dc.creatorBoccoli, Javier
dc.creatorLoidl, Cesar Fabian
dc.creatorLópez, Juan José
dc.creatorPistone Creydt, Virginia
dc.creatorIbarra, Cristina Adriana
dc.creatorGoldstein Raij, Jorge
dc.date.accessioned2017-10-09T18:51:12Z
dc.date.accessioned2018-11-06T11:21:26Z
dc.date.available2017-10-09T18:51:12Z
dc.date.available2018-11-06T11:21:26Z
dc.date.created2017-10-09T18:51:12Z
dc.date.issued2008
dc.identifierBoccoli, Javier; Loidl, Cesar Fabian; López, Juan José; Pistone Creydt, Virginia; Ibarra, Cristina Adriana; et al.; Intracerebroventricular administration of Shiga toxin type 2 altered the expression levels of neuronal nitric oxide synthase and glial fibrillary acidic protein in rat brains; Elsevier Science; Brain Research; 1230; -1-2008; 320-333
dc.identifier0006-8993
dc.identifierhttp://hdl.handle.net/11336/26246
dc.identifier1872-6240
dc.identifierCONICET Digital
dc.identifierCONICET
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1849278
dc.description.abstractShiga toxin (Stx) from enterohemorrhagic Escherichia coli (STEC) is the main cause of hemorrhagic colitis which may derive into Hemolytic Uremic Syndrome (HUS) and acute encephalopathy, one of the major risk factors for infant death caused by the toxin. We have previously demonstrated that intracerebroventricular administration of Stx2 causes neuronal death and glial cell damage in rat brains. In the present work, we observed that the intracerebroventricular administration of Stx2 increased the expression of glial fibrillary acidic protein (GFAP) leading to astrogliosis. Confocal microscopy showed reactive astrocytes in contact with Stx2-containing neurons. Immunocolocalization of increased GFAP and Stx2 in astrocytes was also observed. This insult in the brain was correlated with changes in the expression and activity of neuronal nitric oxide synthase (nNOS) by using the NADPH-diaphorase histochemical technique (NADPH-d HT). A significant decrease in NOS/NADPH-d-positive neurons and NOS/NADPH-d activity was observed in cerebral cortex and striatum, whereas an opposite effect was found in the hypothalamic paraventricular nucleus. We concluded that the i.c.v. administration of Stx2 promotes a typical pattern of brain injury showing reactive astrocytes and an alteration in the number and activity of nNOS/NADPH-d. According to the functional state of nNOS/NADPH-d and to brain cell morphology data, it could be inferred that the i.c.v. administration of Stx2 leads to either a neurodegenerative or a neuroprotective mechanism in the affected brain areas. The present animal model resembles the encephalopathy developed in Hemolytic Uremic Syndrome (HUS) patients by STEC intoxication.
dc.languageeng
dc.publisherElsevier Science
dc.relationinfo:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0006899308017137
dc.relationinfo:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1016/j.brainres.2008.07.052
dc.relationinfo:eu-repo/semantics/altIdentifier/pmid/18675791
dc.rightshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectSHIGA TOXIN 2
dc.subjectNITRIC OXIDE
dc.subjectGFAP
dc.subjectBRAIN INJURY
dc.titleIntracerebroventricular administration of Shiga toxin type 2 altered the expression levels of neuronal nitric oxide synthase and glial fibrillary acidic protein in rat brains
dc.typeArtículos de revistas
dc.typeArtículos de revistas
dc.typeArtículos de revistas


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