Calcium‐dependent regulation of climbing fibre synapse elimination during postnatal cerebellar development. (22nd February 2013)

• Record Type: Journal Article
• Authors: Kano, Masanobu; Nakayama, Hisako; Hashimoto, Kouichi; Kitamura, Kazuo; Sakimura, Kenji; Watanabe, Masahiko
• Is Part Of: Journal of physiology. Volume 591:Number 13(2013:Jul.)
• Page Start: 3151
• Page End: 3158
• Publication Date: 2013-02-22
• Subjects: Physiology -- Periodicals; 612.005
• DOI: 10.1113/jphysiol.2012.248252
• Languages: English
• ISSNs: 0022-3751

Abstract

Abstract : Abstract 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 Ca 2+ 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 Ca 2+ imaging data suggest that GABAA receptor‐mediated inhibition onto PC somata from putative basket cells influences CF‐induced Ca 2+ transients and regulates elimination of redundant CF synapses from PC somata at P10–P16. Thus, regulation of Ca 2+ influx to PCs through VDCCs is crucial for the four phases of CF synapse elimination during postnatal development.