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Research Library

A-Z Conditions  Participate in ORR

Hypothalamic POMC neurons promote cannabinoid-induced feeding

  • Journal : Nature
  • Publication Year : 2015
  • Authors : Marco Koch; Luis Varela; Jae G. Kim; Jung D. Kim; Francisco Hernández-Nuño; Stephanie E. Simonds; Carlos M. Castorena; Claudia R. Vianna; Joel K. Elmquist; Yury M. Morozov; Pasko Rakic; Ingo Bechmann; Michael A. Cowley; Klara Szigeti-Buck; Marcelo O. Dietrich; Xiao-Bing Gao; Sabrina Diano; Tamas L. Horvath

Hypothalamic pro-opiomelanocortin (POMC) neurons promote satiety. Cannabinoid receptor 1 (CB1R) is critical for the central regulation of food intake. Here we test whether CB1R-controlled feeding in sated mice is paralleled by decreased activity of POMC neurons. We show that chemical promotion of CB1R activity increases feeding, and notably, CB1R activation also promotes neuronal activity of POMC cells. This paradoxical increase in POMC activity was crucial for CB1R-induced feeding, because designer-receptors-exclusively-activated-by-designer-drugs (DREADD)-mediated inhibition of POMC neurons diminishes, whereas DREADD-mediated activation of POMC neurons enhances CB1R-driven feeding. The Pomc gene encodes both the anorexigenic peptide α-melanocyte-stimulating hormone, and the opioid peptide β-endorphin. CB1R activation selectively increases β-endorphin but not α-melanocyte-stimulating hormone release in the hypothalamus, and systemic or hypothalamic administration of the opioid receptor antagonist naloxone blocks acute CB1R-induced feeding. These processes involve mitochondrial adaptations that, when blocked, abolish CB1R-induced cellular responses and feeding. Together, these results uncover a previously unsuspected role of POMC neurons in the promotion of feeding by cannabinoids.

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Conditions:

  • Appetite

Research Information:

Research Keywords:

  • alpha-MSH/metabolism, Animals, beta-Endorphin/metabolism, Cannabinoid, Cannabinoids/pharmacology, CB1/agonists, CB1/metabolism, Eating/drug effects, Eating/physiology, Energy Metabolism/drug effects, Hypothalamus/cytology, Hypothalamus/drug effects, Hypothalamus/physiology, Inbred C57BL, Ion Channels/metabolism, Male, Mice, Mitochondria/drug effects, Mitochondria/metabolism, Mitochondrial Proteins/metabolism, Naloxone/pharmacology, Neurons/drug effects, Neurons/metabolism, Pro-Opiomelanocortin/metabolism, Receptor, Satiety Response/drug effects, Satiety Response/physiology, Uncoupling Protein 2

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