The axon initial segment is a specialized compartment that is the site of action potential initiation in central neurons, and is enriched with sodium and potassium channels that mediate the depolarizing and repolarizing phases of spikes. In addition to these channel classes, we recently found that the initial segment is further enriched with low-voltage activated calcium channels (T- and R-type). Since these channels can be active over long durations at hyperpolarized potentials, they play a critical role in the generation of high-frequency volleys of action potentials, termed bursts, and blocking initial segment calcium influx can suppress both spontaneous and evoked bursting. Moreover, initial segment T-type channels are regulated by dopamine in cells expressing Gi-coupled, type 3 dopamine receptors (D3). Upon activation, D3 receptors suppress calcium influx through these initial segment-localized channels, without affecting the function of similar channels expressed in the dendrites, leading to a suppression of burst initiation. Here, I will discuss our recent efforts to understand the molecular signaling cascade that supports dopaminergic modulation of axonal channels, and how calcium channel localization and kinetics contribute to neuronal excitability. These results will advance our understanding of how neuromodulation of axonal excitability can alter the temporal features of spike trains.