The hypothesis that GABA and GABAergic transmission are involved in the pathophysiology of schizophrenia has been one of the representative ideas. Studies of postmortem brain found alterations in the expression of GABAergic transmission-related genes and in particular, reduced expression of a GABA-synthesizing enzyme, glutamate decarboxylase 67 (GAD67). Because of the limitations of the experimental approach in human, it is important to characterize animal models to validate the GABA hypothesis of schizophrenia. Here, we review several animal models for schizophrenia showing both behavioral abnormalities and downregulation of GAD67 expression. The disturbance in GAD67 expression could represent a common molecular pathophysiology for dysfunctions in schizophrenia. We also review the use for GAD67-GFP knock- in mice that have been applied to characterization of psychiatric disease model mice with GABAergic deficit such as disturbance of GABAergic neuron migration, based on the fact that GFP is specifically expressed in GABAergic neurons in these knock- in mice. Establishment of another model animal with GABAergic dysregulation or genetically engineered rodents in GABAergic transmission- related genes will provide an opportunity to further understand the pathogenesis of schizophrenia.