activity, releases accumbal dopamine and increases alcohol consumption in mice (Jerlhag et al. 2007, 2009). Another possible route by which the ghrelin signaling system may alter the sensitivity of the mesolimbic dopamine system and the ability of addictive drugs to activate this system is by interacting with dopamine receptors. This was demonstrated recently in vivo and in vitro studies where GHSR‐1a were found to regulate the activity of tegmental dopamine neurons by heterodimerizing with dopamine D1‐like (Jiang, Betancourt & Smith 2006) and D2 receptors (DRD2) (Kern et al. 2012). Interestingly, GHSR‐1a has been hypothesized to act as an allosteric modulator of dopamine‐DRD2 signaling as effects are seen even in the absence of ligand (i.e. ghrelin) (Kern et al. 2012). This further suggests that GHSR‐1a may function in areas with no ghrelin production and affect neurobiological processes involved in reward. This was further supported by a recently published study showing that when peripherally circulating endogenous ghrelin is pharmacologically hindered from entering the brain (via the high affinity compound Spiegelmer NOX‐B11‐2), there is no subsequent attenuation of the rewarding properties of alcohol in rodents (Jerlhag et al. 2014). Taken together with previous experiments, the importance of central GHSR‐1a receptors in drug‐induced reward
