An extremely anxious temperament early in life is a risk factor for the later development of anxiety, depressive, and substance abuse disorders. Children with an extremely anxious temperament (AT), react to novelty with increased behavioral inhibition and increased levels of physiological arousal. Using a well-validated non-human primate model of AT, our group has been investigating the neurobiology of this early-life risk. In a series of experiments combining behavioral, brain imaging, molecular, and viral vector techniques we have identified specific neuroplasticity-related processes in the extended amygdala as critical contributors to AT. More generally, I will discuss how this translational neuroscience approach can help bridge the gap between psychological and molecular processes.