GABA-MEDIATED SYNCHRONOUS POTENTIALS AND SEIZURE GENERATION

This article summarizes findings related to a synchronous, GABA-mediat ed potential that may contribute to the initiation and spread of epile ptiform discharges within the brain. This phenomenon is observed in co rtical structures such as the hippocampus, the entorhinal cortex, and the neocortex during application of low concentrations of 4-amimopyrid ine and is characterized at the intracellular level by a long-lasting membrane depolarization. The synchronous, GABA-mediated potential cont inues to occur after blockade of excitatory synaptic transmission and relays on the synchronous firing of inhibitory interneurons and conseq uent activation of postsynaptic (mainly type A) GABA receptors leading to a transient elevation of [K+](O). Studies performed in young rat h ippocampus indicate that the synchronous, GABA-mediated potential may play a role in initiating ictal discharges under normal conditions (i. e., when excitatory amino acid receptors are operant). Moreover, a sim ilar phenomenon may also occur in adult rat entorhinal cortex. These f indings therefore indicate a novel role that is played by GABA(A) rece ptors in limbic structures. The ability of this synchronous GABA-media ted potential to propagate in the absence of excitatory synaptic trans mission may also be relevant for the propagation of synchronous activi ty outside conventional neuronal-synapse dependent pathways. This cond ition may occur in brain structures with neuronal loss and consequent disruption of normal excitatory synaptic connections such as mesial li mbic structures of temporal lobe epilepsy patients with Ammon's horn s clerosis.