Motivation remains a central puzzle of neuroscience. Understanding its neural bases is key in developing rational therapies for a broad spectrum of maladies such as drug addiction, obesity, anorexia nervosa, and depression. Salt appetite is a biological drive triggered by a negative body sodium balance that offers a unique model for investigating the central mechanisms of motivated behavior. Sodium appetite fulfills all of the criteria for motivation, as do hunger and thirst, but has some distinct advantages. Its adequate stimulus is simple, the sodium ion, and in the external environment, this stimulus is transduced by a single sensory system, taste. Unlike other sensory systems, except smell, taste has direct neural connections with the limbic system, which is critical to the elaboration of motivation. In most mammals, including humans, recognition of sodium is innate. Thus, when a Na-appetite arises, the significance of the sensory neural activity elicited by sapid sodium changes dramatically. The objective of this project is to understand how the neural systems that control salt appetite effect the change in avidity for salt. The premise is that at least part of the change results from alterations in the gustatory neural code. We already know that, during Na-appetite, changes do occur in the gustatory responses to NaCl on the periphery and in the first central relay, the nucleus of the solitary tract (NST). We also know that lesions of the second central relay, the parabrachial nucleus (PBN), prevent the expression of Na-appetite, but that damage to the third central relay, the thalamic gustatory area (TTA), does not. Finally, chronically decerebrate rats, which have both the NST and PBN intact, but no connections to or from the forebrain, also fail to exhibit a Na-appetite. These facts constrain the hypotheses to interactions between the PBN and the limbic system. Using these constraints, this proposal examines three related hypotheses. During Na-appetite, (1) the sensory neural code for taste in the PBN is altered to make sapid sodium more discriminable from other chemicals, (2) parabrachial gustatory neural activity distributed to the ventral forebrain is necessary and sufficient to change the hedonic value of the salt signal, and (3) the mechanism for the increased discriminability and the changed avidity involves reciprocal interaction between the limbic system and the parabrachial nuclei.