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Requirement of central ghrelin signaling for alcohol reward.

Journal article
Authors Elisabeth Jerlhag
Emil Egecioglu
Sara Landgren
Nicolas Salomé
Markus Heilig
Diederik Moechars
Rakesh Datta
Daniel Perrissoud
Suzanne L. Dickson
Jörgen Engel
Published in Proceedings of the National Academy of Sciences of the United States of America
Volume 106
Issue 27
Pages 11318-23
ISSN 1091-6490
Publication year 2009
Published at Institute of Neuroscience and Physiology, Department of Physiology
Institute of Neuroscience and Physiology, Department of Pharmacology
Pages 11318-23
Language en
Keywords Animals, Central Nervous System, drug effects, metabolism, Conditioning, Classical, drug effects, Dopamine, metabolism, Ethanol, administration & dosage, Ghrelin, administration & dosage, metabolism, pharmacology, Injections, Intraperitoneal, Injections, Intraventricular, Mice, Mice, Inbred C57BL, Models, Biological, Models, Genetic, Motor Activity, drug effects, Nucleus Accumbens, drug effects, metabolism, Receptors, Ghrelin, antagonists & inhibitors, Reward, Signal Transduction, drug effects, Ventral Tegmental Area, drug effects
Subject categories Physiology


The stomach-derived hormone ghrelin interacts with key CNS circuits regulating energy balance and body weight. Here we provide evidence that the central ghrelin signaling system is required for alcohol reward. Central ghrelin administration (to brain ventricles or to tegmental areas involved in reward) increased alcohol intake in a 2-bottle (alcohol/water) free choice limited access paradigm in mice. By contrast, central or peripheral administration of ghrelin receptor (GHS-R1A) antagonists suppressed alcohol intake in this model. Alcohol-induced locomotor stimulation, accumbal dopamine release and conditioned place preference were abolished in models of suppressed central ghrelin signaling: GHS-R1A knockout mice and mice treated with 2 different GHS-R1A antagonists. Thus, central ghrelin signaling, via GHS-R1A, not only stimulates the reward system, but is also required for stimulation of that system by alcohol. Our data suggest that central ghrelin signaling constitutes a potential target for treatment of alcohol-related disorders.

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