Abstract
Maternal stress, inflammation, and nutriture during pregnancy are correlated with a higher prevalence of neurodevelopmental disorders, such as autism spectrum disorder (ASD) , attention‐deficit/hyperactivity disorder, and intellectual disability. In the widely used maternal immune activation (MIA) rodent model, the pathology of ASD has been studied. Administration of the viral mimetic, toll‐like receptor (TLR) ligands, such as lipopolysaccharide or polyinosinic‐polycytidylic acid[poly (I : C) ], is commonly used as experimental tools to study neuronal and dysfunctions in ASD. However, a lot of evidence from investigations suggests that these TLR ligands can vary in terms of their immunogenicity in rodent. Here, we will introduce new research findings of the MIA‐induced ASD pathogenesis as well as the problems inducing inflammation by poly (I : C) administration. In addition, we will explain about the usability for a mouse MIA model by gene transfer system continuously expressing proinflammatory cytokine.
