PUBLICATION
Developmental selenomethionine and methylmercury exposures affect zebrafish learning
- Authors
- Smith, L.E., Carvan, M.J. 3rd, Dellinger, J.A., Ghorai, J.K., White, D.B., Williams, F.E., and Weber, D.N.
- ID
- ZDB-PUB-091023-15
- Date
- 2010
- Source
- Neurotoxicology and teratology 32(2): 246-255 (Journal)
- Registered Authors
- Carvan III, Michael J., Weber, Dan, Williams, Fred
- Keywords
- Developmental exposure, Learning, Mercury, Selenium, Spatial alternation, Zebrafish
- MeSH Terms
-
- Animals
- Brain/drug effects*
- Brain/growth & development
- Brain/physiopathology
- Cell Proliferation/drug effects
- Cytoprotection/drug effects
- Cytoprotection/physiology
- Disease Models, Animal
- Dose-Response Relationship, Drug
- Female
- Learning/drug effects
- Learning/physiology
- Learning Disabilities/chemically induced
- Learning Disabilities/drug therapy*
- Learning Disabilities/physiopathology
- Male
- Methylmercury Compounds/antagonists & inhibitors*
- Methylmercury Compounds/toxicity
- Neuroprotective Agents/pharmacology*
- Neuroprotective Agents/therapeutic use
- Neuropsychological Tests
- Neurotoxicity Syndromes/drug therapy*
- Neurotoxicity Syndromes/physiopathology
- Neurotoxins/antagonists & inhibitors
- Neurotoxins/toxicity
- Selenomethionine/pharmacology*
- Selenomethionine/therapeutic use
- Space Perception/drug effects
- Space Perception/physiology
- Telencephalon/drug effects
- Telencephalon/growth & development
- Telencephalon/physiopathology
- Treatment Outcome
- Zebrafish
- PubMed
- 19800969 Full text @ Neurotoxicol. Teratol.
Citation
Smith, L.E., Carvan, M.J. 3rd, Dellinger, J.A., Ghorai, J.K., White, D.B., Williams, F.E., and Weber, D.N. (2010) Developmental selenomethionine and methylmercury exposures affect zebrafish learning. Neurotoxicology and teratology. 32(2):246-255.
Abstract
Methylmercury (MeHg) is a ubiquitous environmental pollutant and has been shown to affect learning in vertebrates following relatively low exposures. Zebrafish were used to model long-term learning deficits after developmental MeHg exposure. Selenomethionine (SeMet) co-exposure was used to evaluate its role in neuroprotection. Embryos were exposed from 2 to 24h post fertilization to (1) MeHg without SeMet, (2) SeMet without MeHg and (3) in combination of MeHg and SeMet. In case (1), the levels of MeHg were 0.00, 0.01, 0.03, 0.06, 0.10, and 0.30muM. In case (2), the levels of SeMet were 0.00. 0.03, 0.06, 0.10, and 0.30muM. In case (3), co-exposure levels of (MeHg, SeMet) were (0.03, 0.03), (0.03, 0.06), (0.03, 0.10), (0.03, 0.30), (0.10, 0.03), (0.10, 0.06), (0.10, 0.10), and (0.10, 0.30) muM. Learning functions were tested in individual adults, 4months after developmental exposure using a spatial alternation paradigm with food delivery on alternating sides of the aquarium. Low levels of MeHg (<0.1microM) exposure delayed learning in treated fish; fish exposed to higher MeHg levels were unable to learn the task; SeMet co-exposure did not prevent this deficit. These data are consistent with findings in laboratory rodents. The dorsal and lateral telencephalon are the primary brain regions in fish involved in spatial learning and memory. Adult telencephalon cell body density decreased significantly at all MeHg exposures >0.01muM MeHg. SeMet co-exposure ameliorated but did not prevent changes in telencephalon cell body density. In summary, MeHg affected both learning and brain structure, but SeMet only partially reversed the latter.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping