Laboratory of Neuroinformatics, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.
George Mason University, Department of Bioengineering and Krasnow Institute for Advanced Study, MS 2A1, Fairfax, VA, 22030-4444, United States.
Semin Cell Dev Biol. 2019 Nov;95:120-129. doi: 10.1016/j.semcdb.2019.01.006. Epub 2019 Jan 12.
Synaptic plasticity, the activity dependent change in synaptic strength, forms the molecular foundation of learning and memory. Synaptic plasticity includes structural changes, with spines changing their size to accomodate insertion and removal of postynaptic receptors, which are correlated with functional changes. Of particular relevance for memory storage are the long lasting forms of synaptic plasticity which are protein synthesis dependent. Due to the importance of spine structural plasticity and protein synthesis, this review focuses on the signaling pathways that connect synaptic stimulation with regulation of protein synthesis and remodeling of the actin cytoskeleton. We also review computational models that implement novel aspects of molecular signaling in synaptic plasticity, such as the role of neuromodulators and spatial microdomains, as well as highlight the need for computational models that connect activation of memory kinases with spine actin dynamics.
突触可塑性是指突触强度的活动依赖性变化，它构成了学习和记忆的分子基础。突触可塑性包括结构变化，即棘突改变其大小以适应突触后受体的插入和去除，这与功能变化相关。对于记忆存储特别相关的是依赖于蛋白质合成的长时程突触可塑性形式。由于棘突结构可塑性和蛋白质合成的重要性，本综述重点介绍了将突触刺激与蛋白质合成的调节和肌动蛋白细胞骨架的重塑联系起来的信号通路。我们还回顾了实现分子信号转导在突触可塑性中的新方面的计算模型，例如神经调质和空间微区的作用，以及强调需要将记忆激酶的激活与棘突肌动蛋白动力学联系起来的计算模型。
