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The theory that dopaminergic mechanisms play a role in psychosis has evolved since the mid-twentieth century. This followed research which found that the clinical potency of antipsychotics was directly related to their affinity for dopamine receptors and drugs that cause dopamine release caused psychotic symptoms. Molecular imaging studies have found consistent evidence that elevated striatal dopamine synthesis capacity is associated with psychotic symptoms including in people with schizophrenia, people at risk of psychosis and first-degree relatives of people with schizophrenia. Importantly, dopamine elevation has been positively correlated with severity of psychotic symptoms. There is also evidence that dopamine dysfunction may be a transdiagnostic feature of psychosis. The dopamine system plays a key role in cognition, including reward prediction error signaling and salience processing. Dopaminergic dysfunction has been hypothesized to give rise to psychosis through aberrant salience processing. Since stressful experiences are highly salient for an organism’s survival, the dopamine system plays a key role in the brain’s response to stressors. Chronic stressors occurring during development can induce long-term changes in dopamine function and may thus provide a pathway through which environmental risk factors for psychosis alter neurobiology to give rise to psychosis. At least some genetic risk factors for psychosis also converge on the dopamine system. These findings have given rise to a “dual hit” model of dopaminergic dysfunction involving genetic vulnerability and responses to environmental stressors.

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The treatment of attention deficit hyperactivity disorder inTourette's syndrome; a double-blind placebo controlled study with clonidine and desipramine.

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