S-nitrosylation of AMPA receptor GluA1 regulates phosphorylation, single-channel conductance, and endocytosis

被引:74
|
作者
Selvakumar, Balakrishnan [1 ]
Jenkins, Meagan A. [5 ]
Hussain, Natasha K. [1 ]
Huganir, Richard L. [1 ,4 ]
Traynelis, Stephen F. [5 ]
Snyder, Solomon H. [1 ,2 ,3 ]
机构
[1] Johns Hopkins Univ, Sch Med, Solomon H Snyder Dept Neurosci, Baltimore, MD 21205 USA
[2] Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA
[3] Johns Hopkins Univ, Sch Med, Dept Pharmacol & Mol Sci, Baltimore, MD 21205 USA
[4] Johns Hopkins Univ, Sch Med, Howard Hughes Med Inst, Baltimore, MD 21205 USA
[5] Emory Univ, Sch Med, Dept Pharmacol, Atlanta, GA 30322 USA
关键词
LONG-TERM POTENTIATION; PROTEIN-KINASE-II; NITRIC-OXIDE; GLUTAMATE RECEPTORS; SYNAPTIC PLASTICITY; MEDIATED TRANSMISSION; SURFACE EXPRESSION; ENDOTHELIAL-CELLS; GLUR1; SUBUNIT; C ACTIVITY;
D O I
10.1073/pnas.1221295110
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
NMDA receptor activation can elicit synaptic plasticity by augmenting conductance of the AMPA receptor GluA1 subsequent to phosphorylation at S831 by Ca2+-dependent kinases. NMDA receptor activation also regulates synaptic plasticity by causing endocytosis of AMPA receptor GluA1. We demonstrate a unique signaling cascade for these processes mediated by NMDA receptor-dependent NO formation and GluA1 S-nitrosylation. Thus, S-nitrosylation of GluA1 at C875 enhances S831 phosphorylation, facilitates the associated AMPA receptor conductance increase, and results in endocytosis by increasing receptor binding to the AP2 protein of the endocytotic machinery.
引用
收藏
页码:1077 / 1082
页数:6
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