肌球蛋白 IIb 在突触可塑性和记忆形成过程中调节肌动蛋白动力学。
Myosin IIb regulates actin dynamics during synaptic plasticity and memory formation.
机构信息
Department of Psychiatry and Human Behavior, University of California, Irvine, CA 92697, USA.
出版信息
Neuron. 2010 Aug 26;67(4):603-17. doi: 10.1016/j.neuron.2010.07.016.
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.
细胞骨架的重排对于突触可塑性和记忆形成至关重要。目前，这些大脑过程中触发肌动蛋白动力学的机制还知之甚少。在这项研究中，我们表明肌球蛋白 II 的运动活性是 LTP 诱导的下游事件，对于稳定 LTP 的早期阶段的特殊肌动蛋白结构的出现是必需的。我们还证明肌球蛋白 II 的活性对记忆巩固的一个依赖于肌动蛋白的过程有重要贡献。促进肌动蛋白聚合的药理学处理逆转了肌球蛋白 II 抑制剂对 LTP 和记忆的影响。我们的结论是，肌球蛋白 II 分子通过将机械力传递到突触刺激后的脊柱肌动蛋白细胞骨架来调节可塑性。这些细胞骨架力引发了稳定突触可塑性的肌动蛋白结构的出现。我们的研究为理解与突触可塑性和记忆形成相关的细胞骨架动力学提供了一个机械框架。
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