Purkinje cells in mutant med mice who lack expression of the Scn8a gene, which encodes the NaV1.6 protein, have shown a decrease in the rate of spontaneous action-potential firing. Thus, these mice are ataxic.5 Restoring the Purkinje cell output to the normal condition can reduce ataxia in mutant med mice. We propose that BK channel activators and Kv4 channel inhibitors may restore the med Purkinje cell output to normal condition. Proposed drugs for this purpose are acetazolamide (ACTZ), a BK channel-opener, and 4-aminopyridine (4-AP), a Kv4 channel-inhibitor. To determine how the output of med Purkinje cells restore the normal conditions, computer simulations of the electrical behaviors of Purkinje cells can be performed. Computational models of cells have become important tools for investigating different aspects of the behavior of the cells. The simulation environment allows change the properties of the specific ion channels as the possible mechanism of action of neuroprotective drugs. This is a good way to imitate cell response in the presence of channel blockers and activators, without any concern about the blocker side effects or other uncontrollable parameters that may affect the results in the experiments.