GABA and acute psychoses

This is the authors' abstract. We don't add key points for this paper.

Recent attempts to explain acute psychotic behaviour in terms of disordered cerebral neurotransmitter function have largely concerned the monoamines, serotonin, dopamine and noradrenaline Most prominent among these endeavours is the dopamine hypothesis of schizophrenia, which in its current form proposes that the 'positive' symptoms of acute schizophrenia (or Schneider first-rank symptoms) depend on relative overactivity in certain dopaminergic pathways, most probably those in the mesolimbic system Support for this hypothesis is provided by evidence that the neuroleptic drugs which specifically diminish the positive symptoms of acute schizophrenia act at dopamine receptor sites to diminish the biochemical or physiological effects of dopamine. Studies of dopamine turnover in schizophrenic patients However, post-mortem studies do indicate an increase in the dopamine content and in the number of dopamine or butyrophenone receptors in the mesolimbic system and striatum in the brains of chronic schizophrenic patients These observations can be interpreted as showing diminished dopaminergic activity associated with the defect state of chronic schizophrenia