Access to the Published Version May Require Subscription. Published with Permission From: Springer-verlag Ghrelin Receptor Antagonism Attenuates Cocaine-and Amphetamine-induced Locomotor Stimulation, Accumbal Dopamine Release and Conditioned Place Preference

This paper has been peer-reviewed but does not include the final publisher proof-corrections or journal pagination. Ghrelin receptor antagonism attenuates cocaine-and amphetamine-induced locomotor stimulation, accumbal dopamine release, and conditioned place preference. Abstract Recently we demonstrated that genetic or pharmacological suppression of the central ghrelin signalling system, involving the growth hormone secretagogue receptor 1A (GHS-R1A), lead to a reduced reward profile from alcohol. As the target circuits for ghrelin in the brain include a mesolimbic reward pathway that is intimately associated with reward-seeking behaviour, we sought to determine whether the central ghrelin signalling system is required for reward from drugs of abuse other than alcohol, namely cocaine or amphetamine. We found that amphetamine-as well as cocaine-induced locomotor stimulation and accumbal dopamine release were reduced in mice treated with a GHS-R1A antagonist. Moreover, the ability of these drugs to condition a place preference was also attenuated by the GHS-R1A antagonist. Thus GHS-R1A appears to be required not only for alcohol-induced reward, but also for reward induced by psychostimulant drugs. Our data suggest that the central ghrelin signaling system constitutes a novel potential target for treatment of addictive behaviours such as drug dependence.