In previous studies we discovered that NT3-TrkC system plays a role in the regulation of fear in a pathologic setting. TgNTRK3 mice show heighten fear that is resistant to extinction. We showed that an altered brain fear circuit activation and a dysbalance in the excitation/inhibition ratio in the CA1 hippocampal region is responsible for the heightened fear exhibited by this mouse model. Importantly, we could demonstrate that it is possible to rescue these deficits using an agonist of GABA_A receptors (J Neurosci 33: 15259-15271 [2013]). In a second study, we focused our attention in fear extinction and in the prefrontal cortex and I found that transgenic animals, upon fear extinction, do not show an increase in NT3 levels in prefrontal cortex. Moreover, a dysregulation in the NT3/TrkC – MAPK signaling pathway was found to be on the basis of the extinction deficit, which we were able to rescue upon local infusion of NT3 (Neuropsychopharmacol 42: 462–472 [2017]). These results highlighted for the first time the role of NT3 and TrkC in the regulation of fear contributing to understand its pathophysiology, but also to the advancement of knowledge in the field of neurotrophins. Following up this discovery, we are now investigating the neurobiological mechanisms underneath NT3-TrkC action’s in fear, in a physiological context. In the future we aim at translating these results to Humans.