Opioidergic signaling contributes to food-mediated suppression of AgRP neurons

Sayar-Atasoy, N.; Yavuz, Y.; Laule, C.; Dong, C.; Kim, H.; Rysted, J.; Flippo, K.; Davis, D.; Aklan, I.; Yilmaz, B.; Tian, L.; Atasoy, D. ✉

Angol nyelvű Szakcikk (Folyóiratcikk) Tudományos
Megjelent: CELL REPORTS 2211-1247 2211-1247 43 (1) Paper: 113630 2024
  • SJR Scopus - Biochemistry, Genetics and Molecular Biology (miscellaneous): D1
Azonosítók
Opioids are generally known to promote hedonic food consumption. Although much of the existing evidence is primarily based on studies of the mesolimbic pathway, endogenous opioids and their receptors are widely expressed in hypothalamic appetite circuits as well; however, their role in homeostatic feeding remains unclear. Using a fluorescent opioid sensor, deltaLight, here we report that mediobasal hypothalamic opioid levels increase by feeding, which directly and indirectly inhibits agouti-related protein (AgRP)-expressing neurons through the μ-opioid receptor (MOR). AgRP-specific MOR expression increases by energy surfeit and contributes to opioid-induced suppression of appetite. Conversely, its antagonists diminish suppression of AgRP neuron activity by food and satiety hormones. Mice with AgRP neuron-specific ablation of MOR expression have increased fat preference without increased motivation. These results suggest that post-ingestion release of endogenous opioids contributes to AgRP neuron inhibition to shape food choice through MOR signaling. © 2023 The Author(s)
Hivatkozás stílusok: IEEEACMAPAChicagoHarvardCSLMásolásNyomtatás
2024-07-14 06:49