A second measure of model robustness is its ability to replicate physiological data in response to standard channel blockers. In this case we compared model results with  in response to both Na+ and Ca2+ channel blockers while holding all other model parameters fixed.
Figure 9A shows a simulation of TTX block (the conductance of the NaF and NaP channels was set to 0) during a 1.0 nA current injection. Note that the somatic recording showed only attenuated dendritic spikes in the soma, there were no fast somatic spikes, and that there was a sustained plateau potential after the end of the current injection. Subthreshold current injection (0.1 nA) only evoked the plateau current. Similar to the results of  (their Fig. 6), Na+ channel blockers selectively interfered with somatic spikes while having little effect on dendritic spiking and plateau potentials. However, the dendritic spikes in the model were smaller and less sharp than those in experimental recordings. Also, contrary to experimental results, the plateau potential did not decay.
From these simulations one can conclude that dendritic spiking in the model was caused by the slow progressive depolarization induced by the current injection, not by the larger depolarizations during fast somatic spikes.
A simulation of Co2+ block (the conductance of CaT and CaP currents was set to 0) is shown in Fig. 9B. Current injection caused a slow depolarizing response that generated fast somatic action potentials. With increasing amplitude of currents there was less delay before the first action potential, but the spikes also decreased in amplitude and saturated at a sustained plateau depolarization of about -30 mV. These results are comparable with experimental recordings, except that higher-amplitude current injections were necessary in the model to obtain saturation of spiking. As in the case of  (their Fig. 8), Ca2+ channel blockers selectively interfered with dendritic spikes while leaving somatic plateau potentials and somatic spiking intact. However, because the depolarization could not evoke dendritic Ca2+ spikes, there was also no Ca2+-activated hyperpolarization to repolarize the cell and the model settled in sustained plateaus with high-intensity current injection. The model thus confirmed the importance of dendritic Ca2+-activated K+ conductances in repolarizing the somatic depolarizing spike bursts.