Given the importance of GABAergic interneurons throughout the CNS and their often proposed major involvement in the disease etiology and progression of schizophrenia, this study aimed to further elucidate the behavioral consequences of GABAergic depletion in the PrL and the dHPC with regard to schizophrenia-related symptoms such as hyperlocomotion, altered sensorimotor gating and cognitive dysfunction. The gene discussed is PRL; the disease is schizophrenia.