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開催日 2014/9/12
時間 14:00 - 15:00
会場 Poster / Exhibition(Event Hall B)

Homeostatic control of GABA synaptic structure by intracellular calcium

  • P2-030
  • 丹羽 史尋 / Fumihiro Niwa:1 坂内 博子 / Hiroko Bannai:1,2 Mark Sherwood W / Sherwood W Mark:1,5,6 有薗 美沙 / Misa Arizono:1,6,7 宮本 章歳 / Akitoshi Miyamoto:1 杉浦 琴美 / Kotomi Sugiura:1 Levi Sabine / Sabine Levi:3 Triller Antoine / Antoine Triller:4 御子柴 克彦 / Katsuhiko Mikoshiba:1 
  • 1:理研BSI発生神経生物 / Dev. Neurobiol, RIKEN BSI, Saitama, Japan 2:名古屋大院理生命理学 / Dept. Biol. Sci. Nagoya Univ, Aichi, Japan 3:IFM, Paris, France / IFM, Paris, France 4:IBENS, Paris, France / IBENS, Paris, France 5:Inserm U862, Neurocentre Magendie, Bordeaux, France / Inserm U862, Neurocentre Magendie, Bordeaux, France 6:Universite de Bordeaux, Bordeaux, France / Universite de Bordeaux, Bordeaux, France 7:IINS, CNRS UMR 5297, Bordeaux, France / IINS, CNRS UMR 5297, Bordeaux, France 

The regulation of excitation and inhibition balance is indispensible for nervous systems. In neurons, excitatory transmission via ionotopic glutamate receptor-dependent calcium signaling exerts negative control of inhibitory transmission by lateral dispersion of synaptic GABAAR receptor clusters. However, the opposing process for the recovery and stability of inhibition remains unknown. Here, we characterize a homeostatic mechanism that promotes the positive control of inhibitory synaptic structure and transmission. Impairment of slow metabotropic glutamate receptor signaling and IP3 receptor dependent intracellular calcium release resulted in the dispersion of GABAAR synaptic clustering and efficacy. This dispersion was due to lateral diffusion and synaptic escape of GABAARs, and dependent on protein kinase C, and opposed the NMDAR dependent activation of calcineurin for receptor dispersion. These findings show that distinct glutamate receptor signaling pathways activate competing calcium signals to enable dynamic control of the stability and efficacy of inhibitory synapses. This pathway may contribute to the recovery of pathogenic imbalances in transmission.

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