Status epilepticus does not induce acute brain inflammatory response in the Amazon rodent Proechimys, an animal model resistant to epileptogenesis

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dc.citation.volumev. 668
dc.contributor.authorScorza, Carla Alessandra [UNIFESP]
dc.contributor.authorMarques, Marcia Jonathas Guimaraes [UNIFESP]
dc.contributor.authorSilva, Sergio Gomes da [UNIFESP]
dc.contributor.authorNaffah-Mazzacoratti, Maria da Graca [UNIFESP]
dc.contributor.authorScorza, Fulvio Alexandre [UNIFESP]
dc.contributor.authorCavalheiro, Esper Abrão [UNIFESP]
dc.coverageClare
dc.date.accessioned2020-07-20T16:31:16Z
dc.date.available2020-07-20T16:31:16Z
dc.date.issued2018
dc.description.abstractMesial temporal lobe epilepsy is a serious brain disorder in adults that is often preceded by an initial brain insult, such as status epilepticus (SE), that after a latent period leads to recurrent seizures. Post SE models are widely used for studies on epileptogenic processes. Previous findings of our laboratory suggested that the Neotropical rodents Proechimys exhibit endogenous antiepileptogenic mechanisms in post-SE models. Strong body of research supports that SE triggers a rapid and dramatic upregulation of inflammatory mediators and vascular endothelial growth factor (VEGF). In this work we found that, in the epilepsy-resistant Proechimys, hippocampal and cortical levels of inflammatory cytokines (1L-1 beta, 1L-6, IL-10, TNF-alpha) and VEGF remained unchanged 24 h after SE, strongly contrasting to the high levels of post-SE changes observed in Wistar rats. Furthermore, substantial differences in the brain baseline levels of these proteins were encountered between animal species studied. Since inflammatory cytokines and VEGF have been recognized as major orchestrators of the epileptogenic process, our results suggest their role in the antiepileptogenic mechanisms previously described in Proechimys. (C) 2017 Elsevier B.V. All rights reserved.en
dc.description.affiliationUniv Fed Sao Paulo, Escola Paulista Med, Disciplina Neurociencia, Sao Paulo, Brazil
dc.description.affiliationHosp Israelita Albert Einstein, Sao Paulo, SP, Brazil
dc.description.affiliationUniv Mogi das Cruzes, Nucl Pesquisas Tecnol, Mogi Das Cruzes, SP, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Escola Paulista Med, Disciplina Neurociencia, Sao Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFAPESP
dc.description.sponsorshipCAPES
dc.description.sponsorshipCNPq
dc.description.sponsorshipFAPESP/CNPq/MCT-Instituto Nacional de Neurociencia Translacional
dc.format.extent169-173
dc.identifierhttp://dx.doi.org/10.1016/j.neulet.2017.02.049
dc.identifier.citationNeuroscience Letters. Clare, v. 668, p. 169-173, 2018.
dc.identifier.doi10.1016/j.neulet.2017.02.049
dc.identifier.issn0304-3940
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/55834
dc.identifier.wosWOS:000427333700029
dc.language.isoeng
dc.publisherElsevier Ireland Ltd
dc.relation.ispartofNeuroscience Letters
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectStatus epilepticusen
dc.subjectEpileptogenesisen
dc.subjectNeuroinflammationen
dc.subjectProechimysen
dc.titleStatus epilepticus does not induce acute brain inflammatory response in the Amazon rodent Proechimys, an animal model resistant to epileptogenesisen
dc.typeinfo:eu-repo/semantics/review
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