ABSTRACT
Dopamine (DA) has been the centrepiece of schizophrenia research for over three decades. Evidence that antipsychotic drugs increase presynaptic DA metabolism, that they block dopamine receptors, and that dopamimetic drugs are psychotogenic led to the classic dopamine hypothesis of schizophrenia (Carlsson, 2001). In its earliest version, the dopamine hypothesis proposed that DA levels were increased in patients with schizophrenia. The initial tests of this hypothesis involved assays of DA and metabolites in peripheral fluids (e.g. blood, urine and CSF (cerebrospinal fluid)) and directly in postmortem brain tissue. In the main, these efforts were not confirmatory of increased DA levels, turnover, or metabolism (Laruelle, 2003).
