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

Abstract 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 bot...

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Published in:Neurotoxicology and teratology 2011-11, Vol.33 (6), p.727-734
Main Authors: Maximino, Caio, Araujo, Juliana, Leão, Luana Ketlen Reis, Grisolia, Alan Barroso Araújo, Oliveira, Karen Renata Matos, Lima, Monica Gomes, Batista, Evander de Jesus Oliveira, Crespo-López, Maria Elena, Gouveia, Amauri, Herculano, Anderson Manoel
Format: Article
Language:English
Subjects:
Animals
Anxiety
Anxiety - chemically induced
Anxiety - metabolism
Anxiety - physiopathology
Behavior, Animal - drug effects
Brain - drug effects
Brain - metabolism
Chromatography, High Pressure Liquid
Danio rerio
Disease Models, Animal
Dose-Response Relationship, Drug
Emergency
Female
Freshwater
Lipid Peroxidation - drug effects
Male
Medical Education
Mercury Poisoning, Nervous System - physiopathology
Methylmercury
Methylmercury Compounds - toxicity
Oxidative stress
Oxidative Stress - drug effects
Serotonin
Serotonin - metabolism
Subcellular Fractions - metabolism
Zebrafish
Zebrafish - metabolism
Zebrafish - physiology
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Summary:Abstract 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.
ISSN:0892-0362
1872-9738
DOI:10.1016/j.ntt.2011.08.006