Grant: Travel Awards - Institute Community Support

Excessive consumption of palatable energy-dense food can lead to emotional and motivational impairments. In turn this can increase the drive to consume such food and lead to overweight and obesity. The reward system comprises dopamine neurons that originate in the ventral tegmental area (VTA) that are critical for the control of motivation and reward-relevant behaviors. There is evidence that dopamine neurons respond to hormones associated with the nutritional status of the organism such as leptin, insulin and ghrelin. However it is not known if nutrients, in particular fatty acids also impact dopamine neurons. We are interested in the mechanisms by which fatty acids act on the dopamine reward system to influence eating and motivated behavior. We are particularly interested in two classes of fatty acids: the saturated fatty acid palmitate, considered to be a bad type of fat due to its detrimental effects on cardiometabolic health and the monounsaturated fatty acid oleate, considered to be a good type of fat due to its cardioprotective effects. Our results show that oleate but not palmitate decreases food intake when injected in the VTA. Oleate also decreases the motivation of the animals to work for a sucrose reward. Moreover oleate modifies the electrical activity of dopamine neurons of the VTA. Our findings offer a means whereby dietary fatty acids may directly modulate the reward circuitry. Our study is important for the understanding of the central mechanisms involved in food-based motivated behavior and how the disruption of those mechanisms could lead to overconsumption and overweight/obesity.