Maternal Bisphenol A (BPA) Exposure Alters Cerebral Cortical Morphogenesis and Synaptic Function in Mice
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 disrupt...
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| Veröffentlicht in: | Cerebral cortex (New York, N.Y. 1991) N.Y. 1991), 2021-10, Vol.31 (12), p.5598-5612 |
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| container_title | Cerebral cortex (New York, N.Y. 1991) |
| container_volume | 31 |
| creator | Lee, Chang Youn Hyun, Sung-Ae Ko, Moon Yi Kim, Hye Ryeong Rho, Jaerang Kim, Kee K Kim, Woo-Yang Ka, Minhan |
| description | 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. |
| doi_str_mv | 10.1093/cercor/bhab183 |
| format | Article |
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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.</description><identifier>ISSN: 1047-3211</identifier><identifier>EISSN: 1460-2199</identifier><identifier>DOI: 10.1093/cercor/bhab183</identifier><identifier>PMID: 34171088</identifier><language>eng</language><publisher>United States: Oxford University Press</publisher><subject>Animals ; Benzhydryl Compounds - toxicity ; Cerebral Cortex ; Mice ; Neurogenesis ; Phenols - toxicity ; Prenatal Exposure Delayed Effects - chemically induced</subject><ispartof>Cerebral cortex (New York, N.Y. 1991), 2021-10, Vol.31 (12), p.5598-5612</ispartof><rights>The Author(s) 2021. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com 2021</rights><rights>The Author(s) 2021. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c395t-2f7c34121a5fd4fcd2b0b73400268fab42688cb21efba54fc95597b396e5dfb23</citedby><cites>FETCH-LOGICAL-c395t-2f7c34121a5fd4fcd2b0b73400268fab42688cb21efba54fc95597b396e5dfb23</cites><orcidid>0000-0003-3938-6062</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1584,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34171088$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Chang Youn</creatorcontrib><creatorcontrib>Hyun, Sung-Ae</creatorcontrib><creatorcontrib>Ko, Moon Yi</creatorcontrib><creatorcontrib>Kim, Hye Ryeong</creatorcontrib><creatorcontrib>Rho, Jaerang</creatorcontrib><creatorcontrib>Kim, Kee K</creatorcontrib><creatorcontrib>Kim, Woo-Yang</creatorcontrib><creatorcontrib>Ka, Minhan</creatorcontrib><title>Maternal Bisphenol A (BPA) Exposure Alters Cerebral Cortical Morphogenesis and Synaptic Function in Mice</title><title>Cerebral cortex (New York, N.Y. 1991)</title><addtitle>Cereb Cortex</addtitle><description>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.</description><subject>Animals</subject><subject>Benzhydryl Compounds - toxicity</subject><subject>Cerebral Cortex</subject><subject>Mice</subject><subject>Neurogenesis</subject><subject>Phenols - toxicity</subject><subject>Prenatal Exposure Delayed Effects - chemically induced</subject><issn>1047-3211</issn><issn>1460-2199</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkL1PwzAUxC0EoqWwMiKP7ZDWH3GTjG3UAlIrkIA5sp0XGpTawU4k-t9j1MLKdCe9352eDqFbSqaUZHymwWnrZmonFU35GRrSeE4iRrPsPHgSJxFnlA7QlfcfhNCECXaJBjymCSVpOkS7rezAGdngZe3bHRjb4AUeL58XE7z6aq3vHeBFExiPc3CgXEBz67paB7O1rt3ZdzDga4-lKfHLwcg2HPG6N7qrrcG1wdtawzW6qGTj4eakI_S2Xr3mD9Hm6f4xX2wizTPRRaxKdPiOUSmqMq50yRRRCY8JYfO0kioOkmrFKFRKigBkQmSJ4tkcRFkpxkdofOxtnf3swXfFvvYamkYasL0vmIhDgnEhAjo9otpZ7x1URevqvXSHgpLiZ93iuG5xWjcE7k7dvdpD-Yf_zhmAyRGwfftf2Tf4XoYz</recordid><startdate>20211022</startdate><enddate>20211022</enddate><creator>Lee, Chang Youn</creator><creator>Hyun, Sung-Ae</creator><creator>Ko, Moon Yi</creator><creator>Kim, Hye Ryeong</creator><creator>Rho, Jaerang</creator><creator>Kim, Kee K</creator><creator>Kim, Woo-Yang</creator><creator>Ka, Minhan</creator><general>Oxford University Press</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-3938-6062</orcidid></search><sort><creationdate>20211022</creationdate><title>Maternal Bisphenol A (BPA) Exposure Alters Cerebral Cortical Morphogenesis and Synaptic Function in Mice</title><author>Lee, Chang Youn ; Hyun, Sung-Ae ; Ko, Moon Yi ; Kim, Hye Ryeong ; Rho, Jaerang ; Kim, Kee K ; Kim, Woo-Yang ; Ka, Minhan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c395t-2f7c34121a5fd4fcd2b0b73400268fab42688cb21efba54fc95597b396e5dfb23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Benzhydryl Compounds - toxicity</topic><topic>Cerebral Cortex</topic><topic>Mice</topic><topic>Neurogenesis</topic><topic>Phenols - toxicity</topic><topic>Prenatal Exposure Delayed Effects - chemically induced</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Chang Youn</creatorcontrib><creatorcontrib>Hyun, Sung-Ae</creatorcontrib><creatorcontrib>Ko, Moon Yi</creatorcontrib><creatorcontrib>Kim, Hye Ryeong</creatorcontrib><creatorcontrib>Rho, Jaerang</creatorcontrib><creatorcontrib>Kim, Kee K</creatorcontrib><creatorcontrib>Kim, Woo-Yang</creatorcontrib><creatorcontrib>Ka, Minhan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Cerebral cortex (New York, N.Y. 1991)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Chang Youn</au><au>Hyun, Sung-Ae</au><au>Ko, Moon Yi</au><au>Kim, Hye Ryeong</au><au>Rho, Jaerang</au><au>Kim, Kee K</au><au>Kim, Woo-Yang</au><au>Ka, Minhan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Maternal Bisphenol A (BPA) Exposure Alters Cerebral Cortical Morphogenesis and Synaptic Function in Mice</atitle><jtitle>Cerebral cortex (New York, N.Y. 1991)</jtitle><addtitle>Cereb Cortex</addtitle><date>2021-10-22</date><risdate>2021</risdate><volume>31</volume><issue>12</issue><spage>5598</spage><epage>5612</epage><pages>5598-5612</pages><issn>1047-3211</issn><eissn>1460-2199</eissn><abstract>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.</abstract><cop>United States</cop><pub>Oxford University Press</pub><pmid>34171088</pmid><doi>10.1093/cercor/bhab183</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0003-3938-6062</orcidid></addata></record> |
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| source | MEDLINE; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Animals Benzhydryl Compounds - toxicity Cerebral Cortex Mice Neurogenesis Phenols - toxicity Prenatal Exposure Delayed Effects - chemically induced |
| title | Maternal Bisphenol A (BPA) Exposure Alters Cerebral Cortical Morphogenesis and Synaptic Function in Mice |
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