Chronic stress has clear effects on the brain, and exacerbates many symptoms of psychiatric illness. Dopamine (DA) dysregulation, which is involved in many psychiatric conditions, is implicated in emotional dysregulation through amygdala circuits. Corticotropin releasing factor (CRF) is a stress-activated neuromodulator that modulates the DA system. We previously showed that CRF-positive neurons in the primate extended amygdala preferentially target specific DA subpopulations in nonhuman primates. These same DA subpopulations are also a key efferent to the basal nucleus of the amygdala. Since mounting evidence indicates that DA release in the basal nucleus is critical for associative fear learning, driving this system by CRF may alter basal nucleus function. In this renewal, we examine at mesoscopic and ultrastructural levels in primates the idea that CRF-specific inputs from the central nucleus (CeN) are positioned to instigate a feed-forward loop through the lateral VTA (pigmented parabrachial nucleus, PBP) and A8 neurons, to increase DA output to the basal amygdala nucleus. We first characterize cell-type specific inputs and outputs in this loop (Aim 1 and 2). We then test the hypothesis that chronic CeN/CRF-overexpression in monkey results in synaptic alterations at two sites: 1. increased CRF terminals onto PBP/A8 GABA neurons (Aim 3A), 2. increased DA terminals onto basal nucleus neurons (Aim 3B).