Department of Cell Biology and Physiology, and Neuroscience Center, University of North Carolina, Chapel Hill, NC 27514, USA.
Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Kavli Neuroscience Discovery Institute, Johns Hopkins University, Baltimore, MD 21205, USA.
Neuron. 2018 Oct 24;100(2):314-329. doi: 10.1016/j.neuron.2018.10.018.
Changes in the properties and postsynaptic abundance of AMPA-type glutamate receptors (AMPARs) are major mechanisms underlying various forms of synaptic plasticity, including long-term potentiation (LTP), long-term depression (LTD), and homeostatic scaling. The function and the trafficking of AMPARs to and from synapses is modulated by specific AMPAR GluA1-GluA4 subunits, subunit-specific protein interactors, auxiliary subunits, and posttranslational modifications. Layers of regulation are added to AMPAR tetramers through these different interactions and modifications, increasing the computational power of synapses. Here we review the reliance of synaptic plasticity on AMPAR variants and propose "the AMPAR code" as a conceptual framework. The AMPAR code suggests that AMPAR variants will be predictive of the types and extent of synaptic plasticity that can occur and that a hierarchy exists such that certain AMPARs will be disproportionally recruited to synapses during LTP/homeostatic scaling up, or removed during LTD/homeostatic scaling down.
AMPA 型谷氨酸受体 (AMPAR) 的特性和突触后丰度的变化是各种形式的突触可塑性的主要机制，包括长时程增强 (LTP)、长时程抑制 (LTD) 和同型稳态缩放。AMPAR 到突触和从突触的功能和运输是由特定的 AMPAR GluA1-GluA4 亚基、亚基特异性蛋白相互作用物、辅助亚基和翻译后修饰来调节的。通过这些不同的相互作用和修饰，AMPAR 四聚体增加了一层调节，从而增加了突触的计算能力。在这里，我们回顾了突触可塑性对 AMPAR 变体的依赖，并提出了“AMPAR 密码”作为一个概念框架。AMPAR 密码表明，AMPAR 变体将可预测可能发生的突触可塑性的类型和程度，并且存在一种层次结构，使得某些 AMPAR 在 LTP/同型稳态放大期间不成比例地被募集到突触，或者在 LTD/同型稳态缩小期间被去除。
