PT - JOURNAL ARTICLE AU - Courtney Scaramella AU - Joseph B. Alzagatiti AU - Christopher Creighton AU - Samandeep Mankatala AU - Fernando Licea AU - Gabriel M. Winter AU - Jasmine Emtage AU - Joseph R. Wisnieski AU - Luis Salazar AU - Anjum Hussain AU - Faith M. Lee AU - Asma Mammootty AU - Niyaza Mammootty AU - Andrew Aldujaili AU - Kristine A. Runnberg AU - Daniela Hernandez AU - Trevor Zimmerman-Thompson AU - Rikhil Makwana AU - Julien Rouvere AU - Zahra Tahmasebi AU - Gohar Zavradyan AU - Christopher S. Campbell AU - Meghna Komaranchath AU - Javier Carmona AU - Jennifer Trevitt AU - David Glanzman AU - Adam C. Roberts TI - Bisphenol A Exposure Induces Sensory Processing Deficits in Larval Zebrafish during Neurodevelopment AID - 10.1523/ENEURO.0020-22.2022 DP - 2022 May 01 TA - eneuro PG - ENEURO.0020-22.2022 VI - 9 IP - 3 4099 - http://www.eneuro.org/content/9/3/ENEURO.0020-22.2022.short 4100 - http://www.eneuro.org/content/9/3/ENEURO.0020-22.2022.full SO - eNeuro2022 May 01; 9 AB - 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.