Georges Penelope C, Hadzimichalis Norell M, Sweet Eric S, Firestein Bonnie L
Department of Cell Biology and Neuroscience, Rutgers, The State University of New Jersey, 604 Allison Road, Piscataway, NJ 08854-8082, USA.
Mol Neurobiol. 2008 Dec;38(3):270-84. doi: 10.1007/s12035-008-8046-8. Epub 2008 Nov 6.
Actin and microtubules (MT) are targets of numerous molecular pathways that control neurite outgrowth. To generate a neuronal protrusion, coordinated structural changes of the actin and MT cytoskeletons must occur. Neurite formation occurs when actin filaments (F-actin) are destabilized, filopodia are extended, and MTs invade filopodia. This process results in either axon or dendrite formation. Axonal branching involves interplay between F-actin and MTs, with F-actin and MTs influencing polymerization, stabilization, and maintenance of each other. Our knowledge of the mechanisms regulating development of the axon, however, far eclipses our understanding of dendritic development and branching. The two classes of neurites, while fundamentally similar in their ability to elongate and branch, dramatically differ in growth rate, orientation of polarized MT bundles, and mechanisms that initiate branching. In this review, we focus on how F-actin, MTs, and proteins that link the two cytoskeletons coordinate to specifically initiate dendritic events.
肌动蛋白和微管（MT）是众多控制神经突生长的分子途径的靶点。为了产生神经元突起，肌动蛋白和微管细胞骨架必须发生协调的结构变化。当肌动蛋白丝（F-肌动蛋白）不稳定、丝状伪足延伸且微管侵入丝状伪足时，神经突形成。这个过程导致轴突或树突的形成。轴突分支涉及F-肌动蛋白和微管之间的相互作用，F-肌动蛋白和微管相互影响彼此的聚合、稳定和维持。然而，我们对调节轴突发育机制的了解远远超过我们对树突发育和分支的理解。这两类神经突虽然在伸长和分支能力上基本相似，但在生长速度、极化微管束的方向以及启动分支的机制方面有显著差异。在这篇综述中，我们重点关注F-肌动蛋白、微管以及连接这两种细胞骨架的蛋白质如何协调以特异性地启动树突相关事件。
