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Your search keyword '"Quevedo, João"' showing total 23 results
Start Over Author "Quevedo, João" Journal neuroscience letters
23 results on '"Quevedo, João"'

1. Effects of sodium butyrate on aversive memory in rats submitted to sepsis

Author

Steckert, Amanda V., primary, Comim, Clarissa M., additional, Igna, Dhébora M. Dall, additional, Dominguini, Diogo, additional, Mendonça, Bruna P., additional, Ornell, Felipe, additional, Colpo, Gabriela D., additional, Gubert, Carolina, additional, Kapczinski, Flávio, additional, Barichello, Tatiana, additional, Quevedo, João, additional, and Dal-Pizzol, Felipe, additional

Published
2015
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2. Ketamine ameliorates depressive-like behaviors and immune alterations in adult rats following maternal deprivation

Author

Réus, Gislaine Z., primary, Nacif, Marcos Paulo, additional, Abelaira, Helena M., additional, Tomaz, Débora B., additional, dos Santos, Maria Augusta B., additional, Carlessi, Anelise S., additional, da Luz, Jaine R., additional, Gonçalves, Renata C., additional, Vuolo, Francieli, additional, Dal-Pizzol, Felipe, additional, Carvalho, André F., additional, and Quevedo, João, additional

Published
2015
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4. Effects of experimental cerebral malaria in memory, brain-derived neurotrophic factor and acetylcholinesterase acitivity in the hippocampus of survivor mice

Author

Comim, Clarissa M., primary, Reis, Patrícia A., additional, Frutuoso, Valber S., additional, Fries, Gabriel R., additional, Fraga, Daiane B., additional, Kapczinski, Flávio, additional, Zugno, Alexandra I., additional, Barichello, Tatiana, additional, Quevedo, João, additional, and Castro-Faria-Neto, Hugo C., additional

Published
2012
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8. Antibiotic therapy prevents, in part, the oxidative stress in the rat brain after meningitis induced by Streptococcus pneumoniae

Author

Barichello, Tatiana, primary, Savi, Geovana D., additional, Silva, Geruza Z., additional, Generoso, Jaqueline S., additional, Bellettini, Gisele, additional, Vuolo, Francieli, additional, Petronilho, Fabrícia, additional, Feier, Gustavo, additional, Comim, Clarissa M., additional, Quevedo, João, additional, and Dal-Pizzol, Felipe, additional

Published
2010
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11. DNA damage after intracerebroventricular injection of ouabain in rats

Author

Jornada, Luciano K., primary, Valvassori, Samira S., additional, Arent, Camila O., additional, Leffa, Daniela, additional, Damiani, Adriani A., additional, Hainzenreder, Giana, additional, Ferreira, Camila L., additional, Moretti, Morgana, additional, Andrade, Vanessa M., additional, and Quevedo, João, additional

Published
2010
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12. Tumor necrosis factor alpha (TNF-α) levels in the brain and cerebrospinal fluid after meningitis induced by Streptococcus pneumoniae

Author

Barichello, Tatiana, primary, dos Santos, Ivonete, additional, Savi, Geovana D., additional, Florentino, Anelise F., additional, Silvestre, Cintia, additional, Comim, Clarissa M., additional, Feier, Gustavo, additional, Sachs, Daniela, additional, Teixeira, Mauro M., additional, Teixeira, Antonio L., additional, and Quevedo, João, additional

Published
2009
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17. Increased serum glial cell line-derived neurotrophic factor immunocontent during manic and depressive episodes in individuals with bipolar disorder

Author

Rosa, Adriane R., primary, Frey, Benício N., additional, Andreazza, Ana C., additional, Ceresér, Keila M., additional, Cunha, Angelo B.M., additional, Quevedo, João, additional, Santin, Aida, additional, Gottfried, Carmem, additional, Gonçalves, Carlos A., additional, Vieta, Eduard, additional, and Kapczinski, Flávio, additional

Published
2006
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21. Effects of electroconvulsive seizures on Na+,K+-ATPase activity in the rat hippocampus

Author

Streck, Emilio L., Feier, Gustavo, Búrigo, Márcio, Franzon, Renata, Dal-Pizzol, Felipe, Quevedo, João, and Wyse, Angela T.S.

Subjects
*ELECTROCONVULSIVE therapy, *SPASMS, *HIPPOCAMPUS (Brain), *ADENOSINE triphosphatase
Abstract

Abstract: Although several advances have occurred concerning the use of electroconvulsive therapy, little progress has been made in understanding the mechanisms underlying its therapeutic or side effects. Na+,K+-ATPase is an important enzyme of central nervous system, responsible for ionic gradient maintenance and consumption of approximately 40–50% of brain ATP. This work was performed in order to determine Na+,K+-ATPase activity after acute and chronic electroconvulsive shock. Results showed an inhibition of Na+,K+-ATPase activity in the hippocampus 48h, 7, 30, 60 and 90 days after a single electroconvulsive shock. Chronic treatment diminished the enzyme activity in the hippocampus 7 and 30 days after electroconvulsive (ECS) sessions. Our findings demonstrated that Na+,K+-ATPase activity is altered by ECS. [Copyright &y& Elsevier]

Published
2006
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22. Effects of experimental cerebral malaria in memory, brain-derived neurotrophic factor and acetylcholinesterase activity [correction for acitivity] in the hippocampus of survivor mice.

Author

Comim CM, Reis PA, Frutuoso VS, Fries GR, Fraga DB, Kapczinski F, Zugno AI, Barichello T, Quevedo J, and Castro-Faria-Neto HC

Subjects
Animals, Antimalarials therapeutic use, Chloroquine therapeutic use, Habituation, Psychophysiologic, Malaria, Cerebral drug therapy, Mice, Mice, Inbred C57BL, Acetylcholinesterase metabolism, Brain-Derived Neurotrophic Factor metabolism, Hippocampus metabolism, Malaria, Cerebral metabolism, Malaria, Cerebral psychology, Memory
Abstract

Malaria is the most important human parasitic disease and cerebral malaria (CM), its main neurological complication, is characterized by neurological and cognitive damage in both human and animal survivors. The brain-derived neurotrophic factor (BDNF) appears to be involved with activity-dependent synaptic plasticity. There is great interest regarding its role in learning and memory as well as acetylcholinesterase activity (AChE) that is implicated in many cognitive functions and probably plays important roles in neurodegenerative disorders. In the present work, we evaluated BDNF protein levels and AChE activity in the hippocampus and habituation in an animal model of CM using C57BL/6 mice after fifteen days of the induction. The results demonstrated that there was a decrease in BDNF levels in the hippocampus of C57BL/6 mice infected with PbA when compared with C57BL/6 non-infected mice and C57BL/6 non-infected mice that received treatment with chloroquine. However, no difference was observed in AChE activity in the hippocampus. When habituation was evaluated there was memory impairment in the C57BL/6 mice infected with Plasmodium berghei ANKA (PbA). In conclusion, we believe that the decreased BDNF levels in the hippocampus may be related with memory impairment without alterations on AChE activity., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Published
2012
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23. Tumor necrosis factor alpha (TNF-alpha) levels in the brain and cerebrospinal fluid after meningitis induced by Streptococcus pneumoniae.

Author

Barichello T, dos Santos I, Savi GD, Florentino AF, Silvestre C, Comim CM, Feier G, Sachs D, Teixeira MM, Teixeira AL, and Quevedo J

Subjects
Animals, Biomarkers analysis, Biomarkers cerebrospinal fluid, Brain physiopathology, Cerebrospinal Fluid immunology, Cerebrospinal Fluid metabolism, Cerebrospinal Fluid microbiology, Diagnosis, Differential, Disease Models, Animal, Frontal Lobe immunology, Frontal Lobe physiopathology, Hippocampus immunology, Hippocampus physiopathology, Male, Meninges immunology, Meninges microbiology, Meninges pathology, Meningitis, Pneumococcal physiopathology, Predictive Value of Tests, Rats, Streptococcal Infections physiopathology, Tumor Necrosis Factor-alpha analysis, Up-Regulation immunology, Brain immunology, Meningitis, Pneumococcal cerebrospinal fluid, Meningitis, Pneumococcal immunology, Streptococcal Infections cerebrospinal fluid, Streptococcal Infections immunology, Tumor Necrosis Factor-alpha cerebrospinal fluid
Abstract

Bacterial meningitis due to Streptococcus pneumoniae is associated with a significant mortality rate and persisting neurologic sequelae including sensory-motor deficits, seizures, and impairments of learning and memory. The presence of proliferating bacteria within the subarachnoid and ventricular space compartments triggers an intense inflammatory host response at killing the invading microorganism. Proinflammatory mediators released in the process include tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-1beta, IL-6. TNF-alpha have several effects, including cytotoxicity, antiviral activity, transcription factor activation, and immune response regulation. Thus, the aim of this study was to verify the levels of the TNF-alpha after pneumococcal meningitis in male Wistar rats. The animals underwent a magna cistern tap receiving either 10 microL sterile saline as a placebo or an equivalent volume of a S. pneumoniae suspension at the concentration 5 x 10(9)cfu/mL. The animals were killed at 0, 6, 12, 24, 48 and 96 h after induction. The brain was removed and hippocampus, cortex, prefrontal and cerebrospinal fluid (CSF) were isolated and used for the determination of TNF-alpha levels. We found an increase in TNF-alpha levels at 6h after induction of the meningitis in the hippocampus (p<0.01), frontal cortex (p<0.05), and cerebrospinal fluid (p<0.001).There was no alteration in the cortex. Our data suggest that TNF-alpha is involved in the pathophysiology of the pneumococcal meningitis and could be investigated as a putative biomarker for brain damage in the first hours.

Published
2009
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