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Zenki K.C.,Federal University of Rio Grande do Sul | Mussulini B.H.M.,Federal University of Rio Grande do Sul | Rico E.P.,Federal University of Rio Grande do Sul | Rico E.P.,Instituto Nacional Of Ciencia E Tecnologia Em Excitotoxicidade E Neuroprotecao Inct En | And 5 more authors.
Toxicology in Vitro | Year: 2014

Ethanol (EtOH) and its metabolite, acetaldehyde (ALD), induce deleterious effects on central nervous system (CNS). Here we investigate the in vitro toxicity of EtOH and ALD (concentrations of 0.25%, 0.5%, and 1%) in zebrafish brain structures [telencephalon (TE), opticum tectum (OT), and cerebellum (CE)] by measuring the functionality of glutamate transporters, MTT reduction, and extracellular LDH activity. Both molecules decreased the activity of the Na+-dependent glutamate transporters in all brain structures. The strongest glutamate uptake inhibition after EtOH exposure was 58% (TE-1%), and after ALD, 91% (CE-1%). The results of MTT assay and LDH released demonstrated that the actions of EtOH and its metabolite are concentration and structure-dependent, in which ALD was more toxic than EtOH. In summary, our findings demonstrate a differential toxicity in vitro of EtOH and ALD in zebrafish brain structures, which can involve changes on glutamatergic parameters. We suggest that this species may be an interesting model for assessing the toxicological actions of alcohol and its metabolite in CNS. © 2014 Elsevier Ltd.

Mocelin R.,Chapeco Region Community University | Herrmann A.P.,Federal University of Rio Grande do Sul | Marcon M.,Chapeco Region Community University | Rambo C.L.,Grande Rio University | And 11 more authors.
Pharmacology Biochemistry and Behavior | Year: 2015

Despite the recent advances in understanding the pathophysiology of anxiety disorders, the pharmacological treatments currently available are limited in efficacy and induce serious side effects. A possible strategy to achieve clinical benefits is drug repurposing, i.e., discovery of novel applications for old drugs, bringing new treatment options to the market and to the patients who need them. N-acetylcysteine (NAC), a commonly used mucolytic and paracetamol antidote, has emerged as a promising molecule for the treatment of several neuropsychiatric disorders. The mechanism of action of this drug is complex, and involves modulation of antioxidant, inflammatory, neurotrophic and glutamate pathways. Here we evaluated the effects of NAC on behavioral parameters relevant to anxiety in zebrafish. NAC did not alter behavioral parameters in the novel tank test, prevented the anxiety-like behaviors induced by an acute stressor (net chasing), and increased the time zebrafish spent in the lit side in the light/dark test. These data may indicate that NAC presents an anti-stress effect, with the potential to prevent stress-induced psychiatric disorders such as anxiety and depression. The considerable homology between mammalian and zebrafish genomes invests the current data with translational validity for the further clinical trials needed to substantiate the use of NAC in anxiety disorders. © 2015 Elsevier Inc. All rights reserved.

Lima M.G.,Federal University of Para | Maximino C.,Federal University of Para | Maximino C.,Zebrafish Neuroscience Research Consortium ZNRC | Matos Oliveira K.R.,Federal University of Para | And 7 more authors.
Nitric Oxide - Biology and Chemistry | Year: 2014

Nitric oxide (NO) is a highly reactive gas with considerable diffusion power that is produced pre- and post synaptically in the central nervous system (CNS). In the visual system, it is involved in the processing of the visual information from the retina to superior visual centers. In this review we discuss the main mechanisms through which nitric oxide acts, in physiological levels, on the retina, lateral geniculate nucleus (LGN) and primary visual cortex. In the retina, the cGMP-dependent nitric oxide activity initially amplifies the signal, subsequently increasing the inhibitory activity, suggesting that the signal is "filtered". In the thalamus, on dLGN, neuronal activity is amplified by NO derived from brainstem cholinergic cells, in a cGMP-independent mechanism; the result is the amplification of the signal arriving from retina. Finally, on the visual cortex (V1), NO acts through changes on the cGMP levels, increasing signal detection. These observations suggest that NO works like a filter, modulating the signal along the visual pathways. © 2013 Elsevier Inc. All rights reserved.

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