The research in this proposal investigates the influence that a motivated state, sodium appetite, has on gustatory neural responses in the pontine parabrachial nuclei (PBN). These nuclei process gustatory and visceral sensory information involved in salt appetite and a variety of other ingestive behaviors and regulatory systems. Bilateral damage to the PBN prevents a rat from expressing a sodium appetite. Extracellular recordings from single PBN gustatory neurons will be assessed during sapid stimulation with a concentration range of NaCl and at least 3 other standard chemicals, sucrose, citric acid and quinine HCl in rats that are either sodium replete or deficient. Initially, the sodium appetite will be raised by dietary deprivation. Subsequent studies will use a standard diuretic regimen, furosemide, to induce a rapid sodium deficiency. At least the dietary protocol will be performed in both acutely prepared, lightly anesthetized rats and chronically prepared, awake, behaving animals. These parallel studies are desirable both for my own training (acute recording is easier than chronic) and because evidence already exists on the effects of salt appetite from peripheral and the first central gustatory neurons in the nucleus of the solitary tract. With one exception, all these prior studies were in anesthetized rats. The data from these experiments will provide insight into the potential neural mechanisms related to development of a motivated behavior, salt appetite.
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