Cocaine and sugar act as appetitive stimuli, engaging the brain's dopaminergic system to induce positive experiences. While both substances trigger dopamine release, cocaine additionally blocks its reuptake. Dopamine-sensitive neurons, particularly those expressing DRD1 or DRD2, play a pivotal role in mediating these effects. Such cells were recently discovered in the Central Amygdala (CeA), a brain region involved in regulating various emotions, both aversive and appetitive. Given the limited research on the role of dopamine in this brain region, we studied the activity of dopamine-sensitive cells in the CeA in mice exposed to sugar (sucrose self-administration) and cocaine (intraperitoneal injections). Employing two-photon in vivo calcium imaging we investigated how these rewards influence the activity of these neurons. Additionally, with ex vivo electrophysiology experiments we studied whether this modulation leads to neuroplasticity. Our findings reveal differential regulation of CeA dopamine-sensitive neurons by these rewards. Cocaine enhances DRD1 neuron activity while diminishing DRD2 cell activity. Conversely, sucrose activates DRD2 cells while reducing DRD1 activity. Furthermore, we explored these neurons' contribution to cocaine memory retrieval during conditioned place preference (CPP). We found that manipulating DRD2 cells minimally affected the animals’ preference for the conditioned chamber, but blocking DRD1 neurons disrupted cocaine memory. In summary, our study highlights CeA dopamine-sensitive cells' involvement in appetitive behaviors, with distinct regulation during cocaine and sucrose exposure. These findings contribute to a more holistic understanding of the dopaminergic system's role in the brain during reward processing.