Influence of disturbed zinc metabolism on brain excitability measured by Woodbury-Davenport's apparatus and carbonic anhydrase activity in the brain was studied in zinc deficient sucking mice prepared according to Nishimura and in mature mice with zinc intoxication due to a long term administration of zinc chloride. On the other hand, relationship of brain carbonic anhydrase to brain excitability was examined. The observations may be summarized as follows : 1) In zinc deficiency EST showed a rise and MES showed a shortening. In zinc excess EST showed a depression but MES failed to show a significant change. 2) Carbonic anhydrase activity in the brain decreased in zinc deficiency but failed to show a change in zinc excess, being compatible with the present concept that this enzyme is related to MES. 3) Carbonic anhydrase activity in the brain of ep-mice was higher than that of dd-mice. The increase in the cerebellum was most prominent, while that in the hippocampus and dentate gyrus was not significant. This suggests that brain carbonic anhydrase is of secondary importance in the neurochemical mechanism of seizures. 4) The findings in zinc deficient sucklings prepared according to the method of Nishimura probably represents the effect of zinc on the development of seizure activity. Zinc deficiency appears to delay the development of seizure activity.