Effects of dietary Na+ deprivation on epithelial Na+ channel (ENaC), BDNF, and TrkB mRNA expression in the rat tongue

Tao Huang,Frauke Stähler

doi:10.1186/1471-2202-10-19

Abstract

BackgroundIn rodents, dietary Na+ deprivation reduces gustatory responses of primary taste fibers and central taste neurons to lingual Na+ stimulation. However, in the rat taste bud cells Na+ deprivation increases the number of amiloride sensitive epithelial Na+ channels (ENaC), which are considered as the "receptor" of the Na+ component of salt taste. To explore the mechanisms, the expression of the three ENaC subunits (α, β and γ) in taste buds were observed from rats fed with diets containing either 0.03% (Na+ deprivation) or 1% (control) NaCl for 15 days, by using in situ hybridization and real-time quantitative RT-PCR (qRT-PCR). Since BDNF/TrkB signaling is involved in the neural innervation of taste buds, the effects of Na+ deprivation on BDNF and its receptor TrkB expression in the rat taste buds were also examined.ResultsIn situ hybridization analysis showed that all three ENaC subunit mRNAs were found in the rat fungiform taste buds and lingual epithelia, but in the vallate and foliate taste buds, only α ENaC mRNA was easily detected, while β and γ ENaC mRNAs were much less than those in the fungiform taste buds. Between control and low Na+ fed animals, the numbers of taste bud cells expressing α, β and γ ENaC subunits were not significantly different in the fungiform, vallate and foliate taste buds, respectively. Similarly, qRT-PCR also indicated that Na+ deprivation had no effect on any ENaC subunit expression in the three types of taste buds. However, Na+ deprivation reduced BDNF mRNA expression by 50% in the fungiform taste buds, but not in the vallate and foliate taste buds. The expression of TrkB was not different between control and Na+ deprived rats, irrespective of the taste papillae type.ConclusionThe findings demonstrate that dietary Na+ deprivation does not change ENaC mRNA expression in rat taste buds, but reduces BDNF mRNA expression in the fungiform taste buds. Given the roles of BDNF in survival of cells and target innervation, our results suggest that dietary Na+ deprivation might lead to a loss of gustatory innervation in the mouse fungiform taste buds.

Highlights

In rodents, dietary Na+ deprivation reduces gustatory responses of primary taste fibers and central taste neurons to lingual Na+ stimulation
In the nucleus of the solitary tract (NST) and the parabrachial nucleus (PBN), the first and the second relays of central taste system, dietary Na+ deprivation reduces nerve responses to lingual NaCl stimulation [6,7,8]. This indicates that the taste responses to NaCl from chorda tympani (CT) nerves, and NST and PBN taste neurons are consistently reduced following dietary Na+ deprivation, which suggests that the Na+ deprivation might regulate salt taste perception and/or transduction at the peripheral taste system
To explore the gustatory mechanisms of dietary Na+ deprivation we examined epithelial Na+ channels (ENaC) subunit mRNA expression in the taste buds of rats fed with a diet containing either 0.03% NaCl (Na+ deprivation) or 1% NaCl, using in situ hybridization and real-time quantitative RTPCR

Summary

Introduction

Dietary Na+ deprivation reduces gustatory responses of primary taste fibers and central taste neurons to lingual Na+ stimulation. In the rat taste bud cells Na+ deprivation increases the number of amiloride sensitive epithelial Na+ channels (ENaC), which are considered as the "receptor" of the Na+ component of salt taste. In the nucleus of the solitary tract (NST) and the parabrachial nucleus (PBN), the first and the second relays of central taste system, dietary Na+ deprivation reduces nerve responses to lingual NaCl stimulation [6,7,8]. Taken together, this indicates that the taste responses to NaCl from CT nerves, and NST and PBN taste neurons are consistently reduced following dietary Na+ deprivation, which suggests that the Na+ deprivation might regulate salt taste perception and/or transduction at the peripheral taste system. The differential expression and localization of ENaC might lead to an up regulation of ENaC function following Na+ deprivation [13]

Results

Discussion

Conclusion