Abstract

Gestational exposure to methylmercury disrupts dopamine-mediated behavior and produces heightened sensitivity to monoamine agonists later in life. This has been reported and replicated following both pre- and post-natal exposure. Impacts of methylmercury when exposure occurs during the sensitive period of adolescence, a key period of dopaminergic development, remain underexplored. There have been variable results thus far in studies investigating links between adolescent exposure to methylmercury and alterations in executive function and altered sensitivity to monoamine agonists. The current study was designed to investigate adolescent exposure by exposing male mice to 0, 0.3, or 3 ppm methylmercury during adolescence and training them in a hybrid task to assess two executive functions, attention and memory, in adulthood. Behavior in these animals was probed with a range of doses of the dopamine agonist, d-amphetamine, and the norepinephrine agonist, desipramine. Attention and memory in these mice were sensitive to disruption by d-amphetamine and interacted with methylmercury exposure. Choice latencies were also longer in the MeHg-exposed mice. Desipramine did not affect behavior in these animals nor did it interact with methylmercury. It is concluded that methylmercury-related inhibition of behavior observed in this study were differentially sensitive to acute disruption in dopamine, but not norepinephrine, neurotransmission.

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