Acute blood-brain barrier permeabilization in rats after systemic Phoneutria nigriventer venom

dc.creatorRaposo, C
dc.creatorZago, GM
dc.creatorda Silva, GH
dc.creatorHofling, MAD
dc.date2007
dc.dateMAY 29
dc.date2014-11-16T09:49:26Z
dc.date2015-11-26T17:24:23Z
dc.date2014-11-16T09:49:26Z
dc.date2015-11-26T17:24:23Z
dc.date.accessioned2018-03-29T00:11:42Z
dc.date.available2018-03-29T00:11:42Z
dc.identifierBrain Research. Elsevier Science Bv, v. 1149, n. 18, n. 29, 2007.
dc.identifier0006-8993
dc.identifierWOS:000246828200003
dc.identifier10.1016/j.brainres.2007.02.086
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/54189
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/54189
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/54189
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1284068
dc.descriptionA highly controlled transport of substances at the interface between blood and brain characterizes the blood-brain barrier (BBB), fundamental for maintenance of the homeostasis of the cerebral milieu. In this study, we investigated the time course (15 min, 1, 2, and 5 h) of BBB opening induced by intravenous (i.v.) injection of Phoneutria nigriventer spider venom (PNV) using quantitative and morphological approaches on cerebellum and hippocampus vessels for assessment of BBB permeability. The results showed vasogenic edema and tracer extravasation faster and severalfold higher in hippocampus than in cerebellum. Reactive astrocytes with swollen perivascular end-feet processes were found only in cerebellum. An immediate and total degradation of laminin in capillaries occurred resulting in the disappearance of the basement membrane. In medium-sized vessels, this effect was less prominent. The changes were transient, with cerebellum in general presenting a faster recovery. However, at 5 h laminin was overexpressed, principally in hippocampus. The rapid and abrupt shift of laminin expression in capillaries (at 15 min) coincided with the immediate and severe signs of intoxication shown by the animals, but not with the peak of leakage of vessels and vasogenic edema, which occurred later (1-2 h). The findings suggest a complex regulatory mechanism, since the extension of BBB impairment caused by PNV depends on the region of the SNC, and on the vessels types. It is suggested that the components of the BBB (gliovascular unit) have a critical role in these differences. P. nigriventer venom can be a useful tool to explore the mechanisms of BBB. (c) 2007 Elsevier B.V. All rights reserved.
dc.description1149
dc.description18
dc.description29
dc.languageen
dc.publisherElsevier Science Bv
dc.publisherAmsterdam
dc.publisherHolanda
dc.relationBrain Research
dc.relationBrain Res.
dc.rightsfechado
dc.rightshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.sourceWeb of Science
dc.subjectbasal membrane
dc.subjectBBB
dc.subjectlaminin
dc.subjectMET
dc.subjectlanthanum nitrate
dc.subjectPhoneutria nigriventer
dc.subjectExperimental Autoimmune Encephalomyelitis
dc.subjectAppearing White-matter
dc.subjectCentral-nervous-system
dc.subjectSpider Venom
dc.subjectMultiple-sclerosis
dc.subjectIn-vitro
dc.subjectBasement-membrane
dc.subjectCalcium-channels
dc.subjectTight Junctions
dc.subjectToxin
dc.titleAcute blood-brain barrier permeabilization in rats after systemic Phoneutria nigriventer venom
dc.typeArtículos de revistas


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