The epileptogenic property of ouabain was studied in cats including 17 chronic and 13 acute animals. In chronic experiments, infusion of ouabain into the septum by means of an indwelling cannula induced severe rhinencephalic epileptic state followed by a long lasting spike activity in the hippocampus. Several mechanisms responsible for such a self-sustained epileptic activity are discussed by considering the specific metabolic action of ouabain and the site of injection. Intraventricular infusion of 20 µg ouabain, induced a loss of intracellular potassium demonstrated by an increase of potassium concentration in CSF which is followed by a cerebral hyperemia determined by 133 Xe clearance method and later by an epileptic state in the hippocampus. The change in cerebral ionic distribution is considered as a causal factor of both cerebral hyperemia and epileptic activity. The influence of the preconvulsive increase of the cerebral blood flow upon the peculiar intensity of epilepsy induced by ouabain is suspected. From these results the role of potassium in regulating electrical activity and cerebral blood flow and their interrelationship of the latter is emphasized.