| Popis: |
When most omnivores and herbivores become sodium depleted they engage in the motivated behavior of sodium appetite (AKA salt appetite), or the seeking out and ingestion of salty substances. Sodium appetite is associated with psychological processes that serve to enhance the incentive and rewarding value of salty substances in order to attract animals to salty substances and reinforce the ingestion of them. The experience of sodium depletion also produces long-lasting changes in behavior; one of the most apparent changes being a seemingly life-long increase in hypertonic salt intake which indicates sodium appetite is sensitized. Two neural circuits have been implicated in the sensitization of sodium appetite: 1) a forebrain neural circuit that regulates body fluid homeostasis, and 2) the mesolimbic dopamine system which mediates motivated behaviors. This dissertation has three aims that serve the overall purpose of providing a better understanding of the neurobiological mechanisms that mediate the sensitization of sodium appetite. The first aim is to develop a model of sodium depletion that is amenable to pharmacological manipulation in order to determine whether the -blockade of N-methyl-d-aspartate receptors, which are critical for neural plasticity, will prevent the sensitization of sodium appetite. The second aim is to determine whether sensitization is associated with relatively long-term molecular changes in forebrain areas that regulate body fluid homeostasis. The third aim is to identify how forebrain areas involved in body fluid homeostasis may connect to and influence activity in the mesolimbic dopamine system. |
