Alterations of glial cell function in temporal lobe epilepsy.

Abstract

Comparison of extracellular K+ regulation in sclerotic and nonsclerotic epileptic hippocampus. Measurements of K+ signals with double-barreled K+-selective reference microelectrodes in area CAI of slices from human and rat hippocampus, induction of increases in extracellular potassium concentration by repetitive alvear stimulation or iontophoresis. and block of inward-rectifying and background K+ channels in astrocytes by barium. In the CA1 pyramidal layer from normal rat hippocampus, barium augmented extracellular K+ accumulation induced by iontophoresis or antidromic stimulation in a dose-dependent manner. Similarly, barium augmented stimulus-induced K+ signals from nonsclerotic hippocampi (human mesial temporal lobe epilepsy). In contrast, barium failed to do so in sclerotic hippocampi (human mesial temporal lobe epilepsy, rat pilocarpine model). Our findings suggest that in areas of reduced neuronal density (hippocampal sclerosis), glial cells adapt to permit rather large increases in extracellular potassium accumulation. Such increases might be involved in the transmission of activity through the sclerotic area.