The role of chloride regulation in epilepsy. (360G-Wellcome-080543_Z_06_Z)

In both human cases of epilepsy, and in animal models, seizure activity has been shown to lead to abnormal neuronal morphology and connectivity. For example, the inducement of epileptic-like activity in the rat hippocampus leads to a decrease in the density of dendritic spines within pyramidal neurons of around 20-40%. Tissue samples taken from temporal lobe epileptic patients also reveal significant atrophy of the neocortical grey matter with pyramidal cells possessing sparser dendritic trees and reduced spinie density compared to age-matched controls. Such patho-morphological changes are believed to have important consequences with regards to normal neuronal function and may lead to increased susceptibility and likelihood of future epileptic insults. The cellular processes behind these changes are poorly understood and any insights would help to elucidate the mechanisms by which epileptic states are initiated and maintained within neuronal tissue, as well as potentially providing novel therapeutic targets and approaches to treating the disorder.