Reviews evidence for the dopamine (DA) hypothesis--that schizophrenia may be related to a relative excess of DA-dependent neuronal activity. DA is not present uniformly throughout the brain, but is localized in at least 6 distinct neuronal tracts; the functional anatomy of these tracts and their possible relations to schizophrenia are reviewed. Evidence for a role of DA in animals is also examined, focusing on both biochemical and pharmacological studies. Basic mechanisms of the synthesis, catabolism, and regulation of DA chemistry and the effects of selected psychotomimetic and antipsychotic drugs affecting DA metabolism are discussed in relation to clinical findings and the idea of increased DA activity as either a precursor or concomitant of schizophrenia. Evidence for a role of DA in the pathophysiology of schizophrenia is compelling but not irrefutable; future studies should have either a therapeutic intent, the intent of transiently exacerbating symptomatology, or a major focus on neuroendocrine indicators of central dopaminergic activity. The DA hypothesis appears to be functionally correct in that some, maybe even most, schizophrenics will have the equivalent of hyperactivity of DA neurons, although this hyperactivity may probably be secondary to some other basic defect that allows DA activity to be transiently increased during periods of increased CNS arousal created by excessive environmental demands.(15 p ref)(PsycINFO Database Record (c) 2016 APA, all rights reserved)