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1.
PLoS One ; 8(11): e78854, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-24236060

RESUMO

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.


Assuntos
Alcoolismo/fisiopatologia , Antígeno CD11b/metabolismo , Neuroglia/metabolismo , Membro 2 da Família 12 de Carreador de Soluto/metabolismo , Estado Epiléptico/fisiopatologia , Alcoolismo/complicações , Alcoolismo/metabolismo , Alcoolismo/patologia , Animais , Giro Denteado/efeitos dos fármacos , Giro Denteado/patologia , Giro Denteado/fisiopatologia , Etanol/efeitos adversos , Humanos , Técnicas In Vitro , Masculino , Potenciais da Membrana , Neuroglia/efeitos dos fármacos , Ratos , Ratos Wistar , Estado Epiléptico/etiologia , Estado Epiléptico/metabolismo , Estado Epiléptico/patologia
2.
Phys Biol ; 10(5): 056008, 2013 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-24092000

RESUMO

The important role of cation-chloride co-transporters in epilepsy is being supported by an increasing number of investigations. However, enormous complexity is involved since the action of these co-transporters has effects on the ionic homeostasis influencing directly the neuronal excitability and the tissue propensity to sustain seizure. To unravel the complex mechanisms involving the co-transporters action during seizure, this paper shows simulations of non-synaptic epileptiform activity and the effect of the blockage of the two different types of cation-chloride co-transporters present in the brain: Na, K and 2Cl co-transporter (NKCC) and K and Cl co-transporter (KCC). The simulations were performed with an electrochemical model representing the non-synaptic structure of the granule cell layer of the dentate gyrus (DG) of the rat hippocampus. The simulations suggest: (i) the potassium clearance is based on the systemic interplay between the Na/K pump and the NKCC co-transporters; (ii) the simultaneous blockage of the NKCC of the neurons and KCC of glial cells acts efficiently suppressing the epileptiform activities; and (iii) the simulations show that depending on the combined blockage of the co-transporters, the epileptiform activities may be suppressed or enhanced.


Assuntos
Simulação por Computador , Epilepsia/tratamento farmacológico , Simportadores de Cloreto de Sódio-Potássio/efeitos dos fármacos , Simportadores/antagonistas & inibidores , Animais , Eletroencefalografia , Epilepsia/fisiopatologia , Hipocampo/efeitos dos fármacos , Hipocampo/fisiopatologia , Neurônios/efeitos dos fármacos , Neurônios/fisiologia , Ratos , Cotransportadores de K e Cl-
3.
Comput Intell Neurosci ; 2013: 949816, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-23431287

RESUMO

Structural rearrangement of the dentate gyrus has been described as the underlying cause of many types of epilepsies, particularly temporal lobe epilepsy. It is said to occur when aberrant connections are established in the damaged hippocampus, as described in human epilepsy and experimental models. Computer modelling of the dentate gyrus circuitry and the corresponding structural changes has been used to understand how abnormal mossy fibre sprouting can subserve seizure generation observed in experimental models when epileptogenesis is induced by status epilepticus. The model follows the McCulloch-Pitts formalism including the representation of the nonsynaptic mechanisms. The neuronal network comprised granule cells, mossy cells, and interneurons. The compensation theory and the Hebbian and anti-Hebbian rules were used to describe the structural rearrangement including the effects of the nonsynaptic mechanisms on the neuronal activity. The simulations were based on neuroanatomic data and on the connectivity pattern between the cells represented. The results suggest that there is a joint action of the compensation theory and Hebbian rules during the inflammatory process that accompanies the status epilepticus. The structural rearrangement simulated for the dentate gyrus circuitry promotes speculation about the formation of the abnormal mossy fiber sprouting and its role in epileptic seizures.


Assuntos
Giro Denteado/fisiopatologia , Epilepsia/fisiopatologia , Rede Nervosa/fisiologia , Redes Neurais de Computação , Vias Neurais/fisiologia , Sinapses/fisiologia , Algoritmos , Simulação por Computador , Fenômenos Eletrofisiológicos , Humanos , Interneurônios/fisiologia , Modelos Neurológicos , Fibras Musgosas Hipocampais/fisiologia , Agonistas Muscarínicos/farmacologia , Neurônios/fisiologia , Pilocarpina/farmacologia , Receptores de GABA-A/fisiologia , Estado Epiléptico/fisiopatologia , Transmissão Sináptica
4.
J Neural Eng ; 1(2): 117-26, 2004 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-15876630

RESUMO

In the study of the spreading depression (SD) wave phenomenon and its dynamics, it is necessary to describe the ionic movements along the extracellular space, as well as between this and the intracellular space. In both cases, the ionic movement includes a double coupling involving the concentration and the potential gradients and hence must be described by electrodiffusion mechanisms. Based on this, the effects of the ionic composition on the characteristics of the wave propagation can be predicted. The influence of varying extracellular sodium and chloride concentrations on the velocity of propagation of the SD wave was investigated by simulation. The results achieved are close to the experimental measurement from the literature. These findings suggest the potentiality of the model proposed in supporting the interpretation of experimental data in neuronal tissues, particularly the SD.


Assuntos
Cloro/metabolismo , Modelos Neurológicos , Condução Nervosa/fisiologia , Inibição Neural/fisiologia , Disco Óptico/fisiologia , Terminações Pré-Sinápticas/fisiologia , Sódio/metabolismo , Transmissão Sináptica/fisiologia , Animais , Células Cultivadas , Galinhas , Cloro/farmacologia , Simulação por Computador , Relação Dose-Resposta a Droga , Eletroencefalografia/métodos , Sódio/farmacologia
5.
In. Schiabel, Homero; Slaets, Annie France Frère; Costa, Luciano da Fontoura; Baffa Filho, Oswaldo; Marques, Paulo Mazzoncini de Azevedo. Anais do III Fórum Nacional de Ciência e Tecnologia em Saúde. Säo Carlos, s.n, 1996. p.649-650, graf.
Monografia em Português | LILACS | ID: lil-233913

RESUMO

A modelagem da atividade elétrica de células neuronais é de grande interesse para o estudo do comportamento de redes neuronais biológicas. Neste estudo apresenta-se a modelagem de correntes iônicas de células neuronais que são indispensáveis ao estudo de potenciais de ação e respostas sinápticas.


Assuntos
Eletrofisiologia , Rede Nervosa , Modelos Anatômicos , Neurônios , Sódio , Cálcio , Dinâmica não Linear , Potássio
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