the dopamine hypothesis of schizophrenia :

The predominant biological hypothesis for a neurochemical defect in schizophrenia is currently the socalled "dopamine (DA) hypothesis." In its simplest form, this hypothesis states that schizophrenia may be related to a relative excess of DA-dependent neuronal activity. It is derived from pharmacologic evidence that drugs that decrease DA activity (e.g., the phenothiazines) may be antipsychotic and drugs that promote DA activity (e.g., amphetamine) may be psychotomimetic. The particular means by which "too much dopamine" is produced in schizophrenia is not yet known. If, as Karl Popper (1959) says, the value of a hypothesis lies not so much in whether it is right or wrong but in its capacity to stimulate attempts to refute it, then the DA hypothesis of schizophrenia has been extraordinarily successful. Indeed, this hypothesis has stimulated a legion of basic and clinical scientists to investigate the anatomy, biochemistry, and function of DA as it might relate to the behavioral characteristics of schizophrenia. Some of the evidence for the DA hypothesis has been reviewed previously (Klawans, Goetz, and Westheimer 1972, Matthysse 1973 and 1974, Snyder 1972, Snyder, Aghajanian, and Matthysse 1972, and Snyder et al. 1974a). Significant segments of recent symposia on catecholamines or DA are devoted to this topic or are highly relevant (Calne, Chase, and Barbeau 1975, Kety and Matthysse 1972, Usdin 1974, Usdin and Bunney 1975, and Usdin and Snyder 1973). For readers of the