A cell model study of calcium influx mechanism regulated by calcium-dependent potassium channels in Purkinje cell dendrites

The present study was designed to elucidate the roles of dendritic voltage-gated K⁺ channels in Ca²⁺ influx mechanism of a rat Purkinje cell using a computer simulation program. First, we improved the channel descriptions and the maximum conductance in the Purkinje cell model to mimic both the kinetics of ion channels and the Ca²⁺ spikes, which had failed in previous studies. Our cell model is, therefore, much more authentic than those in previous studies. Second, synaptic inputs that mimic stimulation of parallel fibers and induce sub-threshold excitability were simultaneously applied to the spiny dendrites. As a result, transient Ca ²⁺ responses were observed in the stimulation points and they decreased with the faster decay rate in the cell model including high-threshold Ca²⁺-dependent K⁺ channels than in those excluding these channels. Third, when a single synaptic input was applied into a spiny dendrite, Ca²⁺-dependent K⁺ channels suppressed Ca²⁺ increases at stimulation and recording points. Finally, Ca ²⁺-dependent K⁺ channels were also found to suppress the time to peak Ca²⁺ values in the recording points. These results suggest that the opening of Ca²⁺-dependent K⁺ channels by Ca²⁺ influx through voltage-gated Ca²⁺ channels hyperpolarizes the membrane potentials and deactivates these Ca²⁺ channels in a negative feedback manner, resulting in local, weak Ca ²⁺ responses in spiny dendrites of Purkinje cells.