Previous studies demonstrate that lesions to the rodent parabrachial nucleus (PBN) disrupt the formation of gustatory-postingestive associations, while preserving gustatory and viscerosensory functions. This suggests that the rodent PBN functions essentially as an integrative circuit, supporting the conditioning of tastants to postingestive factors. In the case of primates, however, anatomical studies have failed to demonstrate gustatory projections from medullary nuclei to PBN. It should therefore be inferred that the primate PBN lacks the associative functions assigned to its rodent counterpart. Moreover, the ability of rodent midbrain dopaminergic systems to respond to the activation of palatable tastants depends on the integrity of the gustatory PBN. However, recent studies demonstrate that caloric palatable compounds do not require taste signaling to produce elevated brain dopamine levels. This raises the possibility that, in rodents, PBN neurons are important for the detection of postingestive effects of nutrients that occur independently of gustatory input. If confirmed, such function would assign non-associative roles to the rodent PBN, approximating its functional organization to its primate counterpart. We are currently testing this possibility by monitoring the behavioral responses to caloric glucose solutions in sweet-blind mice having sustained bilateral lesions to the PBN. Preliminary results indicate that the rodent PBN regulates nutrient intake even when no gustatory inputs are involved. This favors the assignment of non-gustatory, homeostatic functions to the rodent PBN during feeding, a concept that brings an additional perspective on the rodent versus primate functional discrepancy associated with the anatomy of this pontine nucleus.