ReviewThe Journal of physiology2013
Calcium-dependent regulation of climbing fibre synapse elimination during postnatal cerebellar development.
Review in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed.
- C1ql1-Bai3 signaling is necessary for climbing fiber synapse formation in mature Purkinje cells in coordination with neuronal activity.Molecular brain · 2023Article
- Adult loss of Cacna1a in mice recapitulates childhood absence epilepsy by distinct thalamic bursting mechanisms.Brain : a journal of neurology · 2020Article
- Article
- Type-1 metabotropic glutamate receptor signaling in cerebellar Purkinje cells in health and disease.F1000Research · 2017Review
- Noradrenergic refinement of glutamatergic neuronal circuits in the lateral superior olivary nucleus before hearing onset.Journal of neurophysiology · 2015Article
- Disturbed calcium signaling in spinocerebellar ataxias and Alzheimer's disease.Seminars in cell & developmental biology · 2015Review
- Synapse elimination in the developing cerebellum.Cellular and molecular life sciences : CMLS · 2013Review
- Size matters: formation and function of giant synapses.The Journal of physiology · 2013Article
- Spike timing-dependent selective strengthening of single climbing fibre inputs to Purkinje cells during cerebellar development.Nature communications · 2013Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
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