Abstract
A spontaneous genetic model of cerebellar ataxia in the Syrian hamster (Mesocricetus auratus) is described. The homozygous mutant hamsters are smaller than the unaffected littermates but have a normal appearance. They develop progressive, but moderate ataxia beginning at 7 weeks of age. The major pathologic change in the ataxic mutants is significant cerebellar atrophy, including a rapid and substantial loss of Purkinje cells. In the homozygous hamster brain, expression of Nna1, the gene responsible for the Purkinje cell degeneration (pcd) phenotype in mice, is selectively suppressed.
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References
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Akita, K. (2016). Ataxic Syrian Hamster. In: Gruol, D., Koibuchi, N., Manto, M., Molinari, M., Schmahmann, J., Shen, Y. (eds) Essentials of Cerebellum and Cerebellar Disorders. Springer, Cham. https://doi.org/10.1007/978-3-319-24551-5_61
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DOI: https://doi.org/10.1007/978-3-319-24551-5_61
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