1. Synthesis and release of dopamine as well as firing rates of dopaminergic neurons are controlled by stimulation of autoreceptors via a negative feedback regulation. Investigations on therapeutic effects of autoreceptor-nonselective dopamine agonists in schizophrenia have yielded inconsistent results. 2. With respect to the dopamine hypothesis of schizophrenia, dopamine autoreceptor agonists have been tested in positive schizophrenic symptomatology in order to reduce the postulated excess of central dopaminergic activity. However, administration of selective dopamine autoreceptor agonists like talipexole or roxindole did not result in a significant improvement of psychopathological symptoms. 3. In negative schizophrenic symptomatology, a dopamine deficit rather than an excess has been hypothesized. Current evidence from open clinical trials suggests that dopamine autoreceptor agonists may produce a minor to moderate improvement of symptoms like affective flattening, depressed mood, alogia and avolition.