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Bisphenol A Exposure Induces Sensory Processing Deficits in Larval Zebrafish during Neurodevelopment

Scaramella, Courtney and Alzagatiti, Joseph B. and Creighton, Christopher and Mankatala, Samandeep and Licea, Fernando and Winter, Gabriel M. and Emtage, Jasmine and Wisnieski, Joseph R. and Salazar, Luis and Hussain, Anjum and Lee, Faith M. and Mammootty, Asma and Mammootty, Niyaza and Aldujaili, Andrew and Runnberg, Kristine A. and Hernandez, Daniela and Zimmerman-Thompson, Trevor and Makwana, Rikhil and Rouvere, Julien and Tahmasebi, Zahra and Zavradyan, Gohar and Campbell, Christopher S. and Komaranchath, Meghna and Carmona, Javier and Trevitt, Jennifer and Glanzman, David and Roberts, Adam C. (2022) Bisphenol A Exposure Induces Sensory Processing Deficits in Larval Zebrafish during Neurodevelopment. eNeuro, 9 (3). Art. No. ENEURO.0020-22.2022. ISSN 2373-2822. PMCID PMC9116930. doi:10.1523/eneuro.0020-22.2022. https://resolver.caltech.edu/CaltechAUTHORS:20220523-165193000

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Abstract

Because of their ex utero development, relatively simple nervous system, translucency, and availability of tools to investigate neural function, larval zebrafish are an exceptional model for understanding neurodevelopmental disorders and the consequences of environmental toxins. Furthermore, early in development, zebrafish larvae easily absorb chemicals from water, a significant advantage over methods required to expose developing organisms to chemical agents in utero. Bisphenol A (BPA) and BPA analogs are ubiquitous environmental toxins with known molecular consequences. All humans have measurable quantities of BPA in their bodies. Most concerning, the level of BPA exposure is correlated with neurodevelopmental difficulties in people. Given the importance of understanding the health-related effects of this common toxin, we have exploited the experimental advantages of the larval zebrafish model system to investigate the behavioral and anatomic effects of BPA exposure. We discovered that BPA exposure early in development leads to deficits in the processing of sensory information, as indicated by BPA’s effects on prepulse inhibition (PPI) and short-term habituation (STH) of the C-start reflex. We observed no changes in locomotion, thigmotaxis, and repetitive behaviors (circling). Despite changes in sensory processing, we detected no regional or whole-brain volume changes. Our results show that early BPA exposure can induce sensory processing deficits, as revealed by alterations in simple behaviors that are mediated by a well-defined neural circuit.


Item Type:Article
Related URLs:
URLURL TypeDescription
https://doi.org/10.1523/ENEURO.0020-22.2022DOIArticle
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9116930/PubMed CentralArticle
ORCID:
AuthorORCID
Scaramella, Courtney0000-0002-0021-7117
Glanzman, David0000-0001-5479-0245
Roberts, Adam C.0000-0001-8596-8552
Additional Information:© 2022 Scaramella et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed. Received January 16, 2022. Revision received March 10, 2022. Accepted April 1, 2022. Published online May 4, 2022. We thank RIKEN for the transgenic fish line Tg(elavl3:Kaede). The authors declare no competing financial interests. This work was supported by the National Institutes of Health National Institute of General Medical Sciences Grant SC2 GM130485 (to A.C.R.). Author contributions: C.S., J.B.A., and A.C.R. designed research; C.S., C.C., S.M., F.L., G.M.W., J.E., L.S., and T.Z.-T. performed research; C.S., J.B.A., C.C., S.M., F.L., G.MW., J.R.W., L.S., A.H., F.M.L., A.M., N.M., A.A., K.A.R., D.H., T.Z.T., R.M., J.R., Z.T., G.Z., C.C., M.K., J.C., and A.C.R. analyzed data; C.S., J.B.A., J.T., D.G., and A.C.R. wrote the paper. C.S. and J.B.A. contributed equally to this work.
Funders:
Funding AgencyGrant Number
NIHSC2 GM130485
Subject Keywords:autism spectrum disorder; C-start reflex; habituation; Mauthner cell; prepulse inhibition; zebrafish
Issue or Number:3
PubMed Central ID:PMC9116930
DOI:10.1523/eneuro.0020-22.2022
Record Number:CaltechAUTHORS:20220523-165193000
Persistent URL:https://resolver.caltech.edu/CaltechAUTHORS:20220523-165193000
Official Citation:Bisphenol A Exposure Induces Sensory Processing Deficits in Larval Zebrafish during Neurodevelopment Courtney Scaramella, Joseph B. Alzagatiti, Christopher Creighton, Samandeep Mankatala, Fernando Licea, Gabriel M. Winter, Jasmine Emtage, Joseph R. Wisnieski, Luis Salazar, Anjum Hussain, Faith M. Lee, Asma Mammootty, Niyaza Mammootty, Andrew Aldujaili, Kristine A. Runnberg, Daniela Hernandez, Trevor Zimmerman-Thompson, Rikhil Makwana, Julien Rouvere, Zahra Tahmasebi, Gohar Zavradyan, Christopher S. Campbell, Meghna Komaranchath, Javier Carmona, Jennifer Trevitt, David Glanzman, Adam C. Roberts eNeuro 4 May 2022, 9 (3) ENEURO.0020-22.2022; DOI: 10.1523/ENEURO.0020-22.2022
Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:114884
Collection:CaltechAUTHORS
Deposited By: George Porter
Deposited On:23 May 2022 20:25
Last Modified:23 May 2022 20:25

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