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During paroxysmal neocortical oscillations, sudden depolarization leading to the next cycle occurs when the majority of cortical neurons are hyperpolarized. Both the Ca(2+)-dependent K(+) currents (I(K(Ca))) and disfacilitation play critical roles in the generation of hyperpolarizing potentials. In vivo experiments and computational models are used here to investigate whether the hyperpolarization-activated depolarizing current (I(h)) in cortical neurons also contributes to the generation of paroxysmal onsets. Hyperpolarizing current pulses revealed a depolarizing sag in approximately 20% of cortical neurons. Intracellular recordings from glial cells indirectly indicated an increase in extracellular potassium concentration ([K(+)](o)) during paroxysmal activities, leading to a positive shift in the reversal potential of K(+)-mediated currents, including I(h). In the paroxysmal neocortex, approximately 20% of neurons show repolarizing potentials originating from hyperpolarizations associated with depth-electroencephalogram positive waves of spike-wave complexes. The onset of these repolarizing potentials corresponds to maximal [K(+)](o) as estimated from dual simultaneous impalements from neurons and glial cells. Computational models showed how, after the increased [K(+)](o), the interplay between I(h), I(K(Ca)), and a persistent Na(+) current, I(Na(P)), could organize paroxysmal oscillations at a frequency of 2-3 Hz.

Cortical hyperpolarization-activated depolarizing current takes part in the generation of focal paroxysmal activities