In intracellular recordings in brain slice preparations some Purkinje cells are silent; others fire spontaneously. Our model is quiet without stimulation, with a stable resting potential of -68 mV. For intrasomatic current injections below the spiking threshold, no somatic spikes could be generated regardless of the length of the current pulses (simulation results not shown). Low-amplitude current injections in Purkinje cell somata above this threshold caused firing of fast somatic spikes, with the relatively high minimum spike frequency (30–40 Hz) characteristic of these cells (Figs. 3A, 4A and B, and 6A). Somatic firing frequency increased relatively rapidly with current amplitude (range 22–250 Hz).
In in vitro intracellular recordings there is often a delay between the onset of the current injection and the occurrence of the first somatic spike, which decreases with increasing amplitude of current. This variable delay was also present in the simulations (Figs. 3, 4, 5, and 6B). Note also that in Fig. 4D we reproduce another phenomenon observed in slice. When the injected current amplitude became too high, somatic spiking saturated at a depolarized level of about -30 mV. This saturation could be reversed either spontaneously (at this current amplitude) or by shutting off the current.
In the soma (Fig. 11A), the main active currents were the fast and persistent Na+ channels and the delayed rectifier. NaF currents and Kdr played their classic role in generating the fast action potentials . Note also that the amplitude of these currents was quite large compared with currents in the dendritic compartments; this was caused by the large size of the soma and the large gin the model. The other somatic currents did not play a large role in the firing patterns shown here. KA and CaT currents were transiently activated when the cell was depolarized from resting membrane or hyperpolarized potentials, but inactivated to a large degree during long current steps (data not shown).