Department of Psychiatry, Charité-Universitätsmedizin Berlin, Charité Campus Mitte, 10117 Berlin, Germany.
Schizophr Bull. 2010 May;36(3):472-85. doi: 10.1093/schbul/sbq031. Epub 2010 May 7.
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.
精神分裂症患者中边缘系统多巴胺系统的失调可能导致激励显著性的异常归因，并导致妄想等精神病理症状的出现。多巴胺能信号被概念化为代表预测误差的信号，表明所接收的奖励与所预测的奖励之间的差异。激励显著性假说指出，多巴胺介导了对预测奖励的条件线索的“激励显著性”归因。该假说最初应用于药物成瘾的背景下，然后被转移到精神分裂症精神病学中。据推测，精神分裂症患者纹状体中多巴胺能神经元的过度放电（与紊乱或应激相关）将激励显著性归因于其他不相关的刺激。在这里，我们回顾了直接针对该假说的最新神经影像学研究。它们表明，与多巴胺能信号相关的神经元功能，例如对奖励预测刺激的显著性归因和预测误差的计算，在精神分裂症患者中确实发生了改变，并且这种损伤似乎导致了妄想的形成。
