ArticleMovement disorders : official journal of the Movement Disorder Society2008
Paroxysmal dyskinesias in mice.
Article in Movement disorders : official journal of the Movement Disorder Society, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
31 citing papers in PubMed, 51 citations in OpenAlex.
- Cerebellar α1Cellular and molecular life sciences : CMLS · 2025Article
- Cerebellar contributions to dystonia: unraveling the role of Purkinje cells and cerebellar nuclei.Dystonia (Lausanne, Switzerland) · 2025Article
- Sex Differences in Dystonia.Movement disorders clinical practice · 2024Article
- Article
- Mechanism of stress-induced attacks in an episodic neurologic disorder.Science advances · 2022Article
- Discovery of the First Selective MACS pharmacology & translational science · 2021Article
- Cerebellar 5HT-2A receptor mediates stress-induced onset of dystonia.Science advances · 2021Article
- Aberrant cerebellar Purkinje cell activity as the cause of motor attacks in a mouse model of episodic ataxia type 2.Disease models & mechanisms · 2018Article
- PRRT2 deficiency induces paroxysmal kinesigenic dyskinesia by regulating synaptic transmission in cerebellum.Cell research · 2018Article
- Parkinsonism without dopamine neuron degeneration in aged l-dopa-responsive dystonia knockin mice.Movement disorders : official journal of the Movement Disorder Society · 2017Article
- Using the shared genetics of dystonia and ataxia to unravel their pathogenesis.Neuroscience and biobehavioral reviews · 2017Review
- The Anatomical Basis for Dystonia: The Motor Network Model.Tremor and other hyperkinetic movements (New York, N.Y.) · 2017Review
- A CaV2.1 N-terminal fragment relieves the dominant-negative inhibition by an Episodic ataxia 2 mutant.Neurobiology of disease · 2016Article
- A new knock-in mouse model of l-DOPA-responsive dystonia.Brain : a journal of neurology · 2015Article
- Dystonia and cerebellar degeneration in the leaner mouse mutant.Brain research · 2015Article
- Protein mutated in paroxysmal dyskinesia interacts with the active zone protein RIM and suppresses synaptic vesicle exocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Flocculus Purkinje cell signals in mouse Cacna1a calcium channel mutants of escalating severity: an investigation of the role of firing irregularity in ataxia.Journal of neurophysiology · 2014Article
- The first knockin mouse model of episodic ataxia type 2.Experimental neurology · 2014Article
- Subtle microstructural changes of the cerebellum in a knock-in mouse model of DYT1 dystonia.Neurobiology of disease · 2014Article
- The focal dystonias: current views and challenges for future research.Movement disorders : official journal of the Movement Disorder Society · 2013Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Animal models of human disease are important tools for revealing the underlying mechanisms of pathophysiology and developing therapeutic strategies. Several unique mouse calcium channel mutants have been identified with nonepileptic, episodic dyskinetic movements that are phenotypically similar to human paroxysmal dyskinesias. In this report, video demonstrations of these motor attacks are provided for two previously described mouse mutants, tottering and lethargic, as well as a new one, rocker. Semiquantitative comparisons using two different rating scales reveal differences in attack morphology, severity, and duration among the strains. These mice provide three independent models of paroxysmal dyskinesia and support for prior proposals that channelopathies may underlie the human disorders.
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Registered trials
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.