Current injection steps are often followed by a prolonged plateau potential. In our simulations this phenomenon was always observed after short current steps around firing threshold (Fig. 5) and sometimes after longer current steps also (Fig. 4A). In the model these plateau potentials resulted in depolarizations of between -49 and -55 mV. Similar prolonged plateau potentials after the end of a current injection were found by  (compare their Fig. 5 D with our Fig. 3A). However, in the experimental data these plateaus decay over a time course of ~ 100 ms, whereas in the model they often did not decay at all (Fig. 5).
The model also generated longer duration plateau-type potentials that have been shown to exist in this neuron [5, 7, 8]. It has been demonstrated physiologically that current injection generates a plateau potential in the soma of the cell that is dependent on Na+ conductances. The model generated Na+-dependent somatic plateaus (Figs. 9B and 11). However, it is debated in the literature whether such persistent Na+ currents rely on a special channel (NaP) or depend on the NaF channel itself [2, 3, 6]. In our model the somatic plateau potential was mainly carried by NaF channels in the form of a so-called window current, although the model also included the experimentally demonstrated NaP channel . The plateau-related current in the model flowed through NaF channels at a potential where the steady-state activation and inactivation curves (Fig. 2A) overlap. Although this mechanism was robust in the model, one argument against the existence of such a window current is that it is based on a wrong model of inactivation, because Na+ channel inactivation is probably not voltage dependent . If this is in fact correct, then the term in our equations for steady-state inactivation would be meaningless. Although this possible inaccuracy in the Hodgkin- Huxley model of inactivation  means that our results are not conclusive, the model at least suggests that there may not be a need for separate NaP channels to explain somatic plateaus. In our simulations the NaP channel actually primarily affected the f - I curve.
The model also generated dendritic plateau potentials (Figs. 9 and 11) that have recently been described in more detail  and that may be particularly important during synaptic activation of the Purkinje cell by peripheral stimuli . In the model these dendritic plateau potentials were carried largely by the CaP channels, because the CaT channel inactivated too rapidly to play a major role. In this case again the plateau response resulted from a window current-like mechanism very similar to that found with the NaF channels in the soma, because the dendritic plateau current through the CaP channel occurred at a potential where the CaP channel does not inactivate completely. As a consequence these dendritic plateau potentials did not wane in the model as they do in slice preparations.
 C Alzheimer, Schwindt PC, and Crill WE. Modal gating of na+ channels as a mechanism of persistent na+ current in pyramidal neurons of from rat and cat sensorimotor cortex. Journal of Neuroscience, 13:660–673, 1993.
 RR Llinás and M Sugimori. The electrophysiology of the cerebellar Purkinje cell revisited. In RR Llinás and C Sotelo, editors, The Cerebellum Revisited, pages 167–181. Berlin: Springer-Verlag, 1992.