ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
β-III spectrin is critical for development of purkinje cell dendritic tree and spine morphogenesis.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 81 citations in OpenAlex.
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- Impaired motor activity in a CRISPR SCA5 L253P knock-in mouse is associated with selective β-III-spectrin subcellular redistribution in the cerebellum.bioRxiv : the preprint server for biology · 2026Article
- Versatile high-speed volumetric imaging from microscopic to macroscopic scale by self-adaptive oblique plane microscopy.bioRxiv : the preprint server for biology · 2026Article
- Automated gait analysis indicates efficacy of T-type calcium channel inhibition for mitigation of disrupted calcium signalling in an SCA5 mouse model.Scientific reports · 2025Article
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- SCA14-Associated PKCγ-G118D Mutant Exhibits a Detrimental Effect on Cerebellar Purkinje Cell Dendritic Growth.International journal of molecular sciences · 2025Article
- The spiny relationship between parallel fibers, climbing fibers, and Purkinje cells.Frontiers in physiology · 2025Review
- Molecular consequences of SCA5 mutations in the spectrin-repeat domains of β-III-spectrin.bioRxiv : the preprint server for biology · 2024Article
- The loss of βΙ spectrin alters synaptic size and composition in theFrontiers in neuroscience · 2024Article
- Mettl1-mediated internal mCell & bioscience · 2023Article
- Increased Actin Binding Is a Shared Molecular Consequence of Numerous SCA5 Mutations in β-III-Spectrin.Cells · 2023Article
- Synapse-Specific Defects in Synaptic Transmission in the Cerebellum of W246G Mutant ELOVL4 Rats-a Model of Human SCA34.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Increased actin binding is a shared molecular consequence of numerous spinocerebellar ataxia mutations in β-III-spectrin.bioRxiv : the preprint server for biology · 2023Article
- The Emerging Key Role of the mGluR1-PKCγ Signaling Pathway in the Pathogenesis of Spinocerebellar Ataxias: A Neurodevelopmental Viewpoint.International journal of molecular sciences · 2022Review
- β-III-spectrin N-terminus is required for high-affinity actin binding and SCA5 neurotoxicity.Scientific reports · 2022Article
- Purkinje Neurons with Loss of STIM1 Exhibit Age-Dependent Changes in Gene Expression and Synaptic Components.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Deficiency of TRIM32 Impairs Motor Function and Purkinje Cells in Mid-Aged Mice.Frontiers in aging neuroscience · 2021Article
- Myosin 18Aα targets the guanine nucleotide exchange factor β-Pix to the dendritic spines of cerebellar Purkinje neurons and promotes spine maturation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Nitric Oxide Critically Regulates Purkinje Neuron Dendritic Development Through a Metabotropic Glutamate Receptor Type 1-Mediated Mechanism.Cerebellum (London, England) · 2020Article
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Mutations in the gene encoding β-III spectrin give rise to spinocerebellar ataxia type 5, a neurodegenerative disease characterized by progressive thinning of the molecular layer, loss of Purkinje cells and increasing motor deficits. A mouse lacking full-length β-III spectrin (β-III⁻/⁻) displays a similar phenotype. In vitro and in vivo analyses of Purkinje cells lacking β-III spectrin, reveal a critical role for β-III spectrin in Purkinje cell morphological development. Disruption of the normally well ordered dendritic arborization occurs in Purkinje cells from β-III⁻/⁻ mice, specifically showing a loss of monoplanar organization, smaller average dendritic diameter and reduced densities of Purkinje cell spines and synapses. Early morphological defects appear to affect distribution of dendritic, but not axonal, proteins. This study confirms that thinning of the molecular layer associated with disease pathogenesis is a consequence of Purkinje cell dendritic degeneration, as Purkinje cells from 8-month-old β-III⁻/⁻ mice have drastically reduced dendritic volumes, surface areas and total dendritic lengths compared with 5- to 6-week-old β-III⁻/⁻ mice. These findings highlight a critical role of β-III spectrin in dendritic biology and are consistent with an early developmental defect in β-III⁻/⁻ mice, with abnormal Purkinje cell dendritic morphology potentially underlying disease pathogenesis.
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