Several anxiety-related neuropsychiatric disorders are associated with amygdala dysfunction during early periods of postnatal development, and adolescence is a particularly vulnerable emotional period. Among the cellular mechanisms involved in changes in the activity of individual neurons and their synaptic connections, the mTOR signaling pathway has been proposed as a molecular regulator of emotional memories and could thus constitute a common mechanistic source of the emergence of anxiety symptoms in these disorders. We hypothesize that amygdala mTOR dysfunction during infancy can initiate a cascade of aberrant signaling processes, putting the organism at risk for developing abnormal fear and anxiety behavior during adolescence. Our aim is to determine the effects of mTOR over-activation in the basolateral amygdala (BLA) during infancy on BLA functionality and the emergence of behavioral alterations during adolescence. Rat pups (PN6-PN8) received bilateral BLA injections of either a control lentivirus (Tsc2-CTL) or a lentivirus producing a partial knock-down of the Tsc2 gene (Tsc2-kd), resulting in hyperactivation of mTOR signaling pathway, possibly altering BLA excitability. At adolescence (PN30-PN40), animals were tested for anxiety (light/dark, open-field) and social interaction, and thereafter underwent auditory fear conditioning. We found that Tsc2-kd rats were less prone to exploration and showed impaired social interaction, fear memory extinction and contextual generalization than Tsc2-CTL animals. These results suggest that Tsc2-kd rats have more anxiety and altered fear memory. Ex vivo electrophysiology experiments are underway to investigate associated changes in BLA neural properties induced by Tsc2-kd that could underlie behavioral changes.