Figure 7. P-type voltage-gated Ca²⁺ channels contribute to the activity of both BK and SK channels.

A and B, application of the P-type Ca²⁺ channel blocker ω-Aga-IVA (100 nm) caused a Purkinje neuron to switch from a regular spontaneous firing pattern at a frequency of 40 Hz to a bursting pattern with an intra-burst frequency of 259 Hz. In contrast to cadmium experiments, Ca²⁺ spikes could still be observed in this condition (arrows in A). C, the AHP of spontaneous Na⁺ spikes was reduced in the presence of ω-Aga-IVA (thick trace, representative action potential from the beginning of a burst) compared to Na⁺ spikes recorded from the same neuron before the addition of the blocker (thin trace, average of 10 sequential action potentials in ACSF). D, the Na⁺ spike AHP was measured using the same method as in Fig. 5 F. ω-Aga-IVA significantly reduced the AHP by 54 ± 12 % (n = 4 cells, P < 0.05), while neither 10 μm nifedipine (8 ± 4 % increase in AHP, n = 3 cells) nor 200 nm SNX-482 (6 ± 20 % increase in AHP, n = 3 cells) had a significant effect. E, ω-Aga-IVA significantly increased the spontaneous firing frequency of Purkinje neurons from their baseline rate of 55 ± 11 to 201 ± 48 Hz in the presence of the blocker (n = 5, P < 0.05). The spontaneous firing rate was not affected by nifedipine (36 ± 9 Hz baseline, 33 ± 9 Hz in nifedipine, n = 3 cells) or SNX-482 (41 ± 26 Hz baseline, 41 ± 18 Hz in SNX-482, n = 3 cells).