Energy, water, and electrolyte balance are among the most closely regulated parameters found in vertebrates. Even minor, uncorrected defects in any one system can become life threatening, and obligate loss occurs continuously. Most of the processes involved in these systems regulate physiological parameters and conservation. Only one process, ingestion of foods or fluids, can replenish supplies of nutrients, electrolytes, and water. The goal of the research outlined in this proposal is to understand the neural mechanisms that govern the decision to ingest or reject the contents of the oral cavity. Evidence from this and other laboratories indicates that the substrates for this neural decision are complete in the brainstem -- the midbrain, pons, and medulla. Sensory information from the oral cavity -- tactile, thermal, and gustatory afferent activity -- first reaches the brain in the pons and medulla. Vagal visceral afferent activity can switch the response elicited by oral stimuli from one of ingestion to one of rejection. The vagus nerve also synapses in the medulla. Finally, the motor neurons that produce ingestive behavior are located in the medulla and pons, and the interneurons that project to these oral motor nuclei form a continuous distribution in the medullary and pontine reticular formation. Chronic precollicular decerebrate preparations exhibit normal ingestion and rejection behavior and, given an appropriate visceral stimulus, will switch their response from ingestion to rejection. Using neuroanatomical, electrophysiological, and behavioral analysis, this project will examine the anatomical and physiological relationships among the nucleus of the solitary tract (NST) and the parabrachial nuclei (PBN), the first two sensory relays for oral and visceral afferent activity, as well as the parvicellular reticular formation (PRF). Specific experiments will examine (1) the axonal connections among functionally defined subdivision of NST and PBN and the oral motor interneurons in PRF, (2) the responses of single neurons in NST, PBN, and the parvicellular reticular formation to both oral and visceral stimuli, and (3) the behavioral capacity of preparations with either lesions or axonal disconnections of the solitary or parabrachial nuclei. In addition to contributing toward the basic understanding of how the nervous system coordinates diverse sensory information into precise physiological and behavioral controls, this research has direct relevance to the sensory mechanisms involved in the etiology of a variety of morbid conditions. Specifically, excess ingestion of carbohydrates, fats, and sodium is highly correlated with, and may the causally related to obesity, diabetes, and hypertension.
