ナカヤマ ヒサコ
Hisako Nakayama
中山 寿子 所属 医学部 医学科 職種 准教授 |
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論文種別 | 総説 |
言語種別 | 英語 |
査読の有無 | 査読あり |
表題 | Calcium-dependent regulation of climbing fibre synapse elimination during postnatal cerebellar development. |
掲載誌名 | 正式名:The Journal of physiology 略 称:J Physiol ISSNコード:00223751/14697793 |
掲載区分 | 国外 |
巻・号・頁 | 591(13),pp.3151-3158 |
著者・共著者 | KANO Masanobu†, NAKAYAMA Hisako, HASHIMOTO Kouichi, KITAMURA Kazuo, SAKIMURA Kenji, WATANABE Masahiko* |
担当区分 | 2nd著者 |
発行年月 | 2013/07 |
概要 | Functional neural circuit formation during postnatal development involves massive elimination of early-formed redundant synapses and strengthening of necessary synaptic connections. In the cerebellum, one-to-one connection from a climbing fibre (CF) to a Purkinje cell (PC) is established through four distinct phases: (1) strengthening of a single CF among multiple CFs in each PC at postnatal age P3–P7 days, (2) translocation of a single strengthened CF to PC dendrites from around P9, (3) early-phase (P7 to around P11) and (4) late-phase (around P12–P17) elimination of weak CF synapses from PC somata. Mice with PC-selective deletion of the P/Q-type voltage-dependent Ca2+ channel (VDCC) exhibit severe defects in strengthening of single CFs, dendritic translocation of single CFs and CF elimination from P7. In contrast, mice with a mutation of a single allele for the GABA synthesizing enzyme GAD67 show selective impairment of CF elimination from P10. Electrophysiological and Ca2+ imaging data suggest that GABAA receptor-mediated inhibition onto PC somata from putative basket cells influences CF-induced Ca2+ transients and regulates elimination of redundant CF synapses from PC somata at P10–P16. Thus, regulation of Ca2+ influx to PCs through VDCCs is crucial for the four phases of CF synapse elimination during postnatal development. |
DOI | 10.1113/jphysiol.2012.248252. |
PMID | 23359672 |