Abstract
Schizophrenia is a severe and common psychiatric disease characterized by hallucinations, delusions, deficit in motivation and cognitive dysfunction. Because many patients show poor or partial response to antipsychotic treatment, it is important to develop novel therapeutic interventions with greater efficacy through new mechanism of action. The hypothesis of inflammation‐induced neurodevelopmental impairment and glutamatergic hypofunction have been proposed as the etiology/pathophysiology of schizophrenia. Kynurenine metabolism is activated by inflammation and there are some metabolites which induce neurotoxicity and affect glutamatergic transmission. Based on the epidemiological hypothesis that maternal gestational exposure to human influenza virus induces vulnerability for the onset of the schizophrenia, embryos of mice are exposed the viral mimic polyriboinosinic‐polyribocytidilic acid (poly I : C) during prenatal period to develop the schizophrenia‐like animal model. In this review, we summarize schizophrenia‐like animal model with neurodevelopmental impairment induced by the prenatal poly I : C exposure and an involvement of kynurenine metabolism in the animal model induced by the prenatal poly I : C exposure. No potential conflicts of interest were disclosed.
