Anxiety disorders are among the most common mental disorders, having inappropriate learned fear and resistance to extinction as cardinal features. Exposure therapy represents a promising therapeutic approach, the efficiency of which depends on inter-individual variation in fear extinction learning. Previously we reported that the formation of fear memories is associated with a general downregulation of the tropomyosin receptor kinase C (TrkC) activation in the brain fear network. Particularly, inactivation of TrkC and of the downstream Erk1/2 signaling in the hippocampus is associated with the reconsolidation of fear memories. More recently, we investigated TrkC signaling in a model of extinction learning, whereby fear-conditioned mice were categorized as extinction (EXT)-success or EXT-failure, according to their inherent ability to extinguish fear. We found that during extinction memory consolidation, activation of TrkC in the amygdala of EXT-success mice promoted synaptic plasticity and the extinction of fear. Importantly, neurotrophin-3 (NT3) infusion in the amygdala of EXT-failure mice was sufficient to rescue extinction deficits and the underlying synaptic plasticity, in a GluN2B-dependent mechanism. Instead, during extinction memory reconsolidation, decreased activation of TrkC and decreased Erk1/2 signaling was observed in the hippocampus of EXT-success mice, when compared to EXT-failure mice. Overall, hippocampal TrkC and Erk1/2 inactivation is associated to reconsolidation of both fear and extinction memories, while TrkC activation in the amygdala is critical for the acquisition of extinction memories. Our data suggests that an intricate pattern of timely local TrkC (in)activation is necessary to achieve proper formation of fear and extinction memories and the maintenance thereof.