Since the discovery of the effects of chlorpromazine in the 1950s, treatment of schizophrenia has relied on antipsychotic drugs that target dopamine D2 receptors. The effectiveness of these agents in reducing the intensity of patients' delusions and hallucinations permitted outpatient treatment instead of lifelong institutionalization in state mental hospitals. The many antipsychotic drugs introduced during the next decade were increasingly potent, as medicinal chemists improved the drugs' affinity for the D2 receptor. However, the efficacy of the drugs was similar, since all had the same mechanism of action.1 A troubling problem was that the blockade of dopaminergic neurotransmission in the . . .
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Robert Freedman (2005) studied this question.
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