RT Journal Article
SR Electronic
T1 Bisphenol A Exposure Induces Sensory Processing Deficits in Larval Zebrafish during Neurodevelopment
JF eneuro
JO eNeuro
FD Society for Neuroscience
SP ENEURO.0020-22.2022
DO 10.1523/ENEURO.0020-22.2022
VO 9
IS 3
A1 Courtney Scaramella
A1 Joseph B. Alzagatiti
A1 Christopher Creighton
A1 Samandeep Mankatala
A1 Fernando Licea
A1 Gabriel M. Winter
A1 Jasmine Emtage
A1 Joseph R. Wisnieski
A1 Luis Salazar
A1 Anjum Hussain
A1 Faith M. Lee
A1 Asma Mammootty
A1 Niyaza Mammootty
A1 Andrew Aldujaili
A1 Kristine A. Runnberg
A1 Daniela Hernandez
A1 Trevor Zimmerman-Thompson
A1 Rikhil Makwana
A1 Julien Rouvere
A1 Zahra Tahmasebi
A1 Gohar Zavradyan
A1 Christopher S. Campbell
A1 Meghna Komaranchath
A1 Javier Carmona
A1 Jennifer Trevitt
A1 David Glanzman
A1 Adam C. Roberts
YR 2022
UL http://www.eneuro.org/content/9/3/ENEURO.0020-22.2022.abstract
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.