title: Contribution of intrinsic neuronal factors in the generation of cortically driven electrographic seizures.
abstract: Some electrographic seizures are generated intracortically. The cellular and ionic bases of cortically generated spontaneous seizures are not fully understood. Here we investigated spontaneously occurring seizures consisting of spike-wave complexes intermingled with fast runs in ketamine-xylazine anesthetized cats, using dual intracellular recordings in which one pipette contained a control solution and another pipette contained blockers of K(+), Na(+), or Ca(2+) currents. We show that closely located neocortical neurons display virtually identical fluctuations of the membrane potential during electrographic seizures, thus directly demonstrating a high degree of focal synchrony during paroxysmal activity. In addition to synaptic drives, the persistent Na(+) current [I(Na(p))] and probably the high-threshold Ca(2+) current contributed to the generation of paroxysmal depolarizing shifts (PDSs) during cortically driven seizures. Ca(2+)-activated K(+) current [I(K(Ca))] took also part in the control of the amplitude and duration of PDSs. The hyperpolarizing components of seizures largely depended on Cs(+)-sensitive K(+) currents. I(K(Ca)) played a significant, while not exclusive, role in the mediation of hyperpolarizing potentials related to EEG "waves" during spike-wave seizures. We conclude that intrinsic cellular factors have significant role in the generation of depolarizing and hyperpolarizing components of seizures.
authors.affiliation: Laboratory of Neurophysiology, Faculty of Medicine, Laval University, Quebec G1K 7P4, Canada. Igor.Timofeev@phs.ulaval.ca
authors.forename: Igor
authors.initials: I
authors.lastname: Timofeev
authors.forename: François
authors.initials: F
authors.lastname: Grenier
authors.forename: Mircea
authors.initials: M
authors.lastname: Steriade
mesh_terms: D000200:Action Potentials; D000779:Anesthetics, Local / Q000494:pharmacology; D000818:Animals; D015220:Calcium Channels / Q000378:metabolism; D002415:Cats; D002540:Cerebral Cortex / Q000503:physiopathology*; D002586:Cesium / Q000494:pharmacology; D002614:Chelating Agents / Q000494:pharmacology; D003344:Cortical Synchronization; D004533:Egtazic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology; D004569:Electroencephalography; D004594:Electrophysiology; D008012:Lidocaine / Q000031:analogs & derivatives* / Q000494:pharmacology; D008564:Membrane Potentials; D009474:Neurons; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism; D012640:Seizures / Q000503:physiopathology*; D015222:Sodium Channels / Q000378:metabolism
chemical_list: D000779:Anesthetics, Local; D015220:Calcium Channels; D002614:Chelating Agents; D015221:Potassium Channels; D015222:Sodium Channels; D002586:Cesium; C012647:QX-314; D004533:Egtazic Acid; D008012:Lidocaine; C025603:1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid