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

Area of Science:

• Neuroscience
• Toxicology
• Developmental Biology

Background:

• Bisphenol A (BPA) is a known endocrine disruptor linked to abnormal neurogenesis in the developing neocortex.
• The precise mechanisms of BPA's neurotoxicity, particularly concerning neuroinflammation, remain incompletely understood.

Purpose of the Study:

• To investigate the impact of BPA exposure on microglial morphology and pro-inflammatory cytokine gene expression in the newborn mouse neocortex.
• To elucidate the role of neuroinflammation in BPA-induced neurodevelopmental toxicity.

Main Methods:

• ICR mice were exposed to BPA (200 μg/kg/d) from gestational day 6 through post-partum day 21.
• Microglial morphology and the gene expression of pro-inflammatory factors were assessed in weanlings.

Main Results:

• BPA-exposed weanlings exhibited an increased number of amoeboid-type microglia, indicating altered microglial activation states.
• A disruption in the M1/M2 microglial ratio was observed, suggesting impaired microglial differentiation.
• Abnormal gene expression patterns for pro-inflammatory factors were detected in the neocortex.

Conclusions:

• Prenatal and early postnatal BPA exposure induces microglial activation and neuroinflammation in the developing neocortex.
• These inflammatory changes are likely contributors to the known neurodevelopmental toxicity of BPA.
• Targeting neuroinflammation may offer a strategy to mitigate BPA's adverse effects on brain development.