Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by deficits in social communication, increased repetitive/restricted behaviours and anxiety. The prevalence of autism has been drastically increasing over the past few decades with an associated increase in socioeconomic burden, imposing hardship on many families. Currently, 1 in 66 Canadians are impacted by the disorder and males are four times as likely to be diagnosed with ASD. There is a growing need to understand the underlying mechanisms during development that are contributing to the pathology of ASD in both sexes. Clinical and epidemiological studies suggest exposure to environmental risk factors during pregnancy can impact lipid signaling during development, contributing to the pathology of ASD in children. Previous literature has provided evidence that a bioactive lipid signalling molecule in the brain, known as prostaglandin E2 (PGE2) can be perturbed due to exposure to environmental risk factors during pregnancy, impacting critical processes such as neuronal migration, differentiation and proliferation. Moreover, deficits in hippocampal function are known to contribute to the major symptoms that characterize ASD. In this study, we investigated how prenatal exposure to PGE2 impacts the developing hippocampus in males and females. We examined the effect of PGE2 exposure on dendritic morphology using Golgi-cox staining and proteins that may be driving these morphological changes using western blotting. Our findings suggest that prenatal PGE2 exposure impacts hippocampal dendritic morphology in a sex-dependent manner, which is associated with changes in the expression of proteins involved in cytoskeletal architecture. Ultimately, this study provides us with insight on how perturbed PGE2 signaling impacts cytoskeletal dynamics in the developing hippocampus, contributing to the pathology of autism
