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.

Highlights

  • Published: 11 October 2021Methylmercury (MeHg) is a neurotoxic contaminant generated through methylation of the heavy metal mercury in aquatic environments, where it enters the aquatic food chain

  • Developmental exposure of zebrafish embryos to MeHg resulted in altered behaviour at 6 dpf in response to alternating light and dark conditions (Figure 1, Figure 2 and Figure S1)

  • We found that exposures of zebrafish embryos to three sub‐acute doses of 5, 10 or ways

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Summary

Introduction

Published: 11 October 2021Methylmercury (MeHg) is a neurotoxic contaminant generated through methylation of the heavy metal mercury in aquatic environments, where it enters the aquatic food chain. Human prenatal exposure to low levels of MeHg was linked to early-life neurotoxicity outcomes, including deficits in motor function [2,3], and lasting neurobehavioural impairments [4,5,6,7]. Most recent studies of MeHg neurotoxicity using experimental models have focused on adverse outcome pathways and behavioural effects of developmental low dose exposure. Pre- and perinatal exposures to low-doses of MeHg resulted in adverse emotional, cognitive and neuromotor effects in juveniles and adults, including depressionlike behaviour [4,17,18], deficits in motor coordination and locomotor activity [19] as well as learning disability [20,21], and memory impairment [22].

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