dc.creator | Maciel, Evelise N | |
dc.creator | Kaminski Schierle, Gabriele S | |
dc.creator | Hansson, Oskar | |
dc.creator | Brundin, Patrik | |
dc.creator | Castilho, Roger F | |
dc.date | 2003-Oct | |
dc.date | 2015-11-27T12:52:29Z | |
dc.date | 2015-11-27T12:52:29Z | |
dc.date.accessioned | 2018-03-29T00:58:07Z | |
dc.date.available | 2018-03-29T00:58:07Z | |
dc.identifier | Experimental Neurology. v. 183, n. 2, p. 430-7, 2003-Oct. | |
dc.identifier | 0014-4886 | |
dc.identifier | | |
dc.identifier | http://www.ncbi.nlm.nih.gov/pubmed/14552883 | |
dc.identifier | http://repositorio.unicamp.br/jspui/handle/REPOSIP/195557 | |
dc.identifier | 14552883 | |
dc.identifier.uri | http://repositorioslatinoamericanos.uchile.cl/handle/2250/1295790 | |
dc.description | 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. | |
dc.description | 183 | |
dc.description | 430-7 | |
dc.language | eng | |
dc.relation | Experimental Neurology | |
dc.relation | Exp. Neurol. | |
dc.rights | fechado | |
dc.rights | | |
dc.source | PubMed | |
dc.subject | Adenosine Diphosphate | |
dc.subject | Adenosine Triphosphate | |
dc.subject | Animals | |
dc.subject | Apoptosis | |
dc.subject | Brain Chemistry | |
dc.subject | Calcium | |
dc.subject | Corpus Striatum | |
dc.subject | Cyclosporine | |
dc.subject | Enzyme Inhibitors | |
dc.subject | Female | |
dc.subject | Gene Expression | |
dc.subject | Humans | |
dc.subject | Membrane Potentials | |
dc.subject | Mice | |
dc.subject | Mice, Transgenic | |
dc.subject | Mitochondria | |
dc.subject | Neurotoxins | |
dc.subject | Proto-oncogene Proteins C-bcl-2 | |
dc.subject | Quinolinic Acid | |
dc.subject | Rats | |
dc.subject | Rats, Wistar | |
dc.title | Cyclosporin A And Bcl-2 Do Not Inhibit Quinolinic Acid-induced Striatal Excitotoxicity In Rodents. | |
dc.type | Artículos de revistas | |