ArticleeLife2024
Cerebellar nuclei cells produce distinct pathogenic spike signatures in mouse models of ataxia, dystonia, and tremor.
Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Disinhibition of cerebellar output by loss of restless legs syndrome-associated gene MEIS1.Current biology : CB · 2026Article
- Competitive Olivocerebellar Input Selection Promotes Resilient Circuit Formation.bioRxiv : the preprint server for biology · 2026Article
- Primary Brain Calcification Associated with a Novel XPR1 In-Frame Deletion: Clinical Characterization and Insights into Cerebellar and Basal Ganglia Contributions.Cerebellum (London, England) · 2026Article
- Steady-state Purkinje cell activity has limited predictive power for cerebellar output in disease.The Journal of physiology · 2026Article
- Frequency-dependent cerebellar circuits independently gate social vocalizations and movement.bioRxiv : the preprint server for biology · 2026Article
- Viral vector-mediated SLC9A6 gene replacement reduces cerebellar motor and molecular abnormalities in the shaker rat model of Christianson syndrome.Human molecular genetics · 2026Article
- Integrated approaches for investigating the neural bases of movement-highlights from the 34th Annual Meeting of the Society for the Neural Control of Movement.Journal of neurophysiology · 2026Article
- Cerebellar deep brain stimulation rescues Purkinje cell mitochondrial density in a genetic mouse model of cerebellar ataxia.Brain research bulletin · 2026Article
- Tremor pathophysiology.Clinical parkinsonism & related disorders · 2026Review
- Cerebellar motor and non-motor contributions to dystonia pathophysiology and treatment.Dystonia (Lausanne, Switzerland) · 2026Article
- The cerebellum in dystonia: key player or background support?Arquivos de neuro-psiquiatria · 2025Review
- Cerebellar dysfunction in a mouse model of childhood-onset manganese-induced dystonia parkinsonism.Neurobiology of disease · 2025Article
- Neurobiology of Dystonia: Review of Genetics, Animal Models, and Neuroimaging.Brain sciences · 2025Review
- Processing reliant on granule cells is essential for motor learning but dispensable for social preference and numerous other cerebellar-dependent behaviors.Nature communications · 2025Article
- Accurate Tracking of Locomotory Kinematics in Mice Moving Freely in Three-Dimensional Environments.eNeuro · 2025Article
- Purkinje Cell spike patterns do not correlate with nuclei cell spike patterns in mouse models for cerebellar disease.bioRxiv : the preprint server for biology · 2025Article
- NETSseq reveals inflammatory and aging mechanisms in distinct cell types, driving cerebellar decline in ataxia telangiectasia.Frontiers in neuroscience · 2025Article
- Cerebellar contributions to dystonia: unraveling the role of Purkinje cells and cerebellar nuclei.Dystonia (Lausanne, Switzerland) · 2025Article
- More Than a Small Brain: The Importance of Studying Neural Function during Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Review
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Abstract
The cerebellum contributes to a diverse array of motor conditions, including ataxia, dystonia, and tremor. The neural substrates that encode this diversity are unclear. Here, we tested whether the neural spike activity of cerebellar output neurons is distinct between movement disorders with different impairments, generalizable across movement disorders with similar impairments, and capable of causing distinct movement impairments. Using in vivo awake recordings as input data, we trained a supervised classifier model to differentiate the spike parameters between mouse models for ataxia, dystonia, and tremor. The classifier model correctly assigned mouse phenotypes based on single-neuron signatures. Spike signatures were shared across etiologically distinct but phenotypically similar disease models. Mimicking these pathophysiological spike signatures with optogenetics induced the predicted motor impairments in otherwise healthy mice. These data show that distinct spike signatures promote the behavioral presentation of cerebellar diseases.
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