Alcohol abuse promotes changes in non-synaptic epileptiform activity with concomitant expression changes in cotransporters and glial cells.
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.
Laboratório de Neurociência Experimental e Computacional, Departamento de Engenharia de Biossistemas, Universidade Federal de São João del-Rei, São João del-Rei, Minas Gerais, Brasil.
Luiz Eduardo Canton
LE
Santos
Gilcélio Amaral
GA
da Silveira
Victor Diego Cupertino
VD
Costa
Aline Gisele
AG
Batista
Ana Paula
AP
Madureira
Antônio Márcio
AM
Rodrigues
Carla Alessandra
CA
Scorza
Henrique Alves
HA
Amorim
Ricardo Mário
RM
Arida
Mario Antônio
MA
Duarte
Fúlvio Alexandre
FA
Scorza
Esper Abrão
EA
Cavalheiro
Antônio-Carlos Guimarães
AC
de Almeida
D000437:Alcoholism / Q000150:complications / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D000818:Animals; D039481:CD11b Antigen / Q000378:metabolism*; D018891:Dentate Gyrus / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D000431:Ethanol / Q000009:adverse effects; D006801:Humans; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials; D009457:Neuroglia / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D064506:Solute Carrier Family 12, Member 2 / Q000378:metabolism*; D013226:Status Epilepticus / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*
D039481:CD11b Antigen; C578879:Slc12a2 protein, rat; D064506:Solute Carrier Family 12, Member 2; D000431:Ethanol