In humans and rodents, the serotonin system interacts with early-life stress (ELS) through its various receptors, such as serotonin 3A receptor (HTR3A). Htr3a is exclusively expressed in a subset of interneurons (IN), where it has been shown to play a role in the establishment of developmental processes of cortical and subcortical circuit. Alterations in Htr3a impairs IN-driven homeostasis, leading to E-I imbalance, and may result in maladaptive anxiety-like behaviours. In rodents, deletion of the Htr3a leads to increased fear during cued fear memory retrieval and reduced attenuation during fear extinction, whereas its role in anxiety is equivocal. In my PhD project, I studied the role of HTR3A in ELS using genetic and epigenetic methods in humans. I also studied the role of its deletion on anxiety-like phenotypes and ELS in mice at a behavioural level, and further assessed its role in cued fear memory retrieval at a functional level.