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Feeding Induced by Cannabinoids Is Mediated Independently of the Melanocortin System

  • Sinnayah, Puspha (Division of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University)
  • Jobst, Erin E. (Pacific University)
  • Rathner, Joseph A. (Neurological Science Institute, Beaverton, Oregon)
  • Caldera-Siu, Angela D. (Department of Pharmacology and Experimental Therapeutics and Program in Neuroscience, Tufts University School of Medicine)
  • Tonelli-Lemos, Luciana (Division of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University)
  • Eusterbrock, Aaron J. (Division of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University)
  • Enriori, Pablo J. (Division of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University)
  • Pothos, Emmanuel N. (Department of Pharmacology and Experimental Therapeutics and Program in Neuroscience, Tufts University School of Medicine)
  • Grove, Kevin L. (Division of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University)
  • Cowley, Michael A. (Division of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University / Department of Physiology, Faculty of Medicine, Monash University)
21 May 2008

Abstract

Background: Cannabinoids, the active components of marijuana, stimulate appetite, and cannabinoid receptor-1 (CB1-R) antagonists suppress appetite and promote weight loss. Little is known about how CB1-R antagonists affect the central neurocircuitry, specifically the melanocortin system that regulates energy balance. Methodology/Principal Findings: Here, we show that peripherally administered CB1-R antagonist (AM251) or agonist equally suppressed or stimulated feeding respectively in Ay , which lack a functional melanocortin system, and wildtype mice, demonstrating that cannabinoid effects on feeding do not require melanocortin circuitry. CB1-R antagonist or agonist administered into the ventral tegmental area (VTA) equally suppressed or stimulated feeding respectively, in both genotypes. In addition, peripheral and central cannabinoid administration similarly induced c-Fos activation in brain sites suggesting mediation via motivational dopaminergic circuitry. Amperometry-detected increases in evoked dopamine (DA) release by the CB1-R antagonist in nucleus accumbens slices indicates that AM251 modulates DA release from VTA terminals. Conclusions/Significance: Our results demonstrate that the effects of cannabinoids on energy balance are independent of hypothalamic melanocortin circuitry and is primarily driven by the reward system.


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