ArticleFrontiers in cellular neuroscience2015
Parallel fiber to Purkinje cell synaptic impairment in a mouse model of spinocerebellar ataxia type 27.
Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 39 citations in OpenAlex.
- Purkinje cell intrinsic activity shapes cerebellar development and function.Nature communications · 2026Article
- Impact of Elovl5 Deficiency on Cerebellar Excitatory Synaptic Transmission in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Deletion of Fgf14 confers resilience to basal and stress-induced depressive-like behavior and reduces anxiety in mice.Translational psychiatry · 2025Article
- Ataxia-associated DNA repair genes protect theFrontiers in neural circuits · 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
- Cerebellar Development and Circuit Maturation: A Common Framework for Spinocerebellar Ataxias.Frontiers in neuroscience · 2020Review
- High-throughput screening against protein:protein interaction interfaces reveals anti-cancer therapeutics as potent modulators of the voltage-gated NaScientific reports · 2019Article
- Imaging of the Axon Initial Segment.Current protocols in neuroscience · 2019Article
- Motor Performances of Spontaneous and Genetically Modified Mutants with Cerebellar Atrophy.Cerebellum (London, England) · 2019Review
- Sex-Specific Proteomic Changes Induced by Genetic Deletion of Fibroblast Growth Factor 14 (FGF14), a Regulator of Neuronal Ion Channels.Proteomes · 2019Article
- Changes in the Fluorescence Tracking of NaV1.6 Protein Expression in a BTBR T+Itpr3tf/J Autistic Mouse Model.Neural plasticity · 2019Article
- Ion channel dysfunction in cerebellar ataxia.Neuroscience letters · 2019Review
- Emerging roles of Fgf14 in behavioral control.Behavioural brain research · 2019Article
- Functional Modulation of Voltage-Gated Sodium Channels by a FGF14-Based Peptidomimetic.ACS chemical neuroscience · 2018Article
- Purkinje Cell Signaling Deficits in Animal Models of Ataxia.Frontiers in synaptic neuroscience · 2018Review
- PPARgamma agonists rescue increased phosphorylation of FGF14 at S226 in the Tg2576 mouse model of Alzheimer's disease.Experimental neurology · 2017Article
- Conditional knockout of Fgf13 in murine hearts increases arrhythmia susceptibility and reveals novel ion channel modulatory roles.Journal of molecular and cellular cardiology · 2017Article
- Intracellular Fibroblast Growth Factor 14: Emerging Risk Factor for Brain Disorders.Frontiers in cellular neuroscience · 2017Review
- Familial episodic ataxia in lambs is potentially associated with a mutation in the fibroblast growth factor 14 (FGF14) gene.PloS one · 2017Article
- Fibroblast Growth Factor 14 Modulates the Neurogenesis of Granule Neurons in the Adult Dentate Gyrus.Molecular neurobiology · 2016Article
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
Genetically inherited mutations in the fibroblast growth factor 14 (FGF14) gene lead to spinocerebellar ataxia type 27 (SCA27), an autosomal dominant disorder characterized by heterogeneous motor and cognitive impairments. Consistently, genetic deletion of Fgf14 in Fgf14 (-/-) mice recapitulates salient features of the SCA27 human disease. In vitro molecular studies in cultured neurons indicate that the FGF14 (F145S) SCA27 allele acts as a dominant negative mutant suppressing the FGF14 wild type function and resulting in inhibition of voltage-gated Na(+) and Ca(2+) channels. To gain insights in the cerebellar deficits in the animal model of the human disease, we applied whole-cell voltage-clamp in the acute cerebellar slice preparation to examine the properties of parallel fibers (PF) to Purkinje neuron synapses in Fgf14 (-/-) mice and wild type littermates. We found that the AMPA receptor-mediated excitatory postsynaptic currents evoked by PF stimulation (PF-EPSCs) were significantly reduced in Fgf14 (-/-) animals, while short-term plasticity, measured as paired-pulse facilitation (PPF), was enhanced. Measuring Sr(2+)-induced release of quanta from stimulated synapses, we found that the size of the PF-EPSCs was unchanged, ruling out a postsynaptic deficit. This phenotype was corroborated by decreased expression of VGLUT1, a specific presynaptic marker at PF-Purkinje neuron synapses. We next examined the mGluR1 receptor-induced response (mGluR1-EPSC) that under normal conditions requires a gradual build-up of glutamate concentration in the synaptic cleft, and found no changes in these responses in Fgf14 (-/-) mice. These results provide evidence of a critical role of FGF14 in maintaining presynaptic function at PF-Purkinje neuron synapses highlighting critical target mechanisms to recapitulate the complexity of the SCA27 disease.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.