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神经元成熟和突触可塑性中的树突棘肌动蛋白动力学

Dendritic spine actin dynamics in neuronal maturation and synaptic plasticity.

作者信息

Hlushchenko Iryna, Koskinen Mikko, Hotulainen Pirta

机构信息

Neuroscience Center, University of Helsinki, Helsinki, Finland.

Minerva Foundation Institute for Medical Research, Helsinki, Finland.

出版信息

Cytoskeleton (Hoboken). 2016 Sep;73(9):435-41. doi: 10.1002/cm.21280. Epub 2016 Mar 4.

DOI:10.1002/cm.21280
PMID:26849484
Abstract

The majority of the postsynaptic terminals of excitatory synapses in the central nervous system exist on small bulbous structures on dendrites known as dendritic spines. The actin cytoskeleton is a structural element underlying the proper development and morphology of dendritic spines. Synaptic activity patterns rapidly change actin dynamics, leading to morphological changes in dendritic spines. In this mini-review, we will discuss recent findings on neuronal maturation and synaptic plasticity-induced changes in the dendritic spine actin cytoskeleton. We propose that actin dynamics in dendritic spines decrease through actin filament crosslinking during neuronal maturation. In long-term potentiation, we evaluate the model of fast breakdown of actin filaments through severing and rebuilding through polymerization and later stabilization through crosslinking. We will discuss the role of Ca(2+) in long-term depression, and suggest that actin filaments are dissolved through actin filament severing. © 2016 Wiley Periodicals, Inc.

摘要

中枢神经系统中兴奋性突触的大多数突触后终末存在于树突上被称为树突棘的小球状结构上。肌动蛋白细胞骨架是树突棘正常发育和形态的基础结构元件。突触活动模式迅速改变肌动蛋白动力学,导致树突棘的形态变化。在这篇小型综述中,我们将讨论关于神经元成熟和突触可塑性诱导的树突棘肌动蛋白细胞骨架变化的最新发现。我们提出,在神经元成熟过程中,树突棘中的肌动蛋白动力学通过肌动蛋白丝交联而降低。在长时程增强中,我们评估了通过切断使肌动蛋白丝快速分解、通过聚合重建以及随后通过交联稳定的模型。我们将讨论Ca(2+)在长时程抑制中的作用,并提出肌动蛋白丝通过肌动蛋白丝切断而溶解。© 2016威利期刊公司。

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