Developmental reversal in neuropeptide Y action on feeding in an amphibian.

Neuropeptide Y (NPY) is expressed in the hypothalamus where it exerts orexigenic actions within the feeding control circuit. While NPY stimulates feeding in juvenile and adult animals, it is not known whether NPY influences food intake at earlier life stages. We investigated a role for NPY in regulating feeding at two stages of the life cycle of an amphibian, the Western spadefoot toad Spea hammondii. We administered NPY by intracerebroventricular (i.c.v.) injection to juvenile toads or prometamorphic tadpoles, and monitored locomotion, feeding behavior and/or food intake. Injection of NPY (20 or 200 ng/g BW) into juvenile toads decreased the latency to, and increased the number of strikes at prey, and the number of crickets eaten compared to uninjected or vehicle-injected controls. By contrast, injection of NPY (0.02-20 ng/g BW) into prometamorphic tadpoles caused a dose-dependent decrease in time spent foraging compared to controls. Blocking NPY signaling in the prometamorphic tadpole brain by i.c.v. injection of a general NPY receptor antagonist increased foraging, and partly blocked the action of exogenous NPY on foraging. Taken together, our findings show a developmental reversal in NPY actions on feeding in an amphibian, with the peptide having a characteristic orexigenic action in the juvenile toad, but an inhibitory action on foraging in the prometamorphic tadpole. The anorexigenic action of NPY in the tadpole correlates with a decrease in feeding that occurs at metamorphic climax when the tadpole's gut and cranium remodels for the transition to a carnivorous diet.