The AMPA Receptor Code of Synaptic Plasticity

被引：623

作者：

Diering, Graham H. ^{[1
,2
]}

Huganir, Richard L. ^{[3
,4
]}

机构：

[1] Univ N Carolina, Dept Cell Biol & Physiol, Chapel Hill, NC 27514 USA

[2] Univ N Carolina, Neurosci Ctr, Chapel Hill, NC 27514 USA

[3] Johns Hopkins Univ, Sch Med, Solomon H Snyder Dept Neurosci, Baltimore, MD 21205 USA

[4] Johns Hopkins Univ, Kavli Neurosci Discovery Inst, Baltimore, MD 21205 USA

来源：

NEURON | 2018年 / 100卷 / 02期

关键词：

LONG-TERM DEPRESSION; DOMAIN-CONTAINING PROTEINS; GLUTAMATE-RECEPTOR; GLUR1; SUBUNIT; TYROSINE-PHOSPHORYLATION; KINASE-II; AUXILIARY SUBUNITS; IN-VIVO; REGULATORY PHOSPHORYLATION; HIPPOCAMPAL SYNAPSES;

D O I：

10.1016/j.neuron.2018.10.018

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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.

引用

页码：314 / 329

页数：16

共 150 条

[101] CaMKII Phosphorylation of TARPγ-8 Is a Mediator of LTP and Learning and Memory [J].