SENSORY AND HORMONAL CONTROL OF SALT APPETITE

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Investigations of gustatory processing during salt appetite will focus on two hypotheses. The first hypothesis is that the sensory neural code for taste is altered in a manner that makes oral sodium more salient to the animal. The second hypothesis places the mechanism for the changed avidity in the ventral forebrain, beyond the central gustatory system, within the neural systems that are altered by the hormones controlling fluid balance. The first hypothesis requires behavioral and electrophysiological experiments. Na-appetite can be elicited with variety of procedures, all of which result in increased salt intake. What is not clear is whether a similar change in salt intake reflects the same alterations in the hedonic response to the sodium ion. We plan to use two short term measures, the taste reactivity test and lick pattern analysis, to determine whether the behavioral responses to taste during sodium hunger differ as a function of the method used to raise the appetite. These behavioral experiments were prompted, in part, by electrophysiological data demonstrating that dietary sodium deprivation reduces while diuretics increase central gustatory neural response to NaCl. These data suggest that different procedures for eliciting an appetite produce different perceptual alterations to sapid sodium. Further analysis of these phenomena both on the periphery and further centrally in the parabrachial nuclei (PBN) is dictated. Bilateral lesions of the PBN eliminate the expression of sodium appetite in naive rats, but similar lesions either in the nucleus of the solitary tract or the thalamic gustatory relay do not. Gustatory neurons in the PBN project not only to thalamus, but also to the ventral forebrain. Given the results from the lesion studies, the gustatory projections from the pons to the ventral forebrain take on added significance. Studies of the second hypothesis will focus on neurons within the septo-preoptic continuum that respond selectively to iontophoretically applied angiotensin. The number of such neurons and the magnitude of their responses increases in animals that have been pretreated with DOCA. In fact, the spontaneous activity of the entire region is enhanced by DOCA. During the next project period, a substantial effort will be devoted to examining the range and mechanisms of this steroid effect. Separate observations have demonstrated that, at some locations, minute doses of angiotensin applied iontophoretically can raise blood pressure and even elicit drinking behavior. We also will determine whether PBN influence on neurons in the area can be altered selectively with DOCA pretreatment.