Protein synthesis is required in distinct populations of inhibitory neurons in the mouse amygdala to store memories of danger and safety. To survive in a dynamic environment, animals need to identify and appropriately respond to stimuli that signal danger(1). Survival also depends on suppressing the threat-response during a stimulus that predicts the absence of threat (safety)(2-5). An understanding of the biological substrates of emotional memories during a task in which animals learn to flexibly execute defensive responses to a threat-predictive cue and a safety cue is critical for developing treatments for memory disorders such as post-traumatic stress disorder(5). The centrolateral amygdala is an important node in the neuronal circuit that mediates defensive responses(6-9), and a key brain area for processing and storing threat memories. Here we applied intersectional chemogenetic strategies to inhibitory neurons in the centrolateral amygdala of mice to block cell-type-specific translation programs that are sensitive to depletion of eukaryotic initiation factor 4E (eIF4E) and phosphorylation of eukaryotic initiation factor 2 alpha (p-eIF2 alpha). We show that de novo translation in somatostatin-expressing inhibitory neurons in the centrolateral amygdala is necessary for the long-term storage of conditioned-threat responses, whereas de novo translation in protein kinase C delta-expressing inhibitory neurons in the centrolateral amygdala is necessary for the inhibition of a conditioned response to a safety cue. Our results provide insight into the role of de novo protein synthesis in distinct inhibitory neuron populations in the centrolateral amygdala during the consolidation of long-term memories.