A series of original computational models written in NEURON of increasing physiological and morphological complexity were developed to determine the dominant causes of epileptiform behavior. Current injections to a model hippocampal pyramidal neuron consisting of three compartments produced the sustained depolarizations (SD) and simple paroxysmal depolarizing shifts (PDS) characteristic of ictal and interictal behavior in a cell, respectively. Our results indicate that SDs are the result of the semi-saturation of Na +, Ca 2+ and K + active channels, particularly the Ca N, with regular Na +/K + spikes riding atop a saturated depolarization; PDS rides on a similar semi-saturated depolarization whose shape depends more heavily on interactions between low-threshold voltage-gated Ca 2+ channels (Ca T) and Ca 2+-dependent K + channels. Our results reflect and predict recent physiological data, and we report here a cellular basis of epilepsy whose mechanisms reside mainly in the membrane channels, and not in specific morphology or network interactions, advancing a possible resolution to the cellular/network debate over the etiology of epileptiform activity.