Poster #031
PLX5622 effects on primed microglia in maternal immune activated offspring
Mentor: Yilin Liu, PhD Student
Maternal immune activation (MIA) is a risk factor for neurodevelopmental disorders (NDDs) such as schizophrenia and epilepsy. During MIA, microglia regulate neuroinflammatory responses through increased activation and interaction with cerebral vasculature. Previous research indicates that MIA-induced disruptions to blood-brain barrier (BBB) development cause lifelong BBB hyperpermeability and chronic activation in microglia. However, there are knowledge gaps surrounding the role of microglial activation, morphological changes, and activation in sustaining MIA-mediated BBB disruption throughout life. We hypothesize that microglia primed prenatally by MIA remain activated, leading to sustained MIA-mediated BBB dysfunction. To test this, we induced MIA by injecting immunostimulant poly(I:C) during pregnancy. MIA offspring received PLX5622 treatment, a CSFR1R inhibitor that depletes microglia, and we measured the impact on offspring BBB integrity. Ultimately, our results will demonstrate whether microglia activation and perivascular localization are necessary for MIA-mediated BBB disruption, providing novel insight into the molecular etiology of NDDs.