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[Fundamental study on ataxic mice (wriggle mouse Sagami)]
Jikken Dobutsu. Experimental Animals
|April 1, 1987
Summary
Wriggle mouse Sagami (WMS) exhibits locomotor instability and abnormal gait. Unlike other ataxic mice, WMS shows reduced cerebellar c-GMP, suggesting a distinct neurological mechanism for its movement disorder.
Area of Science:
- Neuroscience
- Genetics
- Animal Models
Context:
- A novel mouse strain, Wriggle mouse Sagami (WMS), a BALB/C substrain, displays unique neurological and motor deficits.
- Characterized by locomotor instability, abnormal gait, and neck wriggling, WMS presents a unique phenotype for studying neurological disorders.
Purpose:
- To investigate the underlying mechanisms of the abnormal gait and locomotor instability in the Wriggle mouse Sagami (WMS) strain.
- To differentiate the WMS ataxia from other known genetically determined ataxic mouse models.
Summary:
- WMS mice exhibit delayed growth and smaller body weight, with brain size proportional to body weight.
- Gross and histological examinations revealed no localized atrophy in the central nervous system.
- Biochemical analysis showed decreased cyclic guanosine monophosphate (c-GMP) levels in the WMS cerebellum, while cyclic adenosine monophosphate (c-AMP) levels remained normal.
- Administration of thyrotropin releasing hormone (TRH) did not significantly improve the ataxic gait.
Impact:
- The findings suggest that the WMS mouse strain possesses a unique etiological basis for its ataxia and abnormal gait.
- This discovery provides a new model for investigating the neurobiological underpinnings of movement disorders.
- Understanding the distinct mechanism in WMS can help differentiate it from other genetic ataxias like Rolling mouse Nagaya (RMN), Purkinje cell degeneration (PCD), Staggerer, and Reeler mice.