美国佛罗里达大学斯克利普斯研究所的科学家发现了一条对长期记忆形成起关键作用的机制。这个发现不仅阐明了记忆是如何形成的，也有助于发展记忆障碍性疾病治疗的新途径。研究结果发表在《Neuron》杂志上。
在研究中科学家们发现了一个记忆形成的主要驱动子myosin II，它是细胞移动和生长的一个关键动力蛋白。“我们第一次证实了myosin II在记忆形成中发挥主要作用，我们也接近于确定导致这个大脑动力蛋白激活的信号途径。”佛罗里达大学斯克利普斯研究所该项研究的负责人Gavin Rumbaugh说：“一旦我们找到关键的信号途径，我们将开始致力开发有效的治疗方法帮助那些存在认知障碍的人们比如阿尔兹海默病的患者恢复记忆。”
Rumbaugh和他的同事们证实myosin II在记忆形成复杂过程中发挥调控作用。myosin II与长时程增强效应启动相关,启动长时程增强效可增强神经元之间的信号传递，稳定神经元突触可塑性以及重组神经元F-actin。
对大脑的刺激激活了了这些myosin动力蛋白，启动了F-actin的生长最后稳定了长时程增强效应。”Rumbaugh说：“大脑记录我们经历的过程就是突触生长和强化的过程。我们现在了解到突触间的物质使得我们的生命经历得以储存下来。”
他在研究中补充说明了F-actin的作用。长时程增强效应依赖于突触结构的改变表明myosinII启动的动态重组是信息编码的早期步骤。
“许多并行大脑处理过程被激活参与信息储存。如果他们中的任何一个被破坏，信息就会失去稳定，记忆就会丧失。myosinII是这个过程的关键调控因子，如果你能通过药物控制myosin II，你就能随意有效地控制记忆。”Rumbaugh说。
推荐原文出处：
Neuron doi：10.1016/j.neuron.2010.07.016
Myosin IIb Regulates Actin Dynamics during Synaptic Plasticity and Memory Formation
Christopher S. Rex, Cristin F. Gavin, Maria D. Rubio, Eniko A. Kramar, Lulu Y. Chen, Yousheng Jia, Richard L. Huganir, Nicholas Muzyczka, Christine M. Gall, Courtney A. Miller, Gary Lynch, Gavin Rumbaugh
Highlights
Defines a mechanical process controlling F-actin reorganization at synapses
Myosin II motor activity is engaged by LTP induction
Myosin II activity produces de novo actin filaments at synapses that maintain LTP
Myosin II activity regulates actin polymerization that supports memory formation
Summary
Reorganization of the actin cytoskeleton is essential for synaptic plasticity and memory formation. Presently, the mechanisms that trigger actin dynamics during these brain processes are poorly understood. In this study, we show that myosin II motor activity is downstream of LTP induction and is necessary for the emergence of specialized actin structures that stabilize an early phase of LTP. We also demonstrate that myosin II activity contributes importantly to an actin-dependent process that underlies memory consolidation. Pharmacological treatments that promote actin polymerization reversed the effects of a myosin II inhibitor on LTP and memory. We conclude that myosin II motors regulate plasticity by imparting mechanical forces onto the spine actin cytoskeleton in response to synaptic stimulation. These cytoskeletal forces trigger the emergence of actin structures that stabilize synaptic plasticity. Our studies provide a mechanical framework for understanding cytoskeletal dynamics associated with synaptic plasticity and memory formation.
