Dopamine in schizophrenia.

The DA hypothesis of schizophrenia is one of the oldest biological hypotheses of schizophrenia with many revised versions. However, it is unlikely that any single neurotransmitter hypothesis is able to explain the biological basis of such a highly heterogenous disorder as schizophrenia in a satisfactory way. Rather, it is evident that the biological vulnerability factors and the 'acute neurophysiology' of schizophrenic symptoms involve a complex set of imbalances of aberrant connections in neuronal circuits in the brain. Dopamine is likely to be one of the transmitter substances involved, as evidenced by recent neuroimaging studies in neuroleptic-naive schizophrenia. Regardless of whether the DA hypothesis of schizophrenia is true or not, the DA hypothesis of neuroleptic drug action still has a relatively solid basis. The DA D2 receptor blockade remains the best characterized clinically useful mechanism of drug action to alleviate psychotic symptoms. The ongoing and future work on the precise role of DA in schizophrenia should focus on first-episode/admission neuroleptic-naive schizophrenic patients. Such studies represent the best opportunity of finding out specific changes in the dopaminergic pathways and relating them in a meaningful way to various dimensions of psychopathology seen in schizophrenic patients.