ArticleThe Journal of physiology2017
Progressive impairment of cerebellar mGluR signalling and its therapeutic potential for cerebellar ataxia in spinocerebellar ataxia type 1 model mice.
Article in The Journal of physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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45 citing papers in PubMed, 77 citations in OpenAlex.
- Long term administration of selective NMDA GluN2B receptor blocker Ro25-6981 attenuates neurodegeneration in mouse model of spinocerebellar ataxia type 1 (SCA1).Cell death discovery · 2026Article
- Translational Relevance of SCA1 Models for the Development of Therapies for Spinocerebellar Ataxia Type 1.Biomedicines · 2025Review
- Anti-Kv1.2 Immunoprecipitation Identifies shared mGluR1-Associated Signalosome Complex proteins and PKC-Mediated Regulation of Kv1.2 in the Cerebellum.bioRxiv : the preprint server for biology · 2025Article
- Neuronal Nitric Oxide Synthase Regulates Cerebellar Parallel Fiber Slow EPSC in Purkinje Neurons by Modulating STIM1-Gated TRPC3-Containing Channels.Cerebellum (London, England) · 2024Article
- Targeted therapy improves cellular dysfunction, ataxia, and seizure susceptibility in a model of a progressive myoclonus epilepsy.Cell reports. Medicine · 2024Article
- Longitudinal single-cell transcriptional dynamics throughout neurodegeneration in SCA1.Neuron · 2024Article
- Dysregulation of alternative splicing in spinocerebellar ataxia type 1.Human molecular genetics · 2024Article
- Article
- Altered calcium signaling in Bergmann glia contributes to spinocerebellar ataxia type-1 in a mouse model of SCA1.Neurobiology of disease · 2023Article
- Gait disorders induced by photothrombotic cerebellar stroke in mice.Scientific reports · 2023Article
- Pathophysiology of Cerebellar Degeneration in Mitochondrial Disorders: Insights from theInternational journal of molecular sciences · 2023Article
- Therapeutic Strategies for Spinocerebellar Ataxia Type 1.Biomolecules · 2023Review
- Viewpoint: spinocerebellar ataxias as diseases of Purkinje cell dysfunction rather than Purkinje cell loss.Frontiers in molecular neuroscience · 2023Review
- Article
- Development of microglia-targeting adeno-associated viral vectors as tools to study microglial behavior in vivo.Communications biology · 2022Article
- Long-term depression-inductive stimulation causes long-term potentiation in mouse Purkinje cells with a mutant thyroid hormone receptor.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Electrophysiological and Imaging Analysis of GFP-Tagged Protein Kinase C γ Translocation in Cerebellar Purkinje Cells.Cerebellum (London, England) · 2022Article
- Effects of the administration of Elovl5-dependent fatty acids on a spino-cerebellar ataxia 38 mouse model.Behavioral and brain functions : BBF · 2022Article
- Article
- Consensus Paper: Strengths and Weaknesses of Animal Models of Spinocerebellar Ataxias and Their Clinical Implications.Cerebellum (London, England) · 2022Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
key pointsSpinocerebellar ataxia type 1 (SCA1) is a progressive neurodegenerative disease caused by a gene defect, leading to movement disorder such as cerebellar ataxia. It remains largely unknown which functional defect contributes to the cerebellar ataxic phenotype in SCA1. In this study, we report progressive dysfunction of metabotropic glutamate receptor (mGluR) signalling, which leads to smaller slow synaptic responses, reduced dendritic Ca ABSTRACT: Spinocerebellar ataxia type 1 (SCA1) is a progressive neurodegenerative disease that presents with cerebellar ataxia and motor learning defects. Previous studies have indicated that the pathology of SCA1, as well as other ataxic diseases, is related to signalling pathways mediated by the metabotropic glutamate receptor type 1 (mGluR1), which is indispensable for proper motor coordination and learning. However, the functional contribution of mGluR signalling to SCA1 pathology is unclear. In the present study, we show that SCA1 model mice develop a functional impairment of mGluR signalling which mediates slow synaptic responses, dendritic Ca
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