The stress response is a homeostatic reaction generated to meet the energetic demands of environmental threats. As such, it is not surprising that continuous exposure to stressful situations is associated with metabolic changes that can range from marked decreases in body weight and food intake, to increases in body weight and calorie consumption3. The metabolic effects of stressors depend on the type of stressor encountered and the duration of the stressor. Chronic unpredictable stressors typically lead to decreased body weight and food intake, and excessive use of carbohydrate stores resulting in altered glucose regulation, an early indicator of insulin resistance. In contrast, repeated restraint or social stress leads to increased food intake, body weight, and adiposity in a wide array of species, including non-human and human primates. My lab studies the mechanisms through which the hormone ghrelin contributes to the adaptations required to meet the energy demands of stressors and may ultimately cause metabolic imbalance if stressors are chronic. In this presentation I will present evidence suggesting that ghrelin signalling in the ventral tegmental area, a region important for motivation and emotion, are critical for stress induced compensatory feeding, and that deficits in ghrelin signalling in this region make animals more vulnerable to stress induced psychopathology.