title: Effects of barium on stimulus-induced rises of [K+]o in human epileptic non-sclerotic and sclerotic hippocampal area CA1.
abstract: In the hippocampus of patients with therapy-refractory temporal lobe epilepsy, glial cells of area CA1 might be less able to take up potassium ions via barium-sensitive inwardly rectifying and voltage-independent potassium channels. Using ion-selective microelectrodes we investigated the effects of barium on rises in [K+]o induced by repetitive alvear stimulation in slices from surgically removed hippocampi with and without Ammon's horn sclerosis (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 was reversible, concentration dependent, and persisted in the presence of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA), N-methyl-D-aspartate (NMDA) and gamma-aminobutyric acid [GABA(A)] receptor antagonists. In AHS tissue, barium caused a decrease in the baseline level of [K+]o. In contrast 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 half time of recovery from the rise was less prolonged (by 57%). Under conditions of blocked synaptic transmission, barium augmented stimulus-induced rises in [K+]o, but only by 40%. In both tissues, barium significantly reduced negative slow-field potentials following repetitive stimulation but did not alter the mean population spike amplitude. The findings suggest a significant contribution of glial barium-sensitive K+-channels to K+-buffering in non-AHS tissue and an impairment of glial barium-sensitive K+-uptake in AHS tissue.
authors.affiliation: Johannes Müller Institut für Physiologie, Universitätsklinikum Charité, Humboldt-Universität, zu Berlin, Germany.
authors.forename: A
authors.initials: A
authors.lastname: Kivi
authors.forename: T N
authors.initials: TN
authors.lastname: Lehmann
authors.forename: R
authors.initials: R
authors.lastname: Kovács
authors.forename: A
authors.initials: A
authors.lastname: Eilers
authors.forename: R
authors.initials: R
authors.lastname: Jauch
authors.forename: H J
authors.initials: HJ
authors.lastname: Meencke
authors.forename: A
authors.initials: A
authors.lastname: von Deimling
authors.forename: U
authors.initials: U
authors.lastname: Heinemann
authors.forename: S
authors.initials: S
authors.lastname: Gabriel
mesh_terms: D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D000328:Adult; D017609:Barium Compounds / Q000494:pharmacology*; D001640:Bicuculline / Q000494:pharmacology; D002021:Buffers; D002712:Chlorides / Q000494:pharmacology*; D004558:Electric Stimulation; D004594:Electrophysiology; D004833:Epilepsy, Temporal Lobe / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D066298:In Vitro Techniques; D011188:Potassium / Q000378:metabolism*; D011810:Quinoxalines / Q000494:pharmacology; D012598:Sclerosis; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology
chemical_list: D017609:Barium Compounds; D002021:Buffers; D002712:Chlorides; D018691:Excitatory Amino Acid Antagonists; D018756:GABA Antagonists; D011810:Quinoxalines; C024986:barium chloride; C062865:2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline; D015763:2-Amino-5-phosphonovalerate; D011188:Potassium; D001640:Bicuculline