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EMBO J. 2006 Jun 21;25(12):2867-77. Epub 2006 May 18.

NR2B tyrosine phosphorylation modulates fear learning as well as amygdaloid synaptic plasticity.

Author information

  • 1Division of Oncology, Department of Cancer Biology, University of Tokyo, Tokyo, Japan.

Abstract

Phosphorylation of neural proteins in response to a diverse array of external stimuli is one of the main mechanisms underlying dynamic changes in neural circuitry. The NR2B subunit of the NMDA receptor is tyrosine-phosphorylated in the brain, with Tyr-1472 its major phosphorylation site. Here, we generate mice with a knockin mutation of the Tyr-1472 site to phenylalanine (Y1472F) and show that Tyr-1472 phosphorylation is essential for fear learning and amygdaloid synaptic plasticity. The knockin mice show impaired fear-related learning and reduced amygdaloid long-term potentiation. NMDA receptor-mediated CaMKII signaling is impaired in YF/YF mice. Electron microscopic analyses reveal that the Y1472F mutant of the NR2B subunit shows improper localization at synapses in the amygdala. We thus identify Tyr-1472 phosphorylation as a key mediator of fear learning and amygdaloid synaptic plasticity.

PMID:
16710293
[PubMed - indexed for MEDLINE]
PMCID:
PMC1500840
Free PMC Article
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