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 Scaramella, Courtney
A1 Alzagatiti, Joseph B.
A1 Creighton, Christopher
A1 Mankatala, Samandeep
A1 Licea, Fernando
A1 Winter, Gabriel M.
A1 Emtage, Jasmine
A1 Wisnieski, Joseph R.
A1 Salazar, Luis
A1 Hussain, Anjum
A1 Lee, Faith M.
A1 Mammootty, Asma
A1 Mammootty, Niyaza
A1 Aldujaili, Andrew
A1 Runnberg, Kristine A.
A1 Hernandez, Daniela
A1 Zimmerman-Thompson, Trevor
A1 Makwana, Rikhil
A1 Rouvere, Julien
A1 Tahmasebi, Zahra
A1 Zavradyan, Gohar
A1 Campbell, Christopher S.
A1 Komaranchath, Meghna
A1 Carmona, Javier
A1 Trevitt, Jennifer
A1 Glanzman, David
A1 Roberts, Adam C.
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.