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Fontana B.D.,Federal University of Santa Maria | Meinerz D.L.,Federal University of Santa Maria | Rosa L.V.C.,Federal University of Santa Maria | Mezzomo N.J.,Federal University of Santa Maria | And 7 more authors.
Pharmacology Biochemistry and Behavior

Alcohol is a potent agent for eliciting aggression in vertebrates. Taurine (TAU) is an amino sulfonic acid with pleiotropic actions on brain function. It is one of the most abundant molecules present in energy drinks frequently used as mixers for alcoholic beverages. However, the combined effects of TAU and ethanol (EtOH) on behavioral parameters such as aggression are poorly understood. Considering that zebrafish is a suitable vertebrate to assess agonistic behaviors using noninvasive protocols, we investigate whether TAU modulates EtOH-induced aggression in zebrafish using the mirror-induced aggression (MIA) test. Since body color can be altered by pharmacological agents and may be indicative of emotional state, we also evaluated the actions of EtOH and TAU on pigment response. Fish were acutely exposed to TAU (42, 150, and 400 mg/L), EtOH (0.25%), or cotreated with both molecules for 1 h and then placed in the test apparatus for 6 min. EtOH, TAU 42, TAU 400, TAU 42/EtOH and TAU 400/EtOH showed increased aggression, while 150 mg/L TAU only increased the latency to attack the mirror. This same concentration also prevented EtOH-induced aggression, suggesting that it antagonizes the effects of acute alcohol exposure. Representative ethograms revealed the existence of different aggressive patterns and our results were confirmed by an index used to estimate aggression in the MIA test. TAU did not alter pigment intensity, while EtOH and all cotreated groups presented a substantial increase in body color. Overall, these data show a biphasic effect of TAU on EtOH-induced aggression of zebrafish, which is not necessarily associated with changes in body color. © 2015 Elsevier Inc.All rights reserved. Source

Nguyen M.,University of Virginia | Nguyen M.,ZENEREI Institute | Stewart A.M.,ZENEREI Institute | Stewart A.M.,International Zebrafish Neuroscience Research Consortium ZNRC | And 3 more authors.
Progress in Neuro-Psychopharmacology and Biological Psychiatry

Depression is a serious psychiatric condition affecting millions of patients worldwide. Unipolar depression is characterized by low mood, anhedonia, social withdrawal and other severely debilitating psychiatric symptoms. Bipolar disorder manifests in alternating depressed mood and 'hyperactive' manic/hypomanic states. Animal experimental models are an invaluable tool for research into the pathogenesis of bipolar/unipolar depression, and for the development of potential treatments. Due to their high throughput value, genetic tractability, low cost and quick reproductive cycle, zebrafish (Danio rerio) have emerged as a promising new model species for studying brain disorders. Here, we discuss the developing utility of zebrafish for studying depression disorders, and outline future areas of research in this field. We argue that zebrafish represent a useful model organism for studying depression and its behavioral, genetic and physiological mechanisms, as well as for anti-depressant drug discovery. © 2014 Elsevier Inc. Source

Stewart A.M.,ZENEREI Institute | Stewart A.M.,International Zebrafish Neuroscience Research Consortium ZNRC | Ullmann J.F.P.,International Zebrafish Neuroscience Research Consortium ZNRC | Ullmann J.F.P.,University of Queensland | And 8 more authors.
Molecular Psychiatry

Due to their well-characterized neural development and high genetic homology to mammals, zebrafish (Danio rerio) have emerged as a powerful model organism in the field of biological psychiatry. Here, we discuss the molecular psychiatry of zebrafish, and its implications for translational neuroscience research and modeling central nervous system (CNS) disorders. In particular, we outline recent genetic and technological developments allowing for in vivo examinations, high-throughput screening and whole-brain analyses in larval and adult zebrafish. We also summarize the application of these molecular techniques to the understanding of neuropsychiatric disease, outlining the potential of zebrafish for modeling complex brain disorders, including attention-deficit/hyperactivity disorder (ADHD), aggression, post-traumatic stress and substance abuse. Critically evaluating the advantages and limitations of larval and adult fish tests, we suggest that zebrafish models become a rapidly emerging new field in modern molecular psychiatry research. © 2015 Macmillan Publishers Limited All rights reserved 1359-4184/15. Source

Braga M.M.,Federal University of Rio Grande do Sul | Braga M.M.,Instituto Nacional Of Ciencia E Tecnologia Em Excitotoxicidade E Neuroprotecao | Braga M.M.,Federal University of Santa Maria | Silva E.S.,Federal University of Rio Grande do Sul | And 17 more authors.
Toxicology Research

The study of the effects of diethyldithiocarbamate (DEDTC) in some diseases has been in focus for many years. However, DEDTC is a metal chelator that can present neurotoxicity as side effect. Here we investigate the effect of DEDTC on the brain zinc (Zn) content and behavior. To address this issue we used adult zebrafish exposed to different concentrations of DEDTC. The animal's behavioral parameters were evaluated during exposure to DEDTC (0.2, 1, 5 mM in home tank water) for 1 h. At the end of the exposure period, the brain levels of DEDTC were measured. The analysis of the reactive Zn content in different regions of the brain and in glutamatergic neurons and radial glial cells was performed using histochemical and immunocytochemical techniques, respectively. We also measured the activity of a Zn-dependent enzyme, δ-aminolevulinate dehydratase (δ-ALA-D). We found that DEDTC exposure at 1 and 5 mM induced seizure-like behavior in the zebrafish and death at 5 mM. DEDTC in the zebrafish brain was detected with exposure to 1 and 5 mM (above 100 mg kg-1 tissue). The reactive Zn was reduced in glutamatergic neurons after 1 and 5 mM DEDTC exposure in radial glial cells. No changes in the brain δ-ALA-D activity were detected. Our results showed that DEDTC can accumulate in the brain, leading to impairment in neural behavior and in the homeostasis of reactive Zn in the brain. © 2015 The Royal Society of Chemistry. Source

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