Maternal Bisphenol A (BPA) Exposure Alters Cerebral Cortical Morphogenesis and Synaptic Function in Mice.
Chang Youn LeeSung-Ae HyunMoon Yi KoHye Ryeong KimJaerang RhoKee K KimWoo-Yang KimMinhan KaPublished in: Cerebral cortex (New York, N.Y. : 1991) (2022)
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.
Keyphrases
- physical activity
- birth weight
- rna seq
- pregnancy outcomes
- signaling pathway
- body mass index
- cell death
- early life
- single cell
- endoplasmic reticulum stress
- oxidative stress
- subarachnoid hemorrhage
- induced apoptosis
- traumatic brain injury
- healthcare
- type diabetes
- pregnant women
- skeletal muscle
- adipose tissue
- genome wide
- blood brain barrier
- brain injury
- dna methylation
- gene expression
- high fat diet
- high fat diet induced
- preterm birth
- white matter
- cerebral blood flow
- genome wide identification
- wild type