Brain Network May Explain Why We Keep Eating Calorie-rich Foods Long After We're Full

Experiments in the past few years have suggested that our wiring for hedonic feeding involves nociceptin, a small protein that works as a signaling molecule in the mammalian nervous system. Kash's laboratory and other groups have found that compounds blocking nociceptin activity - called nociceptin receptor antagonists - have little or no effect on homeostatic feeding by lab rats and mice, but these compounds do curb hedonic bingeing on tasty, calorie-rich foods. Thus, drug developers have eyed these antagonists as potential anti-obesity, anti-binge-eating drugs, and researchers have been eager to identify the specific brain circuits through which they work. The goal would be to develop a more targeted treatment. Identifying this circuit is largely what Kash and colleagues accomplished in their new study. They engineered mice to produce a fluorescent molecule along with nociceptin, literally illuminating the cells that drive nociceptin circuits. There are multiple nociceptin circuits in the brain, but Kash and colleagues observed that one in particular became active when the mice got a chance to binge on calorie-rich food. The circuit projects to different parts of the brain, including those known to regulate feeding. It starts in an emotion-processing region of the brain called the central amygdala. Deleting about half of the nociceptin-making neurons in this circuit reduced the mice's bingeing and kept their weight down when they had access to rich food, without affecting their intake of ordinary chow. https://www.technologynetworks.com/neuroscience/news/the-neurobiology-of-noshing-318609?utm_campaign=NEWSLETTER_TN_Breaking%20Science%20News&utm_source=hs_email&utm_medium=email&utm_content=72076799&_hsenc=p2ANqtz-95kJ92fGhbY3mHb3oZFJ4ACoK8cLST0IfGVCk-dEVkogIQWteSc3wh0J0Ea32OovcUuNog_gNwGJgFo9spOiTRdT5tJw&_hsmi=72076799