Potentiation of synaptic AMPA receptors induced by the deletion of NMDA receptors requires the GluA2 subunit

Wei Lu, John Gray, Adam J. Granger, Matthew J. During, Roger A. Nicoll

Research output: Contribution to journalArticle

12 Scopus citations

Abstract

Deletion of N-methyl-D-aspartate receptors (NMDARs) early in development results in an increase in the number of synaptic AMPA receptors (AMPARs), suggesting a role for NMDARs in negatively regulating AMPAR trafficking at developing synapses. Substantial evidence has shown that AMPAR subunits function differentially in AMPAR trafficking. However, the role of AMPAR subunits in the enhancement of AMPARs following NMDAR ablation remains unknown. We have now performed single-cell genetic deletions in double-floxed mice in which the deletion of GluN1 is combined with the deletion of GluA1 or GluA2. We find that the AMPAR enhancement following NMDAR deletion requires the GluA2 subunit, but not the GluA1 subunit, indicating a key role for GluA2 in the regulation of AMPAR trafficking in developing synapses.

Original languageEnglish (US)
Pages (from-to)923-928
Number of pages6
JournalJournal of Neurophysiology
Volume105
Issue number2
DOIs
StatePublished - Feb 2011
Externally publishedYes

ASJC Scopus subject areas

  • Physiology
  • Neuroscience(all)

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