Effect of Extracellular Chloride Depletion on Non-synaptic Epileptiform Activities

Abstract

Changes in chloride homeostasis are associated with epilepsy. High intracellular levels of this ion promote increased neuronal excitability. It has been observed that the control of transmembrane fluxes of chloride ions involves the operation of channels, pumps and transporters, mechanisms that do not depend directly on the synaptic circuitry. However, there are still differences regarding the modulation of chloride during epileptiform activities. Thus, the present work investigated the extracellular depletion of chloride ions in the non-synaptic epileptiform activities (AENS) induced in hippocampal slices of Wistar rats by means of extracellular electrophysiological records in the dentate gyrus. The low extracellular chloride (7 mM) maneuver caused an increase in the frequency of firing in the first few minutes of perfusion, followed by changes in the extracellular electrical potential morphology. The analysis of the intrinsic optical signal (IOS) also showed a reduction of light transmittance during the maneuver. Changes in extracellular electrical potential were attributed to the possible occurrence of intracellular alkalosis during perfusion with low [Cl−]o, with consequent development of a neuronal hyperexcitability.