A role for dopamine (DA) release in the hallucinations and other positive symptoms associated with schizophrenia has long been inferred from the antipsychotic response to D2 DA receptor antagonists and because the DA releaser amphetamine can be psychotogenic. Recent studies suggest that patients with schizophrenia, including those never exposed to antipsychotic drugs, maintain high presynaptic DA accumulation in the striatum. New laboratory approaches are elucidating mechanisms that control the level of presynaptic DA stores, thus contributing to fundamental understanding of the basic pathophysiologic mechanism in schizophrenia.