S-nitrosylation of N-ethylmaleimide sensitive factor mediates surface expression of AMPA receptors

Yunfei Huang, Heng Ye Man, Yoko Sekine-Aizawa, Yefei Han, Krishna Juluri, Hongbo Luo, Jaime Cheah, Charles Lowenstein, Richard L. Huganir, Solomon H. Snyder

Research output: Contribution to journalArticlepeer-review

Abstract

Postsynaptic AMPA receptor (AMPAR) trafficking mediates some forms of synaptic plasticity that are modulated by NMDA receptor (NMDAR) activation and N-ethylmaleimide sensitive factor (NSF). We report that NSF is physiologically S-nitrosylated by endogenous, neuronally derived nitric oxide (NO). S-nitrosylation of NSF augments its binding to the AMPAR GluR2 subunit. Surface insertion of GluR2 in response to activation of synaptic NMDARs requires endogenous NO, acting selectively upon the binding of NSF to GluR2. Thus, AMPAR recycling elicited by NMDA neurotransmission is mediated by a cascade involving NMDA activation of neuronal NO synthase to form NO, leading to S-nitrosylation of NSF which is thereby activated, enabling it to bind to GluR2 and promote the receptor's surface expression.

Original languageEnglish (US)
Pages (from-to)533-540
Number of pages8
JournalNeuron
Volume46
Issue number4
DOIs
StatePublished - May 19 2005

ASJC Scopus subject areas

  • Neuroscience(all)

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