催产素、多巴胺与杏仁核：精神分裂症社会认知缺陷的神经功能模型。
Oxytocin, dopamine, and the amygdala: a neurofunctional model of social cognitive deficits in schizophrenia.
机构信息
Department of Psychiatry, Columbia University College of Physicians and Surgeons, New York State Psychiatric Institute, New York, NY 10032, USA.
出版信息
Schizophr Bull. 2011 Sep;37(5):1077-87. doi: 10.1093/schbul/sbq015. Epub 2010 Mar 22.
Until recently, the social cognitive impairment in schizophrenia has been underappreciated and remains essentially untreated. Deficits in emotional processing, social perception and knowledge, theory of mind, and attributional bias may contribute to functional social cognitive impairments in schizophrenia. The amygdala has been implicated as a key component of social cognitive circuitry in both animal and human studies. In addition, structural and functional studies of schizophrenia reproducibly demonstrate abnormalities in the amygdala and dopaminergic signaling. Finally, the neurohormone oxytocin plays an important role in multiple social behaviors in several mammals, including humans. We propose a model of social cognitive dysfunction in schizophrenia and discuss its therapeutic implications. The model comprises abnormalities in oxytocinergic and dopaminergic signaling in the amygdala that result in impaired emotional salience processing with consequent social cognitive deficits.
直到最近，精神分裂症的社会认知障碍一直未被充分认识，基本上得不到治疗。情绪处理、社会知觉和知识、心理理论以及归因偏差方面的缺陷可能导致精神分裂症的功能性社会认知障碍。在动物和人类研究中，杏仁核都被认为是社会认知回路的关键组成部分。此外，精神分裂症的结构和功能研究反复证明杏仁核和多巴胺能信号异常。最后，神经激素催产素在包括人类在内的几种哺乳动物的多种社会行为中发挥着重要作用。我们提出了一个精神分裂症社会认知功能障碍的模型，并讨论了其治疗意义。该模型包括杏仁核内催产素能和多巴胺能信号的异常，导致情绪显著性处理受损，进而导致社会认知缺陷。
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