Department of Physiology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Adv Exp Med Biol. 2012;970:81-95. doi: 10.1007/978-3-7091-0932-8_4.
Spine morphogenesis is largely dependent on the remodeling of the actin cytoskeleton. Actin dynamics within spines is regulated by a complex network of signaling molecules, which relay signals from synaptic receptors, through small GTPases and their regulators, to actin-binding proteins. In this chapter, we will discuss molecules involved in dendritic spine plasticity beginning with actin and moving upstream toward neuromodulators and trophic factors that initiate signaling involved in these plasticity events. We will place special emphasis on small GTPase pathways, as they have an established importance in dendritic spine plasticity and pathology. Finally, we will discuss some epigenetic mechanisms that control spine morphogenesis.
脊柱形态发生在很大程度上依赖于肌动蛋白细胞骨架的重塑。脊柱内的肌动蛋白动力学受到信号分子的复杂网络调控，这些信号分子将来自突触受体的信号通过小 GTP 酶及其调节剂传递到肌动蛋白结合蛋白。在这一章中，我们将讨论参与树突棘可塑性的分子，从肌动蛋白开始，向上游移动到启动这些可塑性事件信号的神经调质和营养因子。我们将特别强调小 GTP 酶途径，因为它们在树突棘可塑性和病理学中具有重要的地位。最后，我们将讨论一些控制脊柱形态发生的表观遗传机制。
