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Learning and Long-term Memory

開催日 2014/9/11
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

NR2B-dependent neural plastic changes constitute the initial step of juvenile learning

  • P1-267
  • 中森 智啓 / Tomoharu Nakamori:1,2,3,4 佐藤 勝重 / Katsushige Sato:4 木下 雅恵 / Masae Kinoshita:5 田中 光一 / Kohichi Tanaka:6 浜崎 浩子 / Hiroko Ohki-Hamazaki:1 
  • 1:北里大・教・生物 / College of Liberal Arts and Sciences, Kitasato University, Kanagawa, Japan 2:学振特別研究員 / JSPS Fellows, Tokyo, Japan 3:北里大・医・解剖 / Department of Anatomy, Kitasato University School of Medicine, Kanagawa, Japan 4:駒沢女子大・健康栄養 / Department of Health and Nutrition Sciences, Komazawa Women's University, Tokyo, Japan 5:理研BSI・発生遺伝子制御 / Laboratory for Developmental Gene Regulation, RIKEN Brain Science Institute, Saitama, Japan 6:東京医科歯科・分子神経 / Laboratory of Molecular Neuroscience, Tokyo Medical and Dental University, Tokyo, Japan 

Since learning in infancy has high efficiency, it could occur by a neural mechanism different from learning in adult. Imprinting behavior in birds is one of the suitable models to investigate the neural basis of juvenile learning. In imprinting behavior, the ability of learning is limited from the first to 4 days after hatching in chicks. This developmental stage is the critical period or sensitive period of imprinting behavior. During this critical period, the neural activity and NR2B expression are high in a telencephalic circuit which is responsible for the process of visual imprinting. When the expression of NR2B was suppressed in this neural circuit by RNA interference using shRNA, imprinting was inhibited. On the other hand, when NR2B-containing NMDA receptors (NR2B/NR1) expression was temporary enhanced at synaptic surface by treatment with a casein kinase 2 inhibitor, chicks could be imprinted by a shorter training. In imprinted chick, synaptic current and cell surface expression of AMPA receptors and NR2B/NR1 were upregulated in the cells constituting the telencephalic circuit of imprinting. Enhancement of surface NR2B/NR1 expression could be induced even by the shorter training which is too weak to imprint chicks. Moreover, activation of NR2B/NR1 mediated its own expression on the neural surface, through degradation of synaptic p35 molecules. These results indicate that NR2B dependent neural plastic changes lead to an efficient learning characteristic of juvenile period. Now we are pursuing the neural mechanism which enables developmental changes of NR2B expression.

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