ABSTRACT

The dopamine hypothesis of schizophrenia, which originally emerged in the 1960s, postulated an overactivity of the dopamine systems of the midbrain as the neurobiological anomaly in schizophrenia. In spite of much research effort over more than 30 years, direct evidence for changes in brain dopamine concentrations or in dopamine receptor densities remained frustratingly intangible. However, in recent years a new lease of life has been given to this hypothesis. This has come about first through a paradigm shift in how the dopamine hypothesis is postulated and, secondly, through technical advances allowing the dynamics of dopaminergic neuro-transmission to be assessed in a more sophisticated fashion.