The prolonged and sex-dependent impact of maternal immune activation (MIA) on the molecular pathways of the amygdala, a brain region that influences social, cognitive, and sexually dimorphic behaviors, is only partially understood. To address this gap, the effect of MIA elicited by porcine reproductive and respiratory syndrome virus (PRRSV) infection during gestation on the amygdala transcriptome of pigs was studied. Gene expression levels were measured using RNA-Seq on the amygdala for 3-week-old female and male offspring from MIA and control groups. Among the 328 genes that exhibited an MIA-by-sex effect, the majority annotated to functional categories relevant to behavioral abnormalities, including neuroactive ligand-receptor pathways, glutamatergic functions, and neuropeptide systems. Genes in these categories included corticotropin releasing hormone receptor 2, glutamate metabotropic receptor 4, glycoprotein hormones, alpha polypeptide, parathyroid hormone 1 receptor, vasointestinal peptide receptor 2, neurotensin, proenkephalin, and gastrin releasing peptide. These genes and functional categories have been associated with MIA-related schizophrenia and autism spectrum behavior disorders. The transcript and network dysregulation uncovered in this study advances the understanding necessary to develop treatments that ameliorate the effects of neurodevelopmental disorders caused by gestational MIA exposure. This study is supported by USDA NIFA AFRI, grant number 2018-67015-27413.
