We have developed a model for the rat phrenic motor neuron (PMN) that robustly replicates many experimentally observed behaviors of PMNs in response to pharmacological, ionic, and electrical perturbations using a single set of parameters. Our model suggests that the after-depolarization (ADP) response seen in action potentials is a result of the slow deactivation of the fast sodium channel in the range of the ADP coupled with the activation of the L-type calcium channel (I(CaL)). This current and its interactions with the small and large conductance calcium-activated potassium currents (I(KCaSK) and I(KCaBK), respectively) is also important in the generation of spike frequency adaptation in the repetitive firing mode of activity. Other aspects of the model conform very well to experimental observations in both the action potential and repetitive firing mode of activity, including the role of I(KCaSK) in the medium after-hyperpolarization (AHP) and the role of I(KCaBK) in the fast AHP. We have made a number of predictions using the model, including the characterization of two putative sodium currents (fast and persistent), as well as functional roles for the N- and T-type calcium currents.