Effects of barium on stimulus-induced rises of [K+](o) in human epileptic non-sclerotic and sclerotic hippocampal area CA1

In the hippocampus of patients with therapy-refractory temporal lobe epilep sy, glial cells of area CA1 might be less able to take up potassium ions vi a barium-sensitive inwardly rectifying and voltage-independent potassium ch annels. Using ion-selective microelectrodes we investigated the effects of barium on rises in [K+](o) induced by repetitive alvear stimulation in slic es from surgically removed hippocampi with and without Ammon's horn scleros is (AHS and non-AHS). In non-AHS tissue, barium augmented rises in [K+](o) by 147% and prolonged the half time of recovery by 90%. The barium effect w as reversible, concentration dependent, and persisted in the presence of al pha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA), N-methyl-D-aspar tate (NMDA) and gamma-aminobutyric acid [GABA(A)] receptor antagonists. In AHS tissue, barium caused a decrease in the baseline level of [K+](o). In c ontrast to non-AHS slices, in AHS slices with intact synaptic transmission, barium had no effect on the stimulus-induced rises of [K+](o), and the hal f time of recovery from the rise was less prolonged (by 57%). Under conditi ons of blocked synaptic transmission, barium augmented stimulus-induced ris es in [K+](o), but only by 40%. In both tissues, barium significantly reduc ed negative slow-field potentials following repetitive stimulation but did not alter the mean population spike amplitude. The findings suggest a signi ficant contribution of glial barium-sensitive K+-channels to K+-bufferrng i n non-AHS tissue and an impairment of glial barium-sensitive K+-uptake in A HS tissue.