Nitric Oxide (NO) actively participates in the regulation of neuronal intracellular Ca²⁺ levels by modulating the activity of various channels and receptors. To test the possibility that modulation of Ca²⁺ buffer protein expression level by NO participates in this regulatory effect, we examined expression of calbindin-D28k, calretinin, and parvalbumin in the cerebellum of neuronal NO synthase knock-out (nNOS^(-/-)) mice using immunohistochemistry. We observed that in the cerebellar cortex of the nNOS^(-/-) mice, expression of calbindin-D28k and parvalbumin were significantly increased while expression of calretinin was significantly decreased. These results suggest another mechanism by which NO can participate in the regulation of Ca²⁺ homeostasis.