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Synaptic Plasticity

開催日 2014/9/13
時間 17:10 - 18:10
会場 Room J(313+314)
Chairperson(s) 竹本 さやか / Sayaka Takemoto-Kimu (東京大学大学院医学系研究科 神経生化学教室 / Department of Neurochemistry, Graduate School of Medicine, University of Tokyo, Japan)
安部 健太郎 / Kentaro Abe (京都大学大学院医学研究科 生体情報科学講座 / Department of Biological Sciences, Graduate School of Medecine, Kyoto University, Japan)

Glucose increased during food intake facilitates brain plasticity

  • O3-J-5-4
  • 大村 裕 / Yutaka Oomura:1 粟生 修司 / Shuji Aou:2 片渕 俊彦 / Toshihiko Katafuchi:1 Hosssain Shamin M / Shamin M Hosssain:1 森口 茂樹 / Shigeki Moriguchi:3 福永 浩司 / Kouji Fukunaga:3 
  • 1:九州大院・医・統合生理 / Dept. Integr. Physi., Grad. Sch. Med. Sci., Kyushu Univ., Japan 2:九州工業大院・生命体工学 / Dept Human Intellig Syst, Grad Sch Life Sci Systems Engineer, Kyushu Inst Tech, Kitakyushu, Japan  3:東北大院・薬・薬理 / Dept Pharmacol, Grad Sch Pharmacy, Tohoku Univ, Sendai, Japan 

Glucose concentration increases twice (from 2 to 4 mM) in the brain during food intake. The amplitude of CA1 synaptic potentials in vitro increased greatly and continued for more than 40 min, when 3.5 mM glucose was changed to 7 mM for 15 min. On the augmentation of synaptic potentials, presynaptic transmitter release on CA1 neurons was facilitated, when this was measured by the paired pulse facilitation method. On postsynaptic responses in CA1 neurons by NMDA, AMPA and GABA, NMDA and AMPA responses were augmented. Neurochemically, when the glucose concentration was increased, (i) phosphorylation of presynaptic synapsin I (site III) was facilitated. (ii) Phosphorylation of postsynaptic CaMKII α, β, PKA α, ERK and GluR1 were facilitated. (iii) Phosphorylation of AKT and CREB was facilitated. BDNF (brain derived neurotrophic factor) was increased by glucose treatments in neuronal cell line (Neuro-2A). This increase in BDNF was mediated by CREB (cyclic-AMP response element binding protein). Spatial learning and memory was facilitated when the glucose concentration was increased to 7mM by an intra-hippocampal glucose injection. These findings demonstrate glucose increased during food intake facilitates hippocampal neuronal plasticity via presynaptic and postsynaptic mechanisms to enhance spatial memory and learning which may be beneficial to remember food rich places.

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