Our research has examined the generation of simple and complex spikes in inhibitory “cartwheel” interneurons of the dorsal cochlear nucleus, using slices of the auditory brainstem from P16-24 mice. The term ‘complex spike’ refers to a burst of Na+ spikes riding on a slower Ca2+ dependent depolarization. We find that both simple and complex spikes propagate down the axons of cartwheel cells and trigger the release of a mixture of GABA and glycine from nerve terminals. A variety of Ca2+ channels contribute to these spikes, but the lowest-threshold complex spikes are generated by T-type channels. Two-photon Ca2+ imaging experiments showed that T-type channels are found on the axon initial segments of cartwheel cells. Selective blockade of these channels inhibited both the Ca2+ signals in the initial segment (e.g., with 3 μM mibefradil 58±3% block, n=5) and the generation of complex spikes (e.g., the # of spikelets in evoked complex spikes reduced by half by 50 μM Ni2+; n=9 cells) . Because Ca2+ channels are often the targets of modulators, we explored candidate modulatory systems in the DCN for their effects on complex spikes and on initial segment Ca2+ channels. We found that as little as 500 nM dopamine, acting on a D2-family dopamine receptor (probably D3), altered the mode of spontaneous spiking in cartwheel cells, converting it from a bursting to a tonic firing pattern, effects similar to those of T-type blockers. Moreover, activation of this dopamine receptor also inhibited evoked complex spikes and initial segment Ca2+ signals. PKC may mediate these effects of dopamine, as a phorbol ester (phorbol 12-myristate 13-acetate, 10 uM) mimicked the action of dopamine or the channel antagonists on Ca2+ signals and complex spikes. Although T-type currents were present in the somatodendritic domains as well as on the axon, the dopamine pathway only inhibited the initial segment T-type channels, as assessed by imaging. We conclude that T-type channels of the initial segment play an essential role in controlling the mode of spiking in these interneurons, and that they are selectively modulated by dopamine.