Possible role of serotoninergic system in the neurobehavioral impairment induced by acute methylmercury exposure in zebrafish (Danio rerio)

Adult zebrafish were treated acutely with methylmercury (1.0 or 5.0 μg g− 1, i.p.) and, 24 h after treatment, were tested in two behavioral models of anxiety, the novel tank and the light/dark preference tests. At the smaller dose, methylmercury produced a marked anxiogenic profile in both tests, while the greater dose produced hyperlocomotion in the novel tank test. These effects were accompanied by a decrease in extracellular levels of serotonin, and an increase in extracellular levels of tryptamine-4,5-dione, a partially oxidized metabolite of serotonin. A marked increase in the formation of malondialdehyde, a marker of oxidative stress, accompanied these parameters. It is suggested that methylmercury-induced oxidative stress produced mitochondrial dysfunction and originated tryptamine-4,5-dione, which could have further inhibited tryptophan hydroxylase. These results underscore the importance of assessing acute, low-level neurobehavioral effects of methylmercury.

► We describe an acute effect of methylmercury (MeHg) poisoning in adult zebrafish.
► Behavioral and neurochemical effects were observed 24 h after MeHg poisoning.
► MeHg was anxiogenic at 1.0 μg g− 1, and motor-stimulating at 5.0 μg g− 1.
► MeHg decreased ECF serotonin levels and increased ECF tryptamine-4,5-dione levels.
► An increase in lipid peroxidation in the brain of MeHg-poisoned fish was observed.