GENESIS: Documentation

Related Documentation:

De Schutter: Purkinje Cell Model


One of the principle benefits of modeling neurons at this level of detail is that the interactions between different currents can be explored. All too frequently experimentalists assign very specific roles to particular channel types without taking into account the often complex interactions between different conductances that are actually responsible.

In the current model there are numerous examples of this type of interaction. One of the most striking involves the interaction of the noninactivating K+ channels and the Na+ and Ca2+ channels responsible for the plateaus. At the somatic level these K+ conductances served to counteract the depolarizing effect of the Na+ channels, with their balance determining the voltage of the plateau potential (Fig. 11A).

In the dendrite the Ca2+ -activated K+ channels played a critical role in the dual function of the CaP channel in generating Ca2+ spikes as well as dendritic plateaus. Because the K2 channel is sensitive to small changes in Ca2+ concentration it could effectively increase the threshold for Ca2+ spike generation by counteracting the activation of small numbers of CaP channels. The involvement of the K2 channel in these two very different forms of dendritic response, and the presence of other mechanisms in the Purkinje cell dendrite that through changes in the Ca2+ concentration [23] could activate this channel, suggest interesting possibilities for regulation of more global dendritic response properties by the K2 channel and other Ca2+-inactivated K+ channels that were not included in the model (like the SK or afterhyperpolarization (AHP) current, [1].

The model supports the suggestion that the channels responsible for generating plateau potentials are different in the soma and dendrite citeR:1980ly. However, examination of the model also makes clear that these different plateaus are not physiologically isolated. A somatic plateau potential was always accompanied by a dendritic plateau and vice versa, because any depolarization will spread throughout the cell.

Other interactions between channels, like the activation of the anomalous rectifier during prolonged hyperpolarizations, followed by an activation of CaT channels during the rebound spike, were not explored in detail. The anomalous rectifier did not affect the repetitive firing properties of the model because it was completely deactivated beyond spiking threshold.


[1]   B Lancaster, RA Nicoll, and DJ Perkel. Calcium activates two types of potassium channels in rat hippocampal neurons in culture. Journal of Neuroscience, 11:23–30, 1991.

[2]   I Llano, J Dreessen, M Kano, and A Konnerth. Intradendritic release of calcium induced by glutamate in cerebellar Purkinje cells. Neuron, 7:577–583, 1991.

[3]   K Takei, H Stukenbrok, A Metcalf, GA Mignery, TC Südhof, P Volpe, and P De Camilli. Ca2+ stores in Purkinje neurons: Endoplasmic reticulum subcompartments demonstrated by the heterogeneous distrtibution of the InsP3 receptor, Ca2+-ATPase, and calsequestrin. Journal of Neuroscience, 12:489–505, 1992.