Hisako Nakayama
Department School of Medicine, School of Medicine Position Associate Professor |
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Article types | Review article |
Language | English |
Peer review | Peer reviewed |
Title | Calcium-dependent regulation of climbing fibre synapse elimination during postnatal cerebellar development. |
Journal | Formal name:The Journal of physiology Abbreviation:J Physiol ISSN code:00223751/14697793 |
Domestic / Foregin | Foregin |
Volume, Issue, Page | 591(13),pp.3151-3158 |
Author and coauthor | KANO Masanobu†, NAKAYAMA Hisako, HASHIMOTO Kouichi, KITAMURA Kazuo, SAKIMURA Kenji, WATANABE Masahiko* |
Authorship | 2nd author |
Publication date | 2013/07 |
Summary | 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 |