PUBLICATION

Developmental Exposure to Low Concentrations of Methylmercury Causes Increase in Anxiety-Related Behaviour and Locomotor Impairments in Zebrafish

Authors
Glazer, L., Brennan, C.H.
ID
ZDB-PUB-211025-39
Date
2021
Source
International Journal of Molecular Sciences   22(20): (Journal)
Registered Authors
Brennan, Caroline
Keywords
HPI-axis, anxiety, behaviour, developmental neurotoxicity, dopaminergic system, locomotor activity, methylmercury, zebrafish
MeSH Terms
  • Animals
  • Anxiety/etiology
  • Behavior, Animal/drug effects*
  • Disease Models, Animal
  • Embryo, Nonmammalian/drug effects
  • Embryonic Development/drug effects
  • Gene Expression/drug effects
  • Larva/drug effects
  • Larva/physiology
  • Locomotion/drug effects*
  • Methylmercury Compounds/toxicity*
  • Receptors, Dopamine D2/genetics
  • Receptors, Dopamine D2/metabolism
  • Zebrafish/growth & development
  • Zebrafish/physiology*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed
34681620 Full text @ Int. J. Mol. Sci.
Abstract
Methylmercury (MeHg) is a ubiquitous pollutant shown to cause developmental neurotoxicity, even at low levels. However, there is still a large gap in our understanding of the mechanisms linking early-life exposure to life-long behavioural impairments. Our aim was to characterise the short- and long-term effects of developmental exposure to low doses of MeHg on anxiety-related behaviours in zebrafish, and to test the involvement of neurological pathways related to stress-response. Zebrafish embryos were exposed to sub-acute doses of MeHg (0, 5, 10, 15, 30 nM) throughout embryo-development, and tested for anxiety-related behaviours and locomotor activity at larval (light/dark locomotor activity) and adult (novel tank and tap assays) life-stages. Exposure to all doses of MeHg caused increased anxiety-related responses; heightened response to the transition from light to dark in larvae, and a stronger dive response in adults. In addition, impairment in locomotor activity was observed in the higher doses in both larvae and adults. Finally, the expressions of several neural stress-response genes from the HPI-axis and dopaminergic system were found to be disrupted in both life-stages. Our results provide important insights into dose-dependent differences in exposure outcomes, the development of delayed effects over the life-time of exposed individuals and the potential mechanisms underlying these effects.
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