Journal
SCHIZOPHRENIA BULLETIN
Volume 36, Issue 3, Pages 472-485Publisher
OXFORD UNIV PRESS
DOI: 10.1093/schbul/sbq031
Keywords
psychosis; delusion; reward; ventral striatum; fMRI; FDOPA
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Funding
- German Research Foundation (Deutsche Forschungs-gemeinschaft) [HE 2597/4-3, HE 2597/4-4]
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A dysregulation of the mesolimbic dopamine system in schizophrenia patients may lead to aberrant attribution of incentive salience and contribute to the emergence of psychopathological symptoms like delusions. The dopaminergic signal has been conceptualized to represent a prediction error that indicates the difference between received and predicted reward. The incentive salience hypothesis states that dopamine mediates the attribution of incentive salience to conditioned cues that predict reward. This hypothesis was initially applied in the context of drug addiction and then transferred to schizophrenic psychosis. It was hypothesized that increased firing (chaotic or stress associated) of dopaminergic neurons in the striatum of schizophrenia patients attributes incentive salience to otherwise irrelevant stimuli. Here, we review recent neuroimaging studies directly addressing this hypothesis. They suggest that neuronal functions associated with dopaminergic signaling, such as the attribution of salience to reward-predicting stimuli and the computation of prediction errors, are indeed altered in schizophrenia patients and that this impairment appears to contribute to delusion formation.
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