Abstracts

Although there have been progresses to understand the mechanisms underlying epilepsy, the cellular and molecular basis of epilepsy still is not known yet very well (Patel, 2004; McCorry [italic]et al[/italic]., 2004; Wolfgang and Dieter, 2002;). Therefore, epileptic seizures remain as uncontrolled in at least 30% of all the cases. In order to promote new advances in the development of antiepileptic drugs a better understanding of cellular and molecular mechanisms of epilepsy should be the ultimate goal (Avanzini and Franceschetti, 2003). This can be achieved by beginning to evaluate epilepsy-induced changes in the brain cells. However, beside the consequences of epileptic activity, any possible effect of experimental convulsants on the cells should be under consideration. In order to evaluate the effects of convulsants we initially aimed to investigate the interaction of model membranes with a convulsant agent called picrotoxin (PTX). PTX is a noncompetitive antagonist at GABA-A receptors and it blocks the GABA-activated chloride ionophore (Mazarati [italic]et al[/italic]., 2004)., This study was performed to characterize the effects of PTX on some parameters of dipalmitoylphosphotidylcholine (DPPC) model membrane system. We used differential scanning calorimetry (DSC), electrospin resonance (ESR) spectroscopy and steady-state fluorescence spectroscopy. All studies were carried out with three different concentrations of PTX (1 mol %, 12 mol % and 24 mol %)., The DSC results revealed that PTX has little effect on the melting behavior of DPPC. Indeed, ESR and steady-state fluorescence data indicated that PTX does not significantly affect the order and fluidity of DPPC model membranes., All these results suggest that PTX does not directly interact with membrane lipids, which means that it only acts by binding the membrane protein. Therefore, it can be concluded that the molecular and cellular alterations of chemically induced seizures are only resulted from the consequences of epileptic activity not from convulsant itself., (Supported by Avanzini G., and Franceschetti S., Lancet Neurology 2003; 233[ndash]42.
Manisha Patel M., Free Radical Biology [amp] Medicine (2004) 10: 1951-1962.
Mazarati, A.M., Halaszi, E., Telegdy, G., Brain Res. (1992) 589: 164[ndash] 166.
McCorry D., Chadwick D., and Marson A., Lancet Neurol (2004) 729[ndash]35
Wolfgang L., and Dieter S., Epilepsy Research (2002) 50: 3-16.)