The obvious prominence of Ca2+ conductances in the dendrites of Purkinje cells has led to much discussion, and some disagreement, concerning their nature. In their original report Llinas and Sugimori  explained the electroresponsiveness of the Purkinje cell dendrite by suggesting that two Ca2+ conductances would be present, namely a plateau-generating one and a spike-generating one. When several years later different types of Ca2+ conductances were identified in other neural systems  and in the Purkinje cell [1, 2] it was proposed that a low-threshold Ca2+ channel (T type) would be responsible for generating the dendritic plateau. In the meantime, however, Llinas et al. [6, 6] had discovered a new type of high-threshold Ca2+ conductance in the Purkinje cell, which they named the P channel. Since then there has been debate about whether other Ca2+ channels than the P channel are present in the Purkinje cell [2, 9, 13] and about the physiological role of these channels in generating the dendritic plateaus and spikes.
We believe that there is now ample experimental evidence for the presence of both a CaP and a CaT channel in the Purkinje cell. Voltage-clamp studies have shown the CaT channel to be present in both young and adult animals, with similar I - V relations [4, 11]. Also, channel blocking studies with funnel web spider toxin (FTX) have shown that the CaP channel constitutes only ~ 90 % of the total Ca2+ conductance . This corresponds well to the relative channel densities for CaP and CaT channels in the dendrites in our model (Table 2), which were determined by trial and error before these data became available.
Perhaps of more importance than the presence of these channels, however, is their relative contribution to Purkinje cell responses. Although it is generally accepted that the CaP channel is responsible for the fast dendritic calcium spikes , it has been suggested that the generation of the longer-duration plateau potentials requires the slower kinetics of a channel like the CaT channel . Llinas and Sugimori , on the other hand, have argued that the CaP channel is also capable of producing these prolonged potentials, providing it with a dual role. As described in detail above, our modeling results clearly support the suggestion by Llinas and Sugimori. Both the dendritic plateaus and spikes in the model were carried by the CaP current. Recent Ca2+ imaging results also indicated a common mechanism for plateaus and spiking . Our model suggests that the CaP channel can generate plateaus because it has a relatively low threshold of activation [11, 12] compared with other high-threshold Ca2+ channels  and because of its incomplete inactivation. In our hands, conductance through the CaT channels contributed only to the rebound spike generation after hyperpolarizations.
 P A Fortier, J P Tremblay, J Rafrafi, and R Hawkes. A monoclonal antibody to conotoxin reveals the distribution of a subset of calcium channels in the rat cerebellar cortex. Molecular Brain Research, 9:209–215, 1991.
 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.