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AP-3B-deficient mice and epilepsy Fubito Nakatsu 1 , Hiroshi Ohno 1,2 1Laboratory for Epithelial Immunobiology, RIKEN, RCAI 2Supramolecular Biology, International Graduate School of Arts and Sciences, Yokohama City University Keyword: アダプター(AP)複合体 , シナプス小胞 , 遺伝子欠損マウス pp.693-702
Published Date 2005/10/10
DOI https://doi.org/10.11477/mf.1431100086
  • Abstract
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To elucidate the role of neuron-specific AP-3B, we generated mice lacking μ3B, a subunit of AP-3B.μ3B-/- mice suffered from spontaneous epileptic seizures. Biochemical as well as morphological studies demonstrated the impairment ofγ-aminobutyric acid(GABA)release because of, at least in part, the reduction of vesicular GABA transporter(VGAT)in μ3B-/- mice, which caused facilitated induction of long-term potentiation(LTP)and abnormal propagation of neuronal excitability. Thus, μ3B plays an essential role in the efficient synaptic inhibition by regulating the formation and function of synaptic vesicles in vivo. This study adds a new aspect to the pathogenesis of epilepsy.


Copyright © 2005, Igaku-Shoin Ltd. All rights reserved.

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電子版ISSN 1882-1243 印刷版ISSN 0001-8724 医学書院

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