dc.creatorMaciel, Evelise N
dc.creatorKaminski Schierle, Gabriele S
dc.creatorHansson, Oskar
dc.creatorBrundin, Patrik
dc.creatorCastilho, Roger F
dc.date2003-Oct
dc.date2015-11-27T12:52:29Z
dc.date2015-11-27T12:52:29Z
dc.date.accessioned2018-03-29T00:58:07Z
dc.date.available2018-03-29T00:58:07Z
dc.identifierExperimental Neurology. v. 183, n. 2, p. 430-7, 2003-Oct.
dc.identifier0014-4886
dc.identifier
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/14552883
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/195557
dc.identifier14552883
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1295790
dc.descriptionMitochondrial 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.
dc.description183
dc.description430-7
dc.languageeng
dc.relationExperimental Neurology
dc.relationExp. Neurol.
dc.rightsfechado
dc.rights
dc.sourcePubMed
dc.subjectAdenosine Diphosphate
dc.subjectAdenosine Triphosphate
dc.subjectAnimals
dc.subjectApoptosis
dc.subjectBrain Chemistry
dc.subjectCalcium
dc.subjectCorpus Striatum
dc.subjectCyclosporine
dc.subjectEnzyme Inhibitors
dc.subjectFemale
dc.subjectGene Expression
dc.subjectHumans
dc.subjectMembrane Potentials
dc.subjectMice
dc.subjectMice, Transgenic
dc.subjectMitochondria
dc.subjectNeurotoxins
dc.subjectProto-oncogene Proteins C-bcl-2
dc.subjectQuinolinic Acid
dc.subjectRats
dc.subjectRats, Wistar
dc.titleCyclosporin A And Bcl-2 Do Not Inhibit Quinolinic Acid-induced Striatal Excitotoxicity In Rodents.
dc.typeArtículos de revistas


Este ítem pertenece a la siguiente institución