Maternal inflammation disrupts neurogenesis and neocortical organization, affecting social and stress-related behavior.

It is imperative to acknowledge the potential impact of various environmental factors on the development of developmental disorders. Among these factors, the maternal immune response induced by the onset of infectious diseases during pregnancy emerges as a notable consideration. The study elucidates the behavioral and morphological abnormalities of the cerebral cortex caused by maternal immune response during pregnancy, emphasizing the significance of maternal immunity in this context. To this end, a mouse model of prenatal infection was established, inducing a congenital immune response analogous to viral infection using polyinosinic-polycytidylic acid (poly(I:C)). Pregnant C57BL/6 N mice were administered poly(I:C) (20 mg/kg, intraperitoneally) on gestational day 12.5. This exposure led to specific abnormalities in neural stem cell differentiation and neurogenesis, which manifested as irregularities in the distribution and layering of neurons in the cerebral cortex. Furthermore, an analysis of spontaneous locomotion, social interaction, and social proximity during the developmental and maturation stages of brain function revealed abnormalities in various environments, including novel and familiar environments, as well as single and group-reared environments. Notably, these mice exhibited a heightened sensitivity to stress post-maturation, underscoring the intricate consequences of maternal immune activation (MIA) on neurodevelopment as an environmental factor. These findings underscore the enduring consequences of MIA on brain development, substantiate the association between intrauterine inflammation and neurodevelopmental disorders, and accentuate the potential implications of intrauterine inflammation in modulating stress responses after maturation.