Related Experiment Video
Updated: Jul 10, 2026

10:41
Implantation of Osmotic Pumps and Induction of Stress to Establish a Symptomatic, Pharmacological Mouse Model for DYT/PARK-ATP1A3 Dystonia
Published on: September 12, 2020
Paroxysmal dyskinesias in mice
Thomas L Shirley1, Lekha M Rao, Ellen J Hess
1Department of Neurology, Johns Hopkins University, Baltimore, Maryland, USA.
Movement Disorders : Official Journal of the Movement Disorder Society
|November 14, 2007
Summary
Mouse calcium channel mutants, including tottering, lethargic, and rocker, exhibit episodic movement disorders. These findings support channelopathies as a cause of human paroxysmal dyskinesias.
Area of Science:
- Neuroscience
- Genetics
- Pharmacology
Background:
- Animal models are crucial for understanding human diseases and developing treatments.
- Specific mouse calcium channel mutants display episodic movement disorders resembling human paroxysmal dyskinesias.
Purpose of the Study:
- To present video demonstrations of motor attacks in tottering, lethargic, and rocker mouse mutants.
- To compare the phenotypic characteristics of these mouse models of paroxysmal dyskinesia.
Main Methods:
- Video recording and analysis of motor attacks in three mouse strains.
- Semiquantitative assessment using two distinct rating scales to evaluate attack features.
Main Results:
- Distinct differences in attack morphology, severity, and duration were observed among the tottering, lethargic, and rocker mouse mutants.
- The study provides detailed phenotypical characterization of these three independent models.
Conclusions:
- These mouse mutants serve as valuable models for studying paroxysmal dyskinesia.
- The findings lend support to the hypothesis that channelopathies are implicated in human paroxysmal dyskinesias.

