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Brain dynamics after stroke in a rodent from the Amazon rainforest

Grant number: 16/06879-2
Support type:Regular Research Grants
Duration: December 01, 2016 - November 30, 2018
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal researcher:Carla Alessandra Scorza Bahi
Grantee:Carla Alessandra Scorza Bahi
Home Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil
Assoc. researchers: Antônio Carlos Guimarães de Almeida ; Ésper Abrão Cavalheiro


Isquemic stroke is a major cause of death in the world and a leading cause of disability. In the first month after the stroke the risk of death is about 10% reaching up to 40% in the first year. After an hypoxic-ischemic insult, a multi-faceted complex cascade of events occurs. In addition to vascular injury and neurodegeneration, which are typical hallmarks of stroke, the most conspicuous features are the marked neuroinflammatory response, marked glia cell activation and the blood-brain barrier breakdown. Furthermore, the neuronal electrical activity, which is an essential physiological attribute of the nervous tissue, is also greatly affected. In this scenario, when homeostatic events are drastically disturbed, the dysfunctional compensatory events may result in pathological maladaptive plasticity, a topic of extreme interest. In recent years, our laboratory has been studying Proechimys, a rodent from Amazon forest which exhibits huge resistance to the epileptogenic insults. Since stroke is a clinically important epileptogenic event, Proechimys rodents may be a valuable tool to investigate the impact of cortical ischemic stroke in the brain. To do so, this project was designed to evaluate the acute phase and long-term brain response of the Neotropical rodents Proechimys to ischemic stroke and to compare these findings to those found in the Wistar rats. The findings of the study may provide new research on pathophysiological mechanisms of ischemic stroke and in the search for new therapeutic targets. (AU)

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Scientific publications (5)
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
ORTIZ-VILLATORO, NANCY N.; REYES-GARCIA, SELVIN Z.; FREITAS, LEANDRO; RODRIGUES, LAIS D.; SANTOS, LUIZ E. C.; FABER, JEAN; CAVALHEIRO, ESPER A.; FINSTERER, JOSEF; SCORZA, FULVIO A.; DE ALMEIDA, ANTONIO C. G.; et al. Amazon rainforest rodents (Proechimys) are resistant to post-stroke epilepsy. SCIENTIFIC REPORTS, v. 11, n. 1, . (16/06879-2)
NEJM, MARIANA BOCCA; VICTORINO, DANIELLA BALDUINO; GUIMARAES-MARQUES, MARCIA JONATHAS; SCORZA, CARLA ALESSANDRA; FINSTERER, JOSEF; SCORZA, FULVIO ALEXANDRE; CYSNEIROS, ROBERTA MONTERAZZO. Effects of fish oil supplementation on spatial memory in rats with pilocarpine-induced epilepsy assessed using the Morris Water Maze test. EPILEPTIC DISORDERS, v. 23, n. 3, p. 476-484, . (16/17746-3, 18/18568-7, 16/06879-2)
GUIMARAES MARQUES, MARCIA JONATHAS; REAL, CAROLINE CRISTIANO; VICTORINO, DANIELLA BALDUINO; BRITTO, LUIZ ROBERTO; CAVALHEIRO, ESPER ABRAO; SCORZA, FULVIO ALEXANDRE; FERRAZ, HENRIQUE BALLALAI; SCORZA, CARLA ALESSANDRA. Endogenous protection against the 6-OHDA model of Parkinson's disease in the Amazonian rodent Proechimys. Neuroscience Letters, v. 709, . (16/06879-2, 13/25049-2, 16/17746-3, 12/50329-6)
REYES-GARCIA, SELVIN Z.; DE ALMEIDA, ANTONIO-CARLOS GUIMARAES; ORTIZ-VILLATORO, NANCY N.; SCORZA, FULVIO A.; CAVALHEIRO, ESPER A.; SCORZA, CARLA A.. Robust Network Inhibition and Decay of Early-Phase LTP in the Hippocampal CA1 Subfield of the Amazon Rodent Proechimys. FRONTIERS IN NEURAL CIRCUITS, v. 12, . (16/06879-2)
FÚLVIO ALEXANDRE SCORZA; FRANCISCO SANDRO MENEZES-RODRIGUES; EFRAÍN OLSZEWER; PAOLO RUGGERO ERRANTE; JOSÉ GUSTAVO PATRÃO TAVARES; CARLA ALESSANDRA SCORZA; HENRIQUE BALLALAI FERRAZ; JOSEF FINSTERER; AFONSO CARICATI-NETO. The mitochondrial calcium uniporter: a new therapeutic target for Parkinson’s disease-related cardiac dysfunctions?. Clinics, v. 75, . (17/25565-1, 16/06879-2)

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