The balance between excitatory and inhibitory systems is crucial for the normal functioning of the brain, and dysfunction in the inhibitory system may be a potential mechanism for psychosis. Current studies emphasize parvalbumin-positive (PV+) GABAergic interneurons as a key component in the development of schizophrenia symptoms, with reduced PV protein levels found in cortical PV+ interneurons in individuals with schizophrenia. Rodent models of schizophrenia indicate that the medial prefrontal cortex (mPFC) is the main structure where PV neurons exhibit aberrant function. However, it is still unresolved whether this dysfunction is due to hypo- or hyperactivity. In our study, we aimed to determine whether the inhibition or activation of PV+ interneurons in the mPFC causes schizophrenia-like behavioral alterations. To achieve this, we utilized PV-cre rats with virally transduced either excitatory or inhibitory Designer Receptors Exclusively Activated by Designer Drugs (DREADDs), expressed in the mPFC. Rats were systemically injected with Compound 21, a DREADD agonist, prior to a behavioral task. The behavioral battery consisted of the Carousel maze, a task that requires the segregation of spatial information into relevant and irrelevant streams, making it a sensitive tool for detecting schizophrenia-like symptoms. In addition, prepulse inhibition of the startle reflex was tested. Preliminary results suggest that increased activity of mPFC PV interneurons does not impact behavioral performance in the Carousel maze. Analysis of further tests is ongoing, and the data will provide insights into the role of mPFC PV interneurons in schizophrenia. This work is supported by the GACR grant 23-06546S.