A major developmental change in sodium taste sensitivity occurs in rats such that sodium stimulated taste responses of the chorda tympani nerve are significantly greater in adult rats when compared to neonatal and weanling rats. This increase in sodium sensitivity is gradual, tissue specific and sensitive to the inhibitory effects of amiloride. It is believed that a majority of sodium sensitivity in the taste system of adult rats is transduced through the amiloride-sensitive epithelial sodium channel (ENaC). We hypothesize that the developmental increase in sodium sensitivity directly involves the transcriptional regulation of ENaC. To establish the validity of this hypothesis the following will be accomplished: First, taste buds isolated from fungiform papillae, circumvallate papillae, soft palate and nasoincisor ducts will be subjected to quantitative RT-PCR to determine the expression profiles for each of the ENaC subunits at different developmental time points. Second, we will utilize in situ hybridization analysis to localize the relative expression of the genes encoding the subunits of the sodium channel during development in each tissue. Finally, identical RT-PCR experimentation will be conducted using adult animals that have been sodium-restricted throughout development, as these animals maintain immature chorda tympani sodium response (fungiform taste buds) throughout life. The results of these studies should elucidate whether sodium channel expression is a mechanism by which sodium sensitivity is developmentally regulated.
