Abstract
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.
Highlights
Reviewed by: Dietmar Fuchs, Innsbruck Medical University, Austria Belinda Lennox, University of Oxford, United Kingdom Marie-Eve Tremblay, Laval University, Canada
Thereby, alterations in dopamine levels associated to schizophrenia might affect inflammatory response of immune cells and some behavioral functions, including reference memory, learning, social behavior, and stress resilience
Specially T-cells, microglial cells and peripheral monocytes, have been described to collaborate with the central nervous system (CNS) to carry out some of these cognitive and behavioral functions that are altered in schizophrenia
Summary
Schizophrenia is a mental illness that often appears during late adolescence or early adulthood. Glutamatergic hypofunction has been suggested as one of the mechanisms involved in this dopaminergic dysfunction in schizophrenia (Swerdlow et al, 2009) In this regard, it has been hypothesized that DRD2-antagonism might prevent DRD1-mediated potentiation of N-Methyl-d-aspartate (NMDA) responses in the prefrontal cortex (Paz et al, 2008). It has been shown that in comparison to healthy subjects, dopamine occupies a higher proportion of striatal D2-like receptors (Kegeles et al, 2010), and a bigger fraction of the dopamine transporters (DAT) in sensorimotor striatum (Weinstein et al, 2017) in schizophrenia It has been described a sub-regional heterogeneity in the dopaminergic dysregulation within the striatum. Further research is still needed to better understand the alterations of dopaminergic circuitry associated to the pathophysiological scenario of schizophrenia
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