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Maternal administration of bisphenol A alters the microglial profile in the neocortex of mouse weanlings

Bisphenol A (BPA) is known to cause abnormal neurogenesis in the developing neocortex. The mechanisms of BPA toxicity concerning neuroinflammatory‐related endpoints are incompletely characterized. To evaluate the microglial morphology and the gene expression of pro‐inflammatory cytokines in the newborn neocortex, ICR mice were exposed to BPA 200 μg/kg/d on gestational day 6 through post‐partum day 21. Weanlings exposed during prenatal and postnatal period to BPA showed an increased number of amoeboid‐type microglia, a microglial differentiation disruption (the M1/M2 microglial ratio), and an abnormal expression of genes encoding pro‐inflammatory factors. These findings suggest that the well‐known neurodevelopmental toxicity of BPA may be related to an increased microglial activation and neuroinflammation in the neocortex.