In spite of its proven heuristic value, the dopamine hypothesis of schizoph
renia is now yielding to a multifactorial view, in which the other monoamin
es as well as glutamate and GABA are included, with a focus on neurotransmi
tter interactions in complex neurocircuits. The primary lesion(s) in schizo
phrenia does not necessarily involve any of these neurotransmitters directl
y but could deal with a more general defect, such as a faulty connectivity
of developmental origin. Nevertheless, a precise identification of neurotra
nsmitter aberrations in schizophrenia will probably provide clues for a bet
ter understanding of the disease and for the development of new treatment a
nd prevention strategies.