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dc.contributor.authorCanton Santos, Luiz Eduardo
dc.contributor.authorSilveira, Gilcelio Amaral da
dc.contributor.authorCosta, Victor Diego Cupertino
dc.contributor.authorBatista, Aline Gisele
dc.contributor.authorMadureira, Ana Paula
dc.contributor.authorRodrigues, Antonio Marcio
dc.contributor.authorScorza, Carla Alessandra [UNIFESP]
dc.contributor.authorAmorim, Henrique Alves [UNIFESP]
dc.contributor.authorArida, Ricardo Mario [UNIFESP]
dc.contributor.authorDuarte, Mario Antonio
dc.contributor.authorScorza, Fulvio Alexandre [UNIFESP]
dc.contributor.authorCavalheiro, Esper Abrão [UNIFESP]
dc.contributor.authorAlmeida, Antonio-Carlos Guimaraes de
dc.date.accessioned2016-01-24T14:34:43Z
dc.date.available2016-01-24T14:34:43Z
dc.date.issued2013-11-13
dc.identifierhttp://dx.doi.org/10.1371/journal.pone.0078854
dc.identifier.citationPlos One. San Francisco: Public Library Science, v. 8, n. 11, 10 p., 2013.
dc.identifier.issn1932-6203
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/36976
dc.description.abstractNon-synaptic mechanisms are being considered the common factor of brain damage in status epilepticus and alcohol intoxication. the present work reports the influence of the chronic use of ethanol on epileptic processes sustained by non-synaptic mechanisms. Adult male Wistar rats administered with ethanol (1, 2 e 3 g/kg/d) during 28 days were compared with Control. Non-synaptic epileptiform activities (NEAs) were induced by means of the zero-calcium and high-potassium model using hippocampal slices. the observed involvement of the dentate gyrus (DG) on the neurodegeneration promoted by ethanol motivated the monitoring of the electrophysiological activity in this region. the DG regions were analyzed for the presence of NKCC1, KCC2, GFAP and CD11b immunoreactivity and cell density. the treated groups showed extracellular potential measured at the granular layer with increased DC shift and population spikes (PS), which was remarkable for the group E1. the latencies to the NEAs onset were more prominent also for the treated groups, being correlated with the neuronal loss. in line with these findings were the predispositions of the treated slices for neuronal edema after NEAs induction, suggesting that restrict inter-cell space counteracts the neuronal loss and subsists the hyper-synchronism. the significant increase of the expressions of NKCC1 and CD11b for the treated groups confirms the existence of conditions favorable to the observed edematous necrosis. the data suggest that the ethanol consumption promotes changes on the non-synaptic mechanisms modulating the NEAs. for the lower ethanol dosage the neurophysiological changes were more effective suggesting to be due to the less intense neurodegenertation.en
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de Minas Gerais (FAPEMIG)
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.format.extent10
dc.language.isoeng
dc.publisherPublic Library Science
dc.relation.ispartofPlos One
dc.rightsAcesso aberto
dc.titleAlcohol Abuse Promotes Changes in Non-Synaptic Epileptiform Activity with Concomitant Expression Changes in Cotransporters and Glial Cellsen
dc.typeArtigo
dc.contributor.institutionUniv Fed Sao Joao del Rei
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.description.affiliationUniv Fed Sao Joao del Rei, Dept Engn Biossistemas, Lab Neurociencia Expt & Computac, Sao Joao Del Rei, MG, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Escola Paulista Med, Disciplina Neurol Expt, São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Ciencia & Tecnol, Sao Jose Dos Campos, SP, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Escola Paulista Med, Disciplina Fisiol, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Escola Paulista Med, Disciplina Neurol Expt, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Ciencia & Tecnol, Sao Jose Dos Campos, SP, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Escola Paulista Med, Disciplina Fisiol, São Paulo, Brazil
dc.identifier.fileWOS000327254700057.pdf
dc.identifier.doi10.1371/journal.pone.0078854
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000327254700057


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