Prolactin-Releasing Peptide Mediates Cholecystokinin-Induced Satiety in Mice

We have shown previously that prolactin-releasing peptide (PrRP) plays a role in the regulation of feeding and energy expenditure in rats. We hypothesize that PrRP may have a physiological action through its putative receptor, GPR10, to mediate the central anorexigenic effects of peripheral satiety factors. Here we examine the effects of PrRP and cholecystokinin (CCK) on feeding in mice, including PrRP receptor gene knockout animals (GPR10(-/-)). Intracerebroventricular administration of PrRP (1-4 nmol) inhibited feeding in C57B6/J mice under both fast-induced and nocturnal feeding conditions. In contrast to the observations made in wild-type mice, neither PrRP nor CCK reduced food intake in GRP10(-/-) mice. The reduction in feeding and the release of corticosterone induced by systemic injection of the stressor lipopolysaccharide was similar in both GPR10(+/+) and GPR10(-/-) mice. These findings suggest that PrRP, acting through GPR10, is involved in regulating food intake and may be a key intermediary in the central satiating actions of CCK.