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Defective function of GABA-containing synaptic vesicles in mice lacking the AP-3B clathrin adaptor
http://hdl.handle.net/2297/11853
http://hdl.handle.net/2297/118530ece70a9-2812-4106-8b50-133b6ea4c64e
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
NS-PR-OHNO-M-293.pdf (421.3 kB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2017-10-03 | |||||
| タイトル | ||||||
| タイトル | Defective function of GABA-containing synaptic vesicles in mice lacking the AP-3B clathrin adaptor | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| 著者 |
Nakatsu, Fubito
× Nakatsu, Fubito× Okada, Motohiro× Mori, Fumiaki× Kumazawa, Noriko× Iwasa, Hiroto× Zhu, Gang× Kasagi, Yasufumi× Kamiya, Haruyuki× Harada, Akihiro× Nishimura, Kazuhiro× Takeuchi, Arata× Miyazaki, Taisuke× Watanabe, Masahiko× Yusasa, Shigeki× Manabe, Toshiya× Wakabayashi, Koichi× Kaneko, Sunao× Saito, Takashi× Ohno, Hiroshi |
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| 提供者所属 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | 金沢大学自然科学研究科 理化学研究所・横浜研究所 免疫アレルギー科学総合研究センター(RCAI) 横浜市立大学大学院国際総合科学研究科生体超分子科学専攻 客員教授 | |||||
| 書誌情報 |
Journal of Cell Biology 巻 167, 号 2, p. 293-373, 発行日 2004-10-25 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 0021-9525 | |||||
| NCID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA00694812 | |||||
| DOI | ||||||
| 関連タイプ | isIdenticalTo | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.1083/jcb.200405032 | |||||
| 出版者 | ||||||
| 出版者 | Rockefeller University Press | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | AP-3 is a member of the adaptor protein (AP) complex family that regulates the vesicular transport of cargo proteins in the secretory and endocytic pathways. There are two isoforms of AP-3: the ubiquitously expressed AP-3A and the neuron-specific AP-3B. Although the physiological role of AP-3A has recently been elucidated, that of AP-3B remains unsolved. To address this question, we generated mice lacking μ3B, a subunit of AP-3B. μ3B-/- mice suffered from spontaneous epileptic seizures. Morphological abnormalities were observed at synapses in these mice. Biochemical studies demonstrated the impairment of γ-aminobutyric acid (GABA) release because of, at least in part, the reduction of vesicular GABA transporter in μ3B-/- mice. This facilitated the induction of long-term potentiation in the hippocampus and the abnormal propagation of neuronal excitability via the temporoammonic pathway. Thus, AP-3B plays a critical role in the normal formation and function of a subset of synoptic vesicles. This work adds a new aspect to the pathogenesis of epilepsy. | |||||
| 著者版フラグ | ||||||
| 出版タイプ | VoR | |||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
