leading lower intakes of alcohol, and hence less c-Fos immunoreactivity in pIIIu. To eliminate this possibility, we investigated the effects of D-Lys3-GHRP-6 on c-Fos immunoreactivity induced following systemic injections of 2.5 g/kg ethanol in Experiment 3. Systemic administration results in delivery of identical amounts of ethanol. This experiment showed that D-Lys3-GHRP-6 significantly reduced ethanol-induced c-Fos immunoreactivity in pIIIu despite the delivery of the same amounts of alcohol in saline and D-Lys3-GHRP-6-preinjected animals. The dose of ethanol, 2.5 g/kg, that we administered does not induce locomotor activity and thus, the increase in the number of c-Fos cells after ethanol administration and the decrease produced by D-Lys3-GHRP-6 in ethanol-induced c-Fos was also not secondary to any effects on locomotor activity. Also, previous genetic and lesion studies studies in mice indicate that the pIIIu is involved in regulation of alcohol consumption, but not locomotor activity in mice (Bachtell et al., 2002b; Bachtell et al., 2003; Bachtell et al., 2004; Weitemier and Ryabinin, 2005). Therefore, the result of this experiment indicates that the reduced activity of pIIIu is not secondary to decreased levels of ethanol or any effects on locomotor activity, and is a consequence of the antagonism of ghrelin receptors in the pIIIu.
