The anion in salt taste: a possible role for paracellular pathways.

Published

Journal Article

It is well established from psychophysical and electrophysiological measurements that both Na and Cl contribute to the taste response to NaCl. The contribution of Na to the NaCl response can be studied using amiloride, a drug that inhibits Na transport in taste and other epithelial cells. The pathways involved in response to Cl are less well understood. We undertook a series of experiments in the rat to determine whether tonic chorda tympani responses to NaCl are inhibited by specific inhibitors of anion transport. Whole nerve responses to NaCl were unchanged by bathing the tongue in SITS, DIDS, bumetanide, furosemide, 9-anthracene carboxylic acid, or an antibody that blocks Cl conductance pathways in many epithelia. Thus, Cl co-transporters, exchangers, and channels (at least in the apical membrane of taste cells) are probably not involved in NaCl taste responses. When other anions (acetate, isethionate, methane sulfonate, gluconate, tartrate), which are generally impermeant in other Cl-selective pathways, were substituted for Cl, the dose-response curves for the chorda tympani response were shifted toward higher concentrations than the response to NaCl, but achieved the same maximum value at sufficiently high concentrations (1.0 M Na). For all the organic Na salts, the amiloride-insensitive portion of the response was substantially less than for NaCl. Experiments with Na acetate at different pHs showed that intracellular acidification is not responsible for the differences between NaCl and organic salts of Na. One possibility which remains is that apical stimulation with these other Na salts results in a taste cell membrane potential that is hyperpolarized with respect to the membrane potential in NaCl.(ABSTRACT TRUNCATED AT 250 WORDS)

Full Text

Duke Authors

Cited Authors

  • Elliott, EJ; Simon, SA

Published Date

  • December 3, 1990

Published In

Volume / Issue

  • 535 / 1

Start / End Page

  • 9 - 17

PubMed ID

  • 1963343

Pubmed Central ID

  • 1963343

International Standard Serial Number (ISSN)

  • 0006-8993

Digital Object Identifier (DOI)

  • 10.1016/0006-8993(90)91817-z

Language

  • eng

Conference Location

  • Netherlands