ArticleCerebellum (London, England)2012
Purkinje cell-specific ablation of Cav2.1 channels is sufficient to cause cerebellar ataxia in mice.
Article in Cerebellum (London, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 51 citations in OpenAlex.
- Adrenergic receptor activation triggers stress-induced dystonia in a CACNA1A mutant mouse model.Frontiers in neuroscience · 2026Article
- Spatial genomics of AAV vectors reveals mechanism of transcriptional crosstalk that enables targeted delivery of large genetic cargo.Nature biotechnology · 2026Article
- A Novel Mouse Model for Developmental and Epileptic Encephalopathy by Purkinje Cell-Specific Deletion ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Cerebellar α1Cellular and molecular life sciences : CMLS · 2025Article
- CACNA1A loss-of-function affects neurogenesis in human iPSC-derived neural models.Cellular and molecular life sciences : CMLS · 2025Article
- Arsenic unsettles the cerebellar balance between neurodegeneration and neurogenesis: reversal by folic acid.Apoptosis : an international journal on programmed cell death · 2025Article
- Balance Performance in Aged Mice is Dependent on Unipolar Brush Cells.Cerebellum (London, England) · 2024Article
- Balance performance in aged mice is dependent on unipolar brush cells.bioRxiv : the preprint server for biology · 2024Article
- Article
- Basket to Purkinje Cell Inhibitory Ephaptic Coupling Is Abolished in Episodic Ataxia Type 1.Cells · 2023Article
- Cerebellar neuronal dysfunction accompanies early motor symptoms in spinocerebellar ataxia type 3.Disease models & mechanisms · 2022Article
- Mechanism of stress-induced attacks in an episodic neurologic disorder.Science advances · 2022Article
- Controlling absence seizures from the cerebellar nuclei via activation of the GCellular and molecular life sciences : CMLS · 2022Article
- Vulnerability of Human Cerebellar Neurons to Degeneration in Ataxia-Causing Channelopathies.Frontiers in systems neuroscience · 2022Review
- Reversing frontal disinhibition rescues behavioural deficits in models of CACNA1A-associated neurodevelopment disorders.Molecular psychiatry · 2021Article
- Voltage-Gated CaFrontiers in synaptic neuroscience · 2021Review
- Article
- Cerebellar function and ischemic brain lesions in migraine patients from the general population.Cephalalgia : an international journal of headache · 2017Article
- Cerebellar Intermittent Theta-Burst Stimulation and Motor Control Training in Individuals with Cervical Dystonia.Brain sciences · 2016Article
- Does modulation of the endocannabinoid system have potential therapeutic utility in cerebellar ataxia?The Journal of physiology · 2016Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
The Cacna1a gene encodes the α(1A) subunit of voltage-gated Ca(V)2.1 Ca(2+) channels that are involved in neurotransmission at central synapses. Ca(V)2.1-α(1)-knockout (α1KO) mice, which lack Ca(V)2.1 channels in all neurons, have a very severe phenotype of cerebellar ataxia and dystonia, and usually die around postnatal day 20. This early lethality, combined with the wide expression of Ca(V)2.1 channels throughout the cerebellar cortex and nuclei, prohibited determination of the contribution of particular cerebellar cell types to the development of the severe neurobiological phenotype in Cacna1a mutant mice. Here, we crossed conditional Cacna1a mice with transgenic mice expressing Cre recombinase, driven by the Purkinje cell-specific Pcp2 promoter, to specifically ablate the Ca(V)2.1-α(1A) subunit and thereby Ca(V)2.1 channels in Purkinje cells. Purkinje cell Ca(V)2.1-α(1A)-knockout (PCα1KO) mice aged without difficulties, rescuing the lethal phenotype seen in α1KO mice. PCα1KO mice exhibited cerebellar ataxia starting around P12, much earlier than the first signs of progressive Purkinje cell loss, which appears in these mice between P30 and P45. Secondary cell loss was observed in the granular and molecular layers of the cerebellum and the volume of all individual cerebellar nuclei was reduced. In this mouse model with a cell type-specific ablation of Ca(V)2.1 channels, we show that ablation of Ca(V)2.1 channels restricted to Purkinje cells is sufficient to cause cerebellar ataxia. We demonstrate that spatial ablation of Ca(V)2.1 channels may help in unraveling mechanisms of human 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.