PUBLICATION
Bisphenol A Exposure Induces Sensory Processing Deficits in Larval Zebrafish During Neurodevelopment
- Authors
- Scaramella, C., Alzagatiti, J.B., Creighton, C., Mankatala, S., Licea, F., Winter, G.M., Emtage, J., Wisnieski, J.R., Salazar, L., Hussain, A., Lee, F.M., Mammootty, A., Mammootty, N., Aldujaili, A., Runnberg, K.A., Hernandez, D., Zimmerman-Thompson, T., Makwana, R., Rouvere, J., Tahmasebi, Z., Zavradyan, G., Campbell, C.S., Komaranchath, M., Carmona, J., Trevitt, J., Glanzman, D., Roberts, A.C.
- ID
- ZDB-PUB-220506-10
- Date
- 2022
- Source
- eNeuro 9(3): (Journal)
- Registered Authors
- Keywords
- Autism Spectrum Disorder, C-start reflex, Habituation, Mauthner cell, Prepulse inhibition, Zebrafish
- MeSH Terms
-
- Benzhydryl Compounds*/toxicity
- Humans
- Phenols
- Larva
- Zebrafish*
- Perception
- Animals
- PubMed
- 35508370 Full text @ eNeuro
Citation
Scaramella, C., Alzagatiti, J.B., Creighton, C., Mankatala, S., Licea, F., Winter, G.M., Emtage, J., Wisnieski, J.R., Salazar, L., Hussain, A., Lee, F.M., Mammootty, A., Mammootty, N., Aldujaili, A., Runnberg, K.A., Hernandez, D., Zimmerman-Thompson, T., Makwana, R., Rouvere, J., Tahmasebi, Z., Zavradyan, G., Campbell, C.S., Komaranchath, M., Carmona, J., Trevitt, J., Glanzman, D., Roberts, A.C. (2022) Bisphenol A Exposure Induces Sensory Processing Deficits in Larval Zebrafish During Neurodevelopment. eNeuro. 9(3):.
Abstract
Due to 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 anatomical 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 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.Significance StatementBPA exposure elicits sensory processing deficits in larval zebrafish. Specifically, animals show abnormal PPI and short-term habituation, which are behaviors mediated by a relatively simple neural circuit: the C-start escape circuit. Given the well-defined nature of the circuitry underlying the C-start reflex, the present study should facilitate future investigations of the neurobiological bases of BPA-induced behavioral deficits. Furthermore, the behavioral assays used here can be readily adapted for high-throughput screening of potential therapeutic agents. Finally, the present study provides a model system and a set of assays that can generally be used to investigate sensory processing, locomotion, anxiety, and key anatomical measurements.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping