Abstract
Bursting activities were investigated under conditions of reduced outward K + currents in neocortical slices obtained from rats presenting the γ-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 Ca 2+ antagonists Cd 2+ and Co 2+. 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.
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