title: A potassium current controls burst termination in rat neocortical neurons after GABA withdrawal.
abstract: Bursting activities were investigated under conditions of reduced outward K+ currents in neocortical slices obtained from rats presenting the gamma-aminobutyric acid (GABA)-withdrawal syndrome (GWS), a focal epilepsy consecutive to the interruption of a chronic intracortical GABA infusion into the somatomotor cortex. These bursts were induced by intracellular depolarizing current injection and/or by white matter stimulation. Tetraethylammonium (TEA) at doses which did not change input resistance, spike duration or first interspike time interval abolished the burst terminating process and induced plateau-like potentials (up to 500 ms) which were tetrodotoxin-resistant and blocked by Ca2+ antagonists Cd2+ and Co2+. Therefore, it appears that bursts during GWS are generated by Ca(2+)-dependent plateau potentials which are terminated by a K+ current highly sensitive to TEA.
authors.affiliation: Institut Alfred Fessard, CNRS, Gif-sur-Yvette, France.
authors.forename: C
authors.initials: C
authors.lastname: Silva-Barrat
authors.forename: J
authors.initials: J
authors.lastname: Champagnat
mesh_terms: D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D004594:Electrophysiology; D004827:Epilepsy / Q000503:physiopathology; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
chemical_list: D002121:Calcium Channel Blockers; D015221:Potassium Channels; D013757:Tetraethylammonium Compounds; D005680:gamma-Aminobutyric Acid