Zebrafish Neuroscience Research Consortium ZNRC

United States

Zebrafish Neuroscience Research Consortium ZNRC

United States
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Savio L.E.B.,Federal University of Rio Grande do Sul | Vuaden F.C.,Federal University of Rio Grande do Sul | Kist L.W.,Grande Rio University | Pereira T.C.,Grande Rio University | And 6 more authors.
Neuroscience | Year: 2013

Hyperprolinemia is an inherited disorder of proline metabolism and hyperprolinemic patients can present neurological manifestations, such as seizures, cognitive dysfunctions, and schizoaffective disorders. However, the mechanisms related to these symptoms are still unclear. In the present study, we evaluated the in vivo and in vitro effects of proline on acetylcholinesterase (AChE) activity and gene expression in the zebrafish brain. For the in vivo studies, animals were exposed at two proline concentrations (1.5 and 3.0 mM) during 1 h or 7 days (short- or long-term treatments, respectively). For the in vitro assays, different proline concentrations (ranging from 3.0 to 1000 μM) were tested. Long-term proline exposures significantly increased AChE activity for both treated groups when compared to the control (34% and 39%). Moreover, the proline-induced increase on AChE activity was completely reverted by acute administration of antipsychotic drugs (haloperidol and sulpiride), as well as the changes induced in ache expression. When assessed in vitro, proline did not promote significant changes in AChE activity. Altogether, these data indicate that the enzyme responsible for the control of acetylcholine levels might be altered after proline exposure in the adult zebrafish. These findings contribute for better understanding of the pathophysiology of hyperprolinemia and might reinforce the use of the zebrafish as a complementary vertebrate model for studying inborn errors of amino acid metabolism. © 2013 IBRO.


Braga M.M.,Federal University of Rio Grande do Sul | Braga M.M.,Institute Nacional Of Ciencia E Tecnologia Em Excitotoxicidade E Neuroprotecao | Rico E.P.,Federal University of Rio Grande do Sul | Rico E.P.,Institute Nacional Of Ciencia E Tecnologia Em Excitotoxicidade E Neuroprotecao | And 14 more authors.
Behavioural Brain Research | Year: 2013

Cerebral hypoxia-ischemia can lead to motor and sensory impairments which can be dependent on the extent of infarcted regions. Since a better understanding of the neurochemical mechanisms involved in this injury is needed, the use of zebrafish as a cerebral hypoxia model has become quite promising because it could improve the knowledge about hypoxia-ischemia. In the current study, we aimed to investigate the spontaneous recovery of brain and behavioral impairments induced by hypoxia in adult zebrafish. Brain injury levels were analyzed by spectrophotometric measurement of mitochondrial dehydrogenase activity by staining with 2,3,5-triphenyltetrazolium chloride, and behavioral profiles were assessed by the open tank test. The induction of hypoxia substantially decreased mitochondrial activity in the brain and impaired behavior. The spontaneous recovery of fish subjected to hypoxia was assessed after 1, 3, 6, 24, and 48. h under normoxia. The quantification of brain injury levels showed a significant increase until 24. h after hypoxia, but after 48. h this effect was completely reversed. Regarding behavioral parameters, we verified that locomotor activity and vertical exploration were impaired by hypoxia and these effects were reversed after 3. h under normoxia. Taken together, these results show that zebrafish exhibited transient cerebral and behavioral impairments when submitted to hypoxia, and 1. h under normoxic conditions was insufficient to reverse both effects. Therefore, our data help to elucidate the time window of spontaneous recovery in zebrafish after hypoxia and also the behavioral phenotypes involved in this phenomenon. © 2013 Elsevier B.V.


Dal Santo G.,Chapecó Region Community University | Conterato G.M.M.,Chapecó Region Community University | Barcellos L.J.G.,University Of Passo Fundo | Rosemberg D.B.,Chapecó Region Community University | And 3 more authors.
Neuroscience Letters | Year: 2014

The zebrafish (Danio rerio) has become an emergent model organism for translational approaches focused on the neurobiology of stress due to its genetic, neuroanatomical, and histological similarities with mammalian systems. However, despite the increasing number of studies using zebrafish, reports examining the impact of stress on relevant neurochemical parameters are still elementary when compared to studies using rodents. Additionally, it is important to further validate this model organism by comparing its stress response with those described in other species. Here, we evaluated the effects of an acute restraint stress (ARS) protocol on oxidative stress-related parameters in the zebrafish brain. Our data revealed that ARS significantly decreased catalase activity without altering the activity of superoxide dismutase. Oxidative stress was also indicated by increased levels of lipid peroxides. ARS significantly increased the levels of non-protein thiols, although significant changes in total reduced sulfhydryl content were not detected. These results suggest that ARS is an interesting strategy for evaluating the mechanisms underlying the neurochemical basis of the oxidative profile triggered by acute stressors in the zebrafish brain. Furthermore, this protocol may be suitable for screening new compounds with protective properties against oxidative stress, which plays an increasingly important role in many psychiatric disorders. © 2013 Elsevier Ireland Ltd.


Marcon M.,Chapecó Region Community University | Herrmann A.P.,University of South Santa Catarina | Mocelin R.,Chapecó Region Community University | Rambo C.L.,Grande Rio University | And 10 more authors.
Psychopharmacology | Year: 2016

Rationale: Several model organisms have been employed to study the impacts of stress on biological systems. Different models of unpredictable chronic stress (UCS) have been established in rodents; however, these protocols are expensive, long-lasting, and require a large physical structure. Our group has recently reported an UCS protocol in zebrafish with several advantages compared to rodent models. We observed that UCS induced behavioral, biochemical, and molecular changes similar to those observed in depressed patients, supporting the translational relevance of the protocol. Objectives: Considering that a pharmacological assessment is lacking in this zebrafish model, our aim was to evaluate the effects of anxiolytic (bromazepam) and antidepressant drugs (fluoxetine and nortriptyline) on behavioral (novel tank test), biochemical (whole-body cortisol), and molecular parameters (cox-2, tnf-α, il-6, and il-10 gene expression) in zebrafish subjected to UCS. Results: We replicated previous data showing that UCS induces behavioral and neuroendocrine alterations in zebrafish, and we show for the first time that anxiolytic and antidepressant drugs are able to prevent such effects. Furthermore, we extended the molecular characterization of the model, revealing that UCS increases expression of the pro-inflammatory markers cox-2 and il-6, which was also prevented by the drugs tested. Conclusions: This study reinforces the use of zebrafish as a model organism to study the behavioral and physiological effects of stress. The UCS protocol may also serve as a screening tool for evaluating new drugs that can be used to treat psychiatric disorders with stress-related etiologies. © 2016 Springer-Verlag Berlin Heidelberg


Mocelin R.,Chapecó Region Community University | Herrmann A.P.,Federal University of Rio Grande do Sul | Marcon M.,Chapecó 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.


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.


Lima M.G.,Federal University of Pará | Maximino C.,Federal University of Pará | Maximino C.,Zebrafish Neuroscience Research Consortium ZNRC | Matos Oliveira K.R.,Federal University of Pará | 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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