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.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)Univ Fed Sao Joao del Rei, Dept Engn Biossistemas, Lab Neurociencia Expt & Computac, Sao Joao Del Rei, MG, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Disciplina Neurol Expt, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Ciencia & Tecnol, Sao Jose Dos Campos, SP, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Disciplina Fisiol, São Paulo, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Disciplina Neurol Expt, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Ciencia & Tecnol, Sao Jose Dos Campos, SP, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Disciplina Fisiol, São Paulo, BrazilWeb of Scienc

Epilepsia e atividade física: estudos em humanos e animais

Epilepsy is the most common chronic neurological disorder in the world that influences negatively the quality of people's life affected by this disease. Although the favorable effect of physical activity on general health is unquestionable, the appropriate physical exercise for people with epilepsy is still controversial. Studies have shown beneficial effect of physical exercise on frequency of seizures as well as on life quality. However, people with epilepsy frequently are discouraged and excluded from participation in physical exercise due to the fear that the participation in a physical exercise program can precipitate epileptic seizures. Therefore, the aim of this study was to review the effect of physical exercise based on clinical and experimental studies of epilepsy.A epilepsia é considerada o distúrbio neurológico crônico mais prevalente no mundo, influenciando negativamente a qualidade de vida de indivíduos com epilepsia. Apesar do efeito favorável do exercício físico sobre a saúde ser inquestionável, a realização de um programa de exercício físico por pessoas com epilepsia ainda é um assunto controverso. Estudos têm mostrado efeitos benéficos do exercício físico na freqüência de crises assim como na qualidade de vida. Entretanto, indivíduos com epilepsia são freqüentemente desencorajados e excluídos da participação em programas de exercício físico pelo medo que tal participação possa precipitar crises epilépticas. Sendo assim, o objetivo desse estudo foi revisar o efeito do exercício físico baseado em dados de estudos clínicos e experimentais de epilepsia

Efeitos do exercício físico na frequência de crises epilépticas e no humor em pacientes com epilepsia

OBJETIVO: Esse estudo teve o propósito de avaliar a ocorrência de crises epilépticas e as alterações nos níveis de depressão e ansiedade em pacientes epilépticos após serem submetidos a um programa de exercício físico aeróbio durante doze semanas. MÉTODOS: Foi utilizada uma amostra composta de 30 pacientes epilépticos, voluntários, do sexo masculino, com idade entre 40 e 49 anos, média de 45 anos, sedentários, que não fazem utilização de medicamentos antidepressivos e não possuem contra-indicações à prática de exercícios físicos diagnosticados por meio de avaliação médica. Os participantes do estudo foram submetidos a um programa de atividade física aeróbia durante 12 semanas, com 3 sessões semanais e com duração que variou de 40 a 60 minutos. RESULTADOS: Os resultados desse estudo demonstraram redução nos níveis de depressão e no número de crises. Por outro lado, em relação à ansiedade não foi observada significante alteração. CONCLUSÕES: Conclui-se que a prática de atividade física aeróbia durante 12 semanas pode ser suficiente para decrescer os níveis de depressão e reduzir o número de crises em portadores de epilepsia

Acute effects of moderate-intensity continuous physical exercise performed with different amounts of muscle mass on executive function in healthy young adults: a randomized trial

We examined the effect of amount of muscle mass involved in moderate-intensity continuous physical exercise on executive function. To this end, fifty-five participants completed two acute physical exercise sessions on an airbike ergometer using the upper and lower limbs simultaneously and only the upper limbs, and a resting control session in a randomized order. The physical exercise session lasted 30 min and was performed at moderate intensity (between 64 %-76 % of maximal heart rate evaluated in graded maximal exercise testing). Participants took the Stroop test (congruent and incongruent trials) before and after the sessions to assess executive performance. For the congruent trial, both physical exercise interventions improved executive function performance (pre vs. post, p-value = 0.002 and 0.003 for physical exercise with upper limbs and physical exercise with upper and lower limbs, respectively). Furthermore, executive function performance was higher after the physical exercise interventions than after the control session (p-value = 0.002 and 0.004 for physical exercise with upper limbs and physical exercise with upper and lower limbs, respectively). For the incongruent trial, both physical exercise interventions also improved executive function performance (pre vs. post, p-value < 0.001 for physical exercise with upper limbs and physical exercise with upper and lower limbs, respectively). However, there were no significant differences after both physical exercise interventions and resting control session (p-value = 0.175). Executive function (congruent trial) was positively impacted by acute aerobic physical exercise regardless of the amount of muscle mass involved (upper limbs or upper plus lower limbs). Therefore, we recommend aerobic physical exercise with less or more muscle mass involved to improve cognitive function

Nissl stain analysis.

<p>A: After Nissl staining, the typical morphology of the granule layer of DG for each group investigated (control, E1, E2 and E3) are shown. B: Effect of the non-synaptic activity induction on the cell morphology, performed for the group E3 in comparison with control. Before seizure induction, the normal morphology of the granule layer (a) is replaced by the presence of whitish zones, somas with swelling (thick arrows) and dark cells (thin arrows) (b). After seizure induction, the slices of the control group showed edematous cell bodies and a few dark cells (thin arrows) (c). However, the slices from the group E3 appeared with intense edematous necrosis, as shown in (d). Several cell bodies with intense swelling (thick arrows) and dark cells (thin arrows) can be seen.</p

DG immuno-stained for NKCC1 and KCC2.

<p>Typical images for NKCC1 (Magnification: 400x). All alcohol treated groups expressed more intense staining for NKCC1 than Control (A). For KCC2 the immuno-reactivity was more intense for the group E3 (K) (Magnification: 1000x). The transition between the granule and molecular layers exhibited the most intense staining for both NKCC1, comparing E3 (G) with Control (E), and KCC2, comparing E3 (N) with Control (L). Statistical comparisons were done with one-way ANOVA with Dunnett’s test. Data are presented as mean ± SEM. Error bars indicate SEM. *<i>p</i><0.05.</p

DG immune-stained for CD11b.

<p>(A) Control, E1, E2 e E3 (Magnification 100x). Insets show typical microglial morphology of each group (Magnification 1000x). Arrows head indicate microglial activation also shown in the insets. (B) Optical densitometry analysis of the immuno-reactivity to CD11b. E2 and E3 groups exhibited increased immuno-staining in comparison with Control and E1. Statistical comparisons were done with one-way ANOVA with Dunnett’s test. Data are presented as mean ± SEM. Error bars indicate SEM. *<i>p</i><0.05.</p

Typical non-synaptic epileptiform activities induced in hippocampus slices and recorded in the granular layer of the dentate gyrus according to the groups.

<p>(A) control, (B) E1, (C) E2 and (D) E3.</p

DG immuno-stained for GFAP.

<p>(A) Control section, (B) E1 section, (C) E2 section, (D) E3 section (Magnification 100x). The astrocyte reactivity typical of E3 (G) is absent in the control (E) (Magnification 1000x). (F) Optical densitometry analysis of GFAP immuno-staining showed E3 with significant increase in comparison with the other groups. Statistical comparisons were done with one-way ANOVA with Dunnett’s test. Data are presented as mean ± SEM. Error bars indicate SEM. *<i>p</i><0.05.</p