态发生。有趣的是，最近有关神经系统疾病并伴有认知缺陷的一些研究表明，树突棘中脑啡肽的丧失是突触功能障碍的常见病理特征。在这篇综述中，为了了解肌动蛋白结合蛋白在脊柱形态发生中的重要性，我们首先概述了与非神经元细胞中肌动蛋白细胞骨架有关的公认知识，例如小GTP酶的调控机制，球状体之间的平衡。肌动蛋白（G-actin）和F-actin，以及各种肌动蛋白结合蛋白的独特作用。然后，我们审查了突触发生过程中和响应谷氨酸受体激活过程中德雷布林的动态变化。由于侧结合蛋白位于通过其他肌动蛋白结合蛋白进行肌动蛋白组织的调控途径的上游，因此我们讨论了肌动蛋白细胞骨架的重组，从而使drebrin在脊柱形态调控机制中的重要性。另外，我们讨论了肌动蛋白-肌球蛋白相互作用可能与棘突的形态可塑性有关。

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