The role of the cerebellum in spatial learning has recently been investigated in genetically and non-genetically lesioned animal models, particularly in water mazes, in view of the minimal impact such lesions exert on swimming movements. A dissociation between place and cued learning in the Morris water maze has been observed in several models, including cerebellar mutant mice (Rora(sg) Nna1(pcd-1J), nervous), rats with lesions of either the lateral cerebellar cortex or the dentate nucleus, and rats with selective Purkinje cell loss caused by intracerebroventricular injections of OX-7-saporin, confirming the hypothesis that cerebellar damage may cause a cognitive deficit independently of fine motor control. In addition, the results of hemi-cerebellectomized rats indicate the probable involvement of the cerebellum in working memory and the procedural aspect of maze learning. The findings of impaired maze learning in cerebellar-lesioned mice and rats are concordant with those of deficient visuospatial functions in patients with cerebellar atrophy. The spatial deficits may be ascribed to altered metabolic activity in cerebellar-related pathways.