Schizophrenia, a complex neuropsychiatric condition impacting 0.5-1% of adults, manifests through positive, negative, and cognitive symptoms affecting emotions, thought processes, and perception. Onset typically occurs from late adolescence to early adulthood, with genetic and early-life environmental factors implicated in its strongly neurodevelopmental origin. The dopamine system plays a central role in schizophrenia's pathogenesis, with dopamine 2 receptor antagonists as the first line of treatment since the 1950s. Numerous studies highlight abnormal dopamine functions in schizophrenia patients, including elevated striatal dopamine, which also predicts disease trajectory in at-risk individuals. Importantly, factors such as maternal infection, childhood adversity, and adolescent substance use impact the dopamine system, making it a converging point of schizophrenia pathogenesis. This has led to the hypothesis that elevated dopamine signaling during development may be a major driving force for the transition to schizophrenia, a notion supported by rodent studies. However, most existing animal models of schizophrenia fail to incorporate the region-specific developmental dopamine dysfunctions observed in schizophrenia patients and those at risk. Given the evidence that periadolescent dopamine activity shapes striatal neuronal circuits, perturbation to this system during brain maturation may result in schizophrenia-like manifestations in adulthood – a hypothesis tested here. Specifically, our project aims to establish a novel circuit-based developmental mouse model for schizophrenia to identify specific dopamine circuits driving the pathology. Our initial experiments revealed changes in several behaviors linked to schizophrenia after transient hyper-dopamine signaling during adolescence. Based on this, our next focus is to dissect dopamine subcircuits responsible for schizophrenia-relevant behavioral phenotypes.