Figure 9.

Effects of VDCC antagonists on AP-induced calcium currents, AHP_slow and AP-induced Ca²⁺ transients. (A) Inward calcium currents recorded in isolated nodose neurons evoked by a prerecorded AP waveform from a holding potential of −60 mV. From Left to Right, control inward current in the presence of 2 mM [Ca²⁺]_o and in the presence of 10 μM nifedipine. After reestablishing control conditions, the neuron was exposed to 1 μM ω-conotoxin-GVIA. The effects of 500 μM cadmium were recorded in another neuron; the control current for this cell was similar to the first trace. (B) AHP_slow evoked by a train of four APs (10 Hz) recorded in another nodose neuron. From Left to Right, AHP_slow evoked in control conditions, in the presence of 100 μM CdCl₂, after washout, in the presence of 500 nM ω-conotoxin-GVIA, and after washout. (C) AP-induced Ca²⁺ transients recorded in two nodose neurons. From Left to Right, Ca²⁺ transients evoked by a train of eight APs in normal Locke solution, and in Locke solution containing 10 μM nifedipine. In another neuron, 1 μM ω-conotoxin-GVIA reduced the Ca²⁺ transient ≈50% (see Table 4). APs were evoked by 2.5-ms, 10-Hz depolarizing current pulses.