There is a growing interest in the functional role of microglia in the developing brain. In our laboratory, we have become particularly intrigued as to whether fetal microglia in the embryonic brain are susceptible to maternal challenges in utero (e.g., maternal infection, stress) and, if so, whether their precocious activation could then adversely influence brain development. One such challenge that is newly arising in this field is whether microglia might be downstream targets to endocrine-disrupting chemicals, such as the plasticizer bisphenol A (BPA), which functions in part by mimicking estrogen structure and function. A growing body of evidence demonstrates that gestational exposure to BPA has adverse effects on brain development, although the exact mechanisms are still emerging. Given that microglia express estrogen receptors and steroid-producing enzymes, microglia might be an unappreciated target of BPA. Mechanistically, we propose that BPA binding to estrogen receptors within microglia initiates transcription of downstream target genes, which then leads to activation of microglia that can then perhaps adversely influence brain development. Here, we first briefly outline the current understanding of how microglia may influence brain development and then describe how this literature overlaps with our understanding of BPA's effects during similar time points. We also outline the current literature demonstrating that BPA exposure affects microglia. We conclude by discussing our thoughts on the mechanisms through which exposure to BPA could disrupt normal microglia functions, ultimately affecting brain development that could potentially lead to lasting behavioral effects and perhaps even neuroendocrine diseases such as obesity.
Keywords: bisphenol A; hypothalamus; microglia; obesity.