Whole-cell and sharp microelectrode recordings were obtained from neurons of rat dorsal motor nucleus of the vagus (DMV) in transverse slices of the rat medulla maintained in vitro. Calcium currents were studied with sodium currents blocked with tetrodotoxin, potassium currents blocked by perfusing the cell with caesium as the main cation and using barium as the charge carrier. From a holding potential of -60 mV, inward currents activated at potentials positive of -50 mV and peaked around 0 mV. Voltage clamping the neuron at more hyperpolarised potentials did not reveal any low-threshold inward current. The inward current was effectively blocked by cadmium (100 $\mu $M) and nicked (1 mM), suggesting that it is carried by voltage-dependent calcium channels. The inward current could be separated into three pharmacologically distinct components: 40% of the whole cell current was $\omega $-conotoxin sensitive; 20% of the current was nifedipine sensitive; and the rest was blocked by high concentrations of cadmium and nickel. This remaining current cannot be due to P-type calcium channels as $\omega $-agatoxin had no effect on the inward current. Nifedipine had no significant effect on the action potential. Application of $\omega $-conotoxin reduced the calcium component of the action potential and significantly reduced the potassium current underlying the afterhyperpolarization. Application of charybdotoxin slowed action potential repolarization. When N-type calcium channels were blocked with $\omega $-conotoxin, charybdotoxin was still effective in slowing repolarization. In contrast, charybdotoxin was ineffective when calcium influx was blocked with the non-specific calcium channel blocker cadmium. These results show that, during the action potential, both $\omega $-conotoxin-sensitive and $\omega $-conotoxin-insensitive calcium channels contribute to calcium influx. Calcium influx via N-type channels is responsible for activating potassium channels underlying the afterhyperpolarization. In contrast, influx via $\omega $-CgTx and nifedipine-insensitive channels is responsible for activating potassium channels contributing to action potential repolarization. Calcium-activated potassium channels are thought to be in close proximity to voltage-dependent calcium channels. These results therefore suggest that in vagal neurons different calcium channels are colocalized with different calcium-activated potassium channels that subserve distinct functional roles.