Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/195557
Type: Artigo de periódico
Title: Cyclosporin A And Bcl-2 Do Not Inhibit Quinolinic Acid-induced Striatal Excitotoxicity In Rodents.
Author: Maciel, Evelise N
Kaminski Schierle, Gabriele S
Hansson, Oskar
Brundin, Patrik
Castilho, Roger F
Abstract: Mitochondrial permeability transition (MPT) is a nonselective inner membrane permeabilization that contributes to neuronal cell death under circumstances such as brain trauma, ischemia, and hypoglycemia. Here we study the participation of MPT and the Bcl-2-sensitive apoptotic cell death pathway in glutamate receptor-mediated excitotoxicity. Intrastriatal infusions of the N-methyl-D-aspartate (NMDA) receptor agonist quinolinic acid caused massive striatal neurodegeneration in both rats and mice. Interestingly, transgenic mice overexpressing human Bcl-2 and rats systemically treated with cyclosporin A did not exhibit reduced sensitivity to quinolinic acid-induced striatal toxicity. Both Bcl-2 and cyclosporin A are inhibitors of MPT; in addition Bcl-2 also inhibits apoptotic stimuli-mediated release of mitochondrial apoptogenic factors. Isolated brain mitochondria from cyclosporin A-treated rats showed resistance to Ca(2+)-induced dissipation of the membrane potential, indicating protection against MPT. We conclude that quinolinic acid-mediated striatal excitotoxicity is not dependent on MPT and Bcl-2-sensitive apoptotic cell death pathways.
Subject: Adenosine Diphosphate
Adenosine Triphosphate
Animals
Apoptosis
Brain Chemistry
Calcium
Corpus Striatum
Cyclosporine
Enzyme Inhibitors
Female
Gene Expression
Humans
Membrane Potentials
Mice
Mice, Transgenic
Mitochondria
Neurotoxins
Proto-oncogene Proteins C-bcl-2
Quinolinic Acid
Rats
Rats, Wistar
Rights: fechado
Identifier DOI: 
Address: http://www.ncbi.nlm.nih.gov/pubmed/14552883
Date Issue: 2003
Appears in Collections:Artigos e Materiais de Revistas Científicas - Unicamp

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