ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
A role for myosin Va in cerebellar plasticity and motor learning: a possible mechanism underlying neurological disorder in myosin Va disease.
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 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Genome-Wide Meta-Analysis of Sciatica in Finnish Population.PloS one · 2016Pooled it
- Spatial and single-cell transcriptomics reveal the reorganization of cerebellar microglia with aging.Cell reports · 2025Article
- A novel, rapidly progressive ataxia due to a spontaneous Myo5a mutation in mice impairs transport proteins and alters mitochondria.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- The Impacts of Surgery and Intracerebral Electrodes in C57BL/6J Mouse Kainate Model of Epileptogenesis: Seizure Threshold, Proteomics, and Cytokine Profiles.Frontiers in neurology · 2021Article
- Endoplasmic reticulum visits highly active spines and prevents runaway potentiation of synapses.Nature communications · 2020Article
- Impairment of cerebellar long-term depression and GABAergic transmission in prion protein deficient mice ectopically expressing PrPLP/Dpl.Scientific reports · 2020Article
- Structural basis of Fusarium myosin I inhibition by phenamacril.PLoS pathogens · 2020Article
- mGluR1 in cerebellar Purkinje cells is essential for the formation but not expression of associative eyeblink memory.Scientific reports · 2019Article
- Pleiotropic neuropathological and biochemical alterations associated with Myo5a mutation in a rat Model.Brain research · 2018Article
- Article
- Optimization of single-cell electroporation protocol for forced gene expression in primary neuronal cultures.Molecular biotechnology · 2014Article
- The synaptic targeting of mGluR1 by its carboxyl-terminal domain is crucial for cerebellar function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- BMP-2 overexpression augments vascular smooth muscle cell motility by upregulating myosin Va via Erk signaling.Oxidative medicine and cellular longevity · 2014Article
- Functions of class V myosins in neurons.The Journal of biological chemistry · 2013Review
- Evidence for defective Rab GTPase-dependent cargo traffic in immune disorders.Experimental cell research · 2013Review
- Myosin motors at neuronal synapses: drivers of membrane transport and actin dynamics.Nature reviews. Neuroscience · 2013Review
- Article
- Multifaceted genomic risk for brain function in schizophrenia.NeuroImage · 2012Article
- Role of myosin Va in purinergic vesicular neurotransmission in the gut.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Article
Corrections and comments
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Authors and funding
8 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations of the myosin Va gene cause the neurological diseases Griscelli syndrome type 1 and Elejalde syndrome in humans and dilute phenotypes in rodents. To understand the pathophysiological mechanisms underlying the neurological disorders in myosin Va diseases, we conducted an integrated analysis at the molecular, cellular, electrophysiological, and behavioral levels using the dilute-neurological (d-n) mouse mutant. These mice manifest an ataxic gait and clonic seizures during postnatal development, but the neurological disorders are ameliorated in adulthood. We found that smooth endoplasmic reticulum (SER) rarely extended into the dendritic spines of Purkinje cells (PCs) of young d-n mice, and there were few, if any, IP(3) receptors. Moreover, long-term depression (LTD) at parallel fiber-PC synapses was abolished, consistent with our previous observations in juvenile lethal dilute mutants. Young d-n mice exhibited severe impairment of cerebellum-dependent motor learning. In contrast, adult d-n mice showed restoration of motor learning and LTD, and these neurological changes were associated with accumulation of SER and IP(3) receptors in some PC spines and the expression of myosin Va proteins in the PCs. RNA interference-mediated repression of myosin Va caused a reduction in the number of IP(3) receptor-positive spines in cultured PCs. These findings indicate that myosin Va function is critical for subsequent processes in localization of SER and IP(3) receptors in PC spines, LTD, and motor learning. Interestingly, d-n mice had defects of motor coordination from young to adult ages, suggesting that the role of myosin Va in PC spines is not sufficient for motor coordination.
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Registered trials
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