@article{oai:kanazawa-u.repo.nii.ac.jp:00011067,
 author = {Nakatsu, Fubito and Okada, Motohiro and Mori, Fumiaki and Kumazawa, Noriko and Iwasa, Hiroto and Zhu, Gang and Kasagi, Yasufumi and Kamiya, Haruyuki and Harada, Akihiro and Nishimura, Kazuhiro and Takeuchi, Arata and Miyazaki, Taisuke and Watanabe, Masahiko and Yusasa, Shigeki and Manabe, Toshiya and Wakabayashi, Koichi and Kaneko, Sunao and Saito, Takashi and Ohno, Hiroshi},
 issue = {2},
 journal = {Journal of Cell Biology},
 month = {Oct},
 note = {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., 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},
 pages = {293--373},
 title = {Defective function of GABA-containing synaptic vesicles in mice lacking the AP-3B clathrin adaptor},
 volume = {167},
 year = {2004}
}