The central nucleus of the amygdala (CeA) is a heterogenous region of primarily GABAergic neurons that contributes to numerous behaviors, including fear learning, feeding, reward, and pain. Dopaminergic inputs to the CeA have been shown to regulate many of these behaviors, but how dopamine exerts these effects at the cellular level has not been well characterized. We used the Targeted Recombination in Active Populations (TRAP) mouse line to fluorescently label pain-responsive CeA neurons, and then targeted these cells for patch-clamp recordings in acute slices to test the effects of dopamine agonists. The D1 agonist SKF-38393 and D2 agonist quinpirole both had inhibitory effects, reducing the input resistance and evoked firing and increasing rheobase of labeled CeA neurons. Both agents also inhibited the NMDA component of excitatory postsynaptic currents (EPSCs) evoked by basolateral amygdala (BLA) stimulation, but did not affect the AMPA component. D1 activation, but not D2, also had a possible presynaptic effect, increasing the frequency of spontaneous EPSCs. These results provide new insights into how dopamine regulates activity within pain-responsive CeA networks.