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.

Effect of co-transporter blockers on non-synaptic epileptiform activity-computational simulation.

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).

Simulation of the effect of Na+ and Cl- on the velocity of a spreading depression wave using a simplified electrochemical model of synaptic terminals.

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.