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Central administration of the anorexigenic peptide neuromedin U decreases alcohol intake and attenuates alcohol-induced reward in rodents

Journal article
Authors Daniel Vallöf
Lisa Ulenius
Emil Egecioglu
Jörgen Engel
Elisabeth Jerlhag
Published in Addiction Biology
Volume 22
Issue 3
Pages 640–651
ISSN 1355-6215
Publication year 2017
Published at Institute of Neuroscience and Physiology, Department of Pharmacology
Pages 640–651
Language en
Keywords Addiction, Appetite regulation, Dopamine, Food intake, Gut-brain axis, Obesity, Reward
Subject categories Neuroscience, Pharmacology


© 2016 The Authors Addiction Biology published by John Wiley & Sons Ltd.By investigating the neurochemical mechanisms through which alcohol activates the brain reward systems, novel treatment strategies for alcohol use disorder (AUD), a chronic relapsing disease, can be developed. In contrast to the common view of the function of gut-brain peptides, such as neuromedin U (NMU), to regulate food intake and appetite, a novel role in reinforcement mediation has been implied. The anorexigenic effects of NMU are mediated via NMU2 receptors, preferably in the arcuate nucleus and paraventricular nucleus. The expression of NMU2 receptors is also expressed in several reward-related areas in the brain, suggesting a role in reward regulation. The present experiments were therefore set up to investigate the effect of intracerebroventricular administration of NMU on alcohol-mediated behaviors in rodents. We found that central administration of NMU attenuated alcohol-induced locomotor stimulation, accumbal dopamine release and the expression of conditioned place preference in mice. In addition, NMU dose dependently decreased alcohol intake in high, but not in low, alcohol-consuming rats. Central NMU administration did not alter the blood alcohol concentrations nor change the corticosterone levels in rodents. Given that AUD is a major health-care challenge causing an enormous cost to society and novel treatment strategies are warranted, our data suggest that NMU analogues deserve to be evaluated as novel treatment of AUD in humans.

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