Ataxic Syrian hamster

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 signifi cant 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.