Thalamic opioids from POMC satiety neurons gate sugar appetite
Sweet, high-sugar containing foods are extremely palatable and often consumed in the absence of caloric needs, thereby driving positive energy balance and accelerating obesity development. Pharmacological studies suggest that endogenous opioid signaling in the brain mediates this specific appetite for sugar in satiety states; however, the cellular and circuit mechanisms remain unknown. We find that pro-opiomelanocortin (POMC) neurons, which are well known for their satiety promoting effects via the melanocortin-4 receptor system, selectively inhibit postsynaptic neurons in the paraventricular