Selective Removal of Sodium Salt Taste Disrupts the Maintenance of Dendritic Architecture of Second Order Taste Neurons in the Mouse Nucleus of the Solitary Tract

Neuronal activity plays critical roles in the development of sensory circuits in the mammalian brain. Recently, experimental manipulations have become available to alter gustatory activity from specific taste transduction pathways to investigate the roles taste experience play in the development of central gustatory circuits. Here we used a previously vetted mouse knockout model in which the transduction channel necessary for sodium taste is removed from taste bud cells throughout life. In these knockout mice, the terminal fields that carry taste information from the periphery into the nucleus of the solitary tract (NST) fail to develop, suggesting that neural sodium taste activity is important for the proper development of central gustatory circuits. Using this model, we tested the hypothesis that the development and maintenance of the dendritic architecture of NST relay cells, the primary postsynaptic partner of gustatory nerve terminal fields, are similarly dependent upon sodium taste activity from this single transduction pathway. The dendritic fields of NST relay cells, from adult male and female mice in which the alpha-subunit of the epithelial sodium channel was conditionally deleted in taste bud cells (ENaC knockout mice) throughout life, were up to 2.4x larger and more complex than that of age-matched control mice. Interestingly, these differences in dendritic architecture were not present in postnatal day 20 (P20) mice of either sex. Overall, our results suggest that ENaC-mediated sodium taste activity is necessary for the maintenance of dendritic fields of relay cells in the gustatory NST.