Vidal Pia M, Pacheco Rodrigo
Department of Basic Science, Biomedical Science Research Lab, Faculty of Medicine, Universidad Católica de la Santísima Concepción, Concepción, Chile.
Laboratorio de Neuroinmunología, Fundación Ciencia & Vida, Santiago, Chile.
Front Pharmacol. 2020 Mar 31;11:394. doi: 10.3389/fphar.2020.00394. eCollection 2020.
Dopamine is one of the neurotransmitters whose transmission is altered in a number of neural pathways in the brain of schizophrenic patients. Current evidence indicates that these alterations involve hyperactive dopaminergic transmission in mesolimbic areas, striatum, and hippocampus, whereas hypoactive dopaminergic transmission has been reported in the prefrontal cortex of schizophrenic patients. Consequently, schizophrenia is associated with several cognitive and behavioral alterations. Of note, the immune system has been found to collaborate with the central nervous system in a number of cognitive and behavioral functions, which are dysregulated in schizophrenia. Moreover, emerging evidence has associated schizophrenia and inflammation. Importantly, different lines of evidence have shown dopamine as a major regulator of inflammation. In this regard, dopamine might exert strong regulation in the activity, migration, differentiation, and proliferation of immune cells that have been shown to contribute to cognitive functions, including T-cells, microglial cells, and peripheral monocytes. Thereby, alterations in dopamine levels associated to schizophrenia might affect inflammatory response of immune cells and consequently some behavioral functions, including reference memory, learning, social behavior, and stress resilience. Altogether these findings support the involvement of an active cross-talk between the dopaminergic and immune systems in the physiopathology of schizophrenia. In this review we summarize, integrate, and discuss the current evidence indicating the involvement of an altered dopaminergic regulation of immunity in schizophrenia.
多巴胺是一种神经递质,其在精神分裂症患者大脑中的多个神经通路中的传递发生改变。目前的证据表明,这些改变涉及中脑边缘区域、纹状体和海马体中多巴胺能传递亢进,而在精神分裂症患者的前额叶皮质中,多巴胺能传递则被报道为减退。因此,精神分裂症与多种认知和行为改变相关。值得注意的是,免疫系统已被发现与中枢神经系统在一些认知和行为功能方面存在协作,而这些功能在精神分裂症中失调。此外,新出现的证据将精神分裂症与炎症联系起来。重要的是,不同的证据线索表明多巴胺是炎症的主要调节因子。在这方面,多巴胺可能对免疫细胞的活性、迁移、分化和增殖发挥强有力的调节作用,这些免疫细胞已被证明对包括T细胞、小胶质细胞和外周单核细胞在内的认知功能有贡献。因此,与精神分裂症相关的多巴胺水平改变可能会影响免疫细胞的炎症反应,进而影响一些行为功能,包括参考记忆、学习、社会行为和应激恢复力。所有这些发现都支持多巴胺能系统与免疫系统之间的活跃相互作用参与了精神分裂症的病理生理过程。在这篇综述中,我们总结、整合并讨论了当前的证据,这些证据表明多巴胺能调节免疫功能的改变与精神分裂症有关。