Developmental selenomethionine and methylmercury exposures affect zebrafish learning

Department of Mathematical Sciences, University of Wisconsin—Milwaukee, United States
Neurotoxicology and Teratology (Impact Factor: 3.22). 03/2010; DOI: 10.1016/

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 24 h 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 0.30 μM. In case (2), the levels of SeMet were 0.00. 0.03, 0.06, 0.10, and 0.30 μM. 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) μM. Learning functions were tested in individual adults, 4 months after developmental exposure using a spatial alternation paradigm with food delivery on alternating sides of the aquarium. Low levels of MeHg (< 0.1 µM) 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 > 0.01 μM 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.

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    ABSTRACT: Lead (Pb) exposure has long been recognized to cause neurological alterations in both adults and children. While most of the studies in adults are related to higher dose exposure, epidemiological studies indicate cognitive decline and neurobehavioral alterations in children associated with lower dose environmental Pb exposure (a blood Pb level of 10 μg/dL and below). Recent animal studies also now report that an early-life Pb exposure results in pathological hallmarks of Alzheimer's disease later in life. While previous studies evaluating higher Pb exposures in adult animal models and higher occupational Pb exposures in humans have suggested a link between higher dose Pb exposure during adulthood and neurodegenerative disease, these newer studies now indicate a link between an early-life Pb exposure and adult neurodegenerative disease. These studies are supporting the “fetal/developmental origin of adult disease” hypothesis and present a new challenge in our understanding of Pb neurotoxicity. There is a need to expand research in this area and additional model systems are needed. The zebrafish presents as a complementary vertebrate model system with numerous strengths including high genetic homology. Several zebrafish genes orthologous to human genes associated with neurodegenerative diseases including Alzheimer's and Parkinson's diseases are identified and this model is starting to be applied in neurodegenerative disease research. Moreover, the zebrafish is being used in developmental Pb neurotoxicity studies to define genetic mechanisms of toxicity and associated neurobehavioral alterations. While these studies are in their infancy, the genetic and functional conservation of genes associated with neurodegenerative diseases and application in developmental Pb neurotoxicity studies supports the potential for this in vivo model to further investigate the link between developmental Pb exposure and adult neurodegenerative disease pathogenesis. In this review, the major factors influencing the pathogenesis of neurodegenerative diseases, Pb neurotoxicity, the developmental origin of adult disease paradigm, and the zebrafish as a model system to investigate the developmental origin of low-dose Pb-induced neurodegenerative diseases is discussed.
    NeuroToxicology 07/2014; 43. DOI:10.1016/j.neuro.2014.03.008 · 3.05 Impact Factor
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    ABSTRACT: The present study investigated the neurobehavioral effects of embryonic exposure to methylmercury (MeHg) in zebrafish using avoidance conditioning as the behavioral paradigm. In this study, adult zebrafish developmentally exposed as embryos to 0.00, 0.01, 0.03, 0.1, or 0.3 µ µ µ µM of MeHg were trained and tested for avoidance responses. The results showed that control zebrafish hatched from embryos unexposed to MeHg learned avoidance responses during training and showed significantly increased avoidance responses during testing. Zebrafish developmentally exposed to MeHg as embryos were hyperactive as they frequently swam back and forth, and showed no significant changes in avoidance responses from training to testing. Results of the present study suggested that embryonic methylmercury exposure produced hyperactivity and impaired avoidance learning.
  • دومین همایش ملی و تخصصی پژوهش های محیط زیست ایران, همدان، ایران; 08/2014


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May 21, 2014