PMID:16710293

Citation	Nakazawa, T, Komai, S, Watabe, AM, Kiyama, Y, Fukaya, M, Arima-Yoshida, F, Horai, R, Sudo, K, Ebine, K, Delawary, M, Goto, J, Umemori, H, Tezuka, T, Iwakura, Y, Watanabe, M, Yamamoto, T and Manabe, T (2006) NR2B tyrosine phosphorylation modulates fear learning as well as amygdaloid synaptic plasticity. EMBO J. 25:2867-77
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.
Links	PubMed PMC1500840 Online version:10.1038/sj.emboj.7601156
Keywords	Amygdala/cytology; Amygdala/physiology; Amygdala/ultrastructure; Animals; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Calcium-Calmodulin-Dependent Protein Kinases/metabolism; Conditioning, Classical; Fear/physiology; Learning/physiology; Mice; Mutation/genetics; Neuronal Plasticity; Phosphorylation; Phosphotyrosine/metabolism; Protein Transport; Receptors, N-Methyl-D-Aspartate/metabolism; Receptors, N-Methyl-D-Aspartate/ultrastructure; Synapses/metabolism; Synaptic Transmission; Tetany
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