ReviewProceedings of the Japan Academy. Series B, Physical and biological sciences2024
Molecular and cellular mechanisms of developmental synapse elimination in the cerebellum: Involvement of autism spectrum disorder-related genes.
Review in Proceedings of the Japan Academy. Series B, Physical and biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Frequency-dependent cerebellar circuits independently gate social vocalizations and movement.bioRxiv : the preprint server for biology · 2026Article
- Cerebellar purkinje cell dysfunction contributes to gait impairments in Shank3-mutant mice.Molecular autism · 2026Article
- Foxp2 mutations and abnormal brain and gastrointestinal development: insights from animal models of speech-language and autism spectrum disorders.Frontiers in neuroanatomy · 2026Review
- Contributions of Retinoid Signaling to Autism-like Behaviors Induced by Early Postnatal Lead Exposure in the Mouse Cerebellum.Current issues in molecular biology · 2025Article
- Autism Spectrum Disorder: The Cerebellum, Genes, and Pathways.Neurology international · 2025Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neural circuits are initially created with excessive synapse formation until around birth and undergo massive reorganization until they mature. During postnatal development, necessary synapses strengthen and remain, whereas unnecessary ones are weakened and eventually eliminated. These events, collectively called "synapse elimination" or "synapse pruning", are thought to be fundamental for creating functionally mature neural circuits in adult animals. In the cerebellum of neonatal rodents, Purkinje cells (PCs) receive synaptic inputs from multiple climbing fibers (CFs). Then, inputs from a single CF are strengthened and those from the other CFs are eliminated, and most PCs become innervated by single CFs by the end of the third postnatal week. These events are regarded as a representative model of synapse elimination. This review examines the molecular and cellular mechanisms of CF synapse elimination in the developing cerebellum and argues how autism spectrum disorder (ASD)-related genes are involved in CF synapse development. We introduce recent studies to update our knowledge, incorporate new data into the known scheme, and discuss the remaining issues and future directions.
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Registered trials
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