In many respects, sodium appetite differs little from other biological motivations.  As with sex, hunger, and thirst, it is the behavioral expression of a larger physiological system that deals with a fundamental problem of life, in this case electrolyte balance.  As with other motivations, salt appetite is hormonally driven and the hormones produce much of their influence on behavior (and physiology) by acting on neurons in the ventral forebrain.  One advantage of salt appetite as a model for studying biological motivation is that its adequate stimulus is simple, the sodium ion, and in the external environment this stimulus is transduced by a single sensory system, taste.  Because the neuroanatomy of the gustatory system has been documented, it should be possible to follow gustatory afferent information into the brain and to determine where and by what mechanisms it interacts with the neural areas that are sensitive to the relevant hormone fluxes.  The experiments outlined in this proposal investigate such interaction.  Neurons in anteroventral third-ventricular forebrain areas will be tested iontophoretically for their sensitivity to two of the principal hormones implicated in eliciting sodium appetite, aldosterone and angiotensin II.  The same neurons also will be tested for responsiveness to electrical stimulation in the parabrachial nuclei, which contains a gustatory relay that projects directly to the ventral forebrain.  Neurons that respond to parabrachial stimulation, in turn, will be examined for responses to sapid stimuli, The results will determine whether neurons that respond to local changes in the concentration of either aldosterone or angiotensin II also receive direct afferent neural influence from the gustatory apparatus.