Alcohol Abuse Promotes Changes in Non-Synaptic Epileptiform Activity with Concomitant Expression Changes in Cotransporters and Glial Cells

Alcohol Abuse Promotes Changes in Non-Synaptic Epileptiform Activity with Concomitant Expression Changes in Cotransporters and Glial Cells

Author Canton Santos, Luiz Eduardo Google Scholar
Silveira, Gilcelio Amaral da Google Scholar
Costa, Victor Diego Cupertino Google Scholar
Batista, Aline Gisele Google Scholar
Madureira, Ana Paula Google Scholar
Rodrigues, Antonio Marcio Google Scholar
Scorza, Carla Alessandra Autor UNIFESP Google Scholar
Amorim, Henrique Alves Autor UNIFESP Google Scholar
Arida, Ricardo Mario Autor UNIFESP Google Scholar
Duarte, Mario Antonio Google Scholar
Scorza, Fulvio Alexandre Autor UNIFESP Google Scholar
Cavalheiro, Esper Abrão Autor UNIFESP Google Scholar
Almeida, Antonio-Carlos Guimaraes de Google Scholar
Institution Univ Fed Sao Joao del Rei
Universidade Federal de São Paulo (UNIFESP)
Abstract Non-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.
Language English
Sponsor Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Fundação de Amparo à Pesquisa do Estado de Minas Gerais (FAPEMIG)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Date 2013-11-13
Published in Plos One. San Francisco: Public Library Science, v. 8, n. 11, 10 p., 2013.
ISSN 1932-6203 (Sherpa/Romeo, impact factor)
Publisher Public Library Science
Extent 10
Access rights Open access Open Access
Type Article
Web of Science ID WOS:000327254700057

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