An early-life anxious temperament (AT) is a risk factor for the development of anxiety, depression, and comorbid substance abuse. We validated a nonhuman primate (NHP) model of early-life AT and identified the dorsal amygdala as a core component of AT’s neural circuit. Here, we combine RNA sequencing, viral-vector gene manipulation, functional brain imaging, and behavioral phenotyping to uncover AT’s molecular substrates.In response to potential threat, AT and brain metabolism were assessed in forty-six young rhesus monkeys. We identified AT-related transcripts using RNA-seq data from dorsal amygdala tissue (including central nucleus of the amygdala [Ce] and dorsal regions of the basal nucleus). Based on the results, we overexpressed the neurotrophin 3 gene (NTF3) in the dorsal amygdala using intraoperative MRI guided surgery (n=5/group).This discovery-based approach identified AT-related alterations in the expression of well-established and novel genes, including an inverse association between neurotrophin receptor kinase 3 (NTRK3) expression and AT. NTRK3 is an interesting target because it is a relatively unexplored neurotrophic factor that modulates intracellular neuroplasticity pathways. Overexpression of the transcript for NTRK3’s endogenous ligand, NTF3, in the dorsal amygdala resulted in reduced AT and altered function in AT’s neural circuit.Together, these data implicate NT-3/NTRK3 signaling in the dorsal amygdala in mediating primate anxiety. More generally, this approach provides an important step towards understanding the molecular underpinnings of early-life AT and will be useful in guiding the development of treatments to prevent the development of stress-related psychopathology.