The A(1) receptor agonist R-Pia reduces the imbalance between cerebral glucose metabolism and blood flow during status epilepticus: Could this mechanism be involved with neuroprotection?

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dc.contributor.authorSilva, Lara Ribeiro [UNIFESP]
dc.contributor.authorNehlig, Astrid
dc.contributor.authorRosim, Fernanda Elisa [UNIFESP]
dc.contributor.authorVignoli, Thiago [UNIFESP]
dc.contributor.authorPersike, Daniele Suzete [UNIFESP]
dc.contributor.authorFerrandon, Arielle
dc.contributor.authorSinigaglia-Coimbra, Rita [UNIFESP]
dc.contributor.authorSilva Fernandes, Maria Jose da [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniv Strasbourg
dc.date.accessioned2016-01-24T14:05:58Z
dc.date.available2016-01-24T14:05:58Z
dc.date.issued2011-01-01
dc.description.abstractIt is well known that the uncoupling between local cerebral glucose utilization (LCGU) and local cerebral blood flow (LCBF), i.e. decrease in LCBF rates with high LCGU, is frequently associated with seizure-induced neuronal damage. This study was performed to assess if the neuroprotective effect of the adenosinergic A(1) receptor agonist R-N-phenylisopropyladenosine (R-Pia) injected prior to pilocarpine is able to reduce the uncoupling between LCGU and LCBF during status epilepticus (SE). Four groups of rats were studied: Saline, Pilo, R-Pia + Saline and R-Pia + Pilo. for LCGU and LCBF studies, rats were subjected to autoradiography using [C-14]-2-deoxyglucose and [C-14]-iodoantypirine, respectively. Radioligands were injected 4 h after SE onset. Neuronal loss was evaluated by Fluorojade-B (FJB) at two time points after SE onset (24 h and 7 days). the results showed a significant increase in LCGU in almost all brain regions studied in the Pilo and R-Pia + Pilo groups compared to controls. However, in R-Pia pretreated rats, the uncoupling between LCGU and LCBF was moderated in a limited number of structures as substantia nigra pars reticulata and hippocampal formation rather in favor of hyperperfusion. Significant increases in LCBF were observed in the entorhinal cortex, thalamic nuclei, mammillary body, red nucleus, zona incerta, pontine nucleus and visual cortex. the neuroprotective effect of R-Pia assessed by FJB showed a lower density of degenerating cells in the hippocampal formation, piriform cortex and basolateral amygdala. in conclusion our data shows that the neuroprotective effect of R-Pia was accompanied by a compensatory metabolic input in brain areas involved with seizures generation. Published by Elsevier Inc.en
dc.description.affiliationUniversidade Federal de São Paulo, Dept Neurol & Neurocirurg, Disciplina Neurol Expt, BR-04039032 São Paulo, Brazil
dc.description.affiliationUniv Strasbourg, INSERM, Unite 465, Strasbourg, France
dc.description.affiliationUniversidade Federal de São Paulo, Ctr Microscopia Eletron, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Neurol & Neurocirurg, Disciplina Neurol Expt, BR-04039032 São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Ctr Microscopia Eletron, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.format.extent169-176
dc.identifierhttp://dx.doi.org/10.1016/j.nbd.2010.09.004
dc.identifier.citationNeurobiology of Disease. San Diego: Academic Press Inc Elsevier Science, v. 41, n. 1, p. 169-176, 2011.
dc.identifier.doi10.1016/j.nbd.2010.09.004
dc.identifier.issn0969-9961
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/33283
dc.identifier.wosWOS:000285036400018
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofNeurobiology of Disease
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.subjectPilocarpineen
dc.subjectNeuroprotectionen
dc.subjectAdenosine receptoren
dc.subjectR-Pia, glucose metabolismen
dc.subjectCerebral blood flowen
dc.titleThe A(1) receptor agonist R-Pia reduces the imbalance between cerebral glucose metabolism and blood flow during status epilepticus: Could this mechanism be involved with neuroprotection?en
dc.typeinfo:eu-repo/semantics/article
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