Selective Removal of Sodium Salt Taste Disrupts the Maintenance of Dendritic Architecture of Gustatory Relay Neurons in the Mouse Nucleus of the Solitary Tract.

Neuronal activity plays critical roles in the development of sensory circuits in the mammalian brain. Experimental procedures are now available to alter the function of specific taste transduction pathways and have been especially useful in studying how stimulus-specific taste activity influences the development of central gustatory circuits. We previously used a mouse knock-out (KO) model in which the transduction channel necessary for sodium taste is removed from taste bud cells throughout life. In these KO mice, the terminal fields that carry taste information from taste buds into the nucleus of the solitary tract (NST) fail to mature, suggesting that sodium-elicited taste activity is important for the proper development of central gustatory circuits. Here, 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 on sodium-elicited taste activity. The dendritic fields of NST relay cells, from adult male and female mice in which the α-subunit of the epithelial sodium channel (αENaC) was conditionally deleted in taste bud cells throughout life, were up to 2.4× larger and more complex than that of age-matched control mice. Interestingly, these differences in dendritic architecture did not appear until after the age when terminal fields begin "pruning," after postnatal day (P)20. 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.

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