We described a mechanism by which stress may increase food drive in rats. This new discovery, published in the journal Neuron, could provide important insight into why stress is thought to be one of the underlying contributors to obesity. We looked specifically at neurons in the dorsomedial hypothalamus, a region thought to be important in integrating stress and satiety signals.
Normally, neurons her produce endocannabinoids that help to precisely regulate synaptic signals. In this study, we found that the absence of food causes a functional re-wiring in the dorsomedial hypothalamus that temporarily eliminates endocannabinoid signaling. This functional re-wiring relies on circulating glucocorticoids that are increased as a result of the activation of the brain’s stress response due to the lack of food.
This work was conducted jointly between our lab and that of Dr. Quentin Pittman. The study was driven by Karen Crosby, a graduate student and Wataru Inoue, a Postdoctoral Fellow.
These results lay the foundation for future studies to investigate the use of therapies that affect these systems in order to manipulate food intake. They also open the door to studies looking at whether or not the stress, brought about by lack of food, affects other systems where endocannabinoids are known to play a role.