AI Article Synopsis
- Early exposure to bisphenol A (BPA), a synthetic compound found in plastics, is linked to cognitive and emotional issues later in life.
- Maternal BPA exposure disrupted the growth of neural progenitor cells in the brain, leading to fewer neurons and more glial cells, along with impaired synapse formation.
- Behavioral tests on mice showed that those whose mothers were exposed to BPA exhibited hyperactivity and social challenges, suggesting that BPA affects brain structure and function, possibly through autophagy mechanisms.
Article Abstract
Early-life exposure to bisphenol A (BPA), synthetic compound used in polycarbonate plastic, is associated with altered cognitive and emotional behavior later in life. However, the brain mechanism underlying the behavioral deficits is unknown. Here, we show that maternal BPA exposure disrupted self-renewal and differentiation of neural progenitors during cortical development. The BPA exposure reduced the neuron number, whereas it increased glial cells in the cerebral cortex. Also, synaptic formation and transmission in the cerebral cortex were suppressed after maternal BPA exposure. These changes appeared to be associated with autophagy as a gene ontology analysis of RNA-seq identified an autophagy domain in the BPA condition. Mouse behavioral tests revealed that maternal BPA caused hyperactivity and social deficits in adult offspring. Together, these results suggest that maternal BPA exposure leads to abnormal cortical architecture and function likely by activating autophagy.
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| http://dx.doi.org/10.1093/cercor/bhab183 | DOI Listing |
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