Life stress modulates decision making, particularly in the face of risk, in some cases prompting vulnerable populations to make suboptimal, life-altering choices. In the brain, stress is known to alter the extracellular release of catecholamines in structures such as basolateral amygdala (BLA) and nucleus accumbens (NAc). To study the role of catecholamines in risky decision-making in rats, we combined a touch screen task, systemic neuropharmacological manipulation, and direct measurement of norepinephrine (NE) and dopamine (DA) release using fiber photometry. Long-Evans rats were trained on an operant touchscreen decision-making task in which they chose between a safe stimulus that delivered a certain 50μl sucrose, or a risky stimulus that delivered either a 'loss' (10μl sucrose 75% of the time) or 'win' (170μl sucrose 25% of the time). Following the pharmacological induction of stress by administration of the inverse GABAA agonist, FG7142, rats were biased in their decisions towards safe choices and the avoidance of loss. This exaggerated loss aversion was blocked by co-treatment with the a2A receptor antagonist, yohimbine. Direct optical measurement of NE release in the BLA and DA release in the NAc revealed temporal dynamics time-locked to the task events and directly related to the outcome of each trial. In both structures, pharmacological stress altered catecholamine release, with systemic yohimbine showing opposing modulation. These findings highlight the catecholamine basis of loss aversion and neuromodulation of critical brain structures during stress.