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

نویسندگان

  • Takanobu Nakazawa
  • Shoji Komai
  • Ayako M Watabe
  • Yuji Kiyama
  • Masahiro Fukaya
  • Fumiko Arima-Yoshida
  • Reiko Horai
  • Katsuko Sudo
  • Kazumi Ebine
  • Mina Delawary
  • June Goto
  • Hisashi Umemori
  • Tohru Tezuka
  • Yoichiro Iwakura
  • Masahiko Watanabe
  • Tadashi Yamamoto
  • Toshiya Manabe
چکیده

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.

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عنوان ژورنال:
  • The EMBO journal

دوره 25 12  شماره 

صفحات  -

تاریخ انتشار 2006