Electrophysiological responses to non-electrolytes in lingual nerve of rat and in lingual epithelia of dog.

Published

Journal Article

Epithelial and neural mechanisms underlying the trigeminal chemoreception of non-electrolytes were investigated in whole-nerve recordings from lingual nerve and in Ussing-chamber studies of isolated lingual epithelia. The non-electrolytes included menthol, amyl acetate, phenethyl alcohol, toluene, methanol, ethanol, propanol, butanol, hexanol and octanol. They produced different lingual nerve responses: methanol and ethanol only increased ongoing activity; longer-chain alcohols initially increased but then suppressed activity below baseline; phenethyl alcohol and toluene only suppressed activity. Their threshold concentrations for lingual nerve responses, with the exception of menthol, were proportional to the octanol:water partition coefficients of the stimuli. The threshold concentration for menthol was significantly lower than predicted by this coefficient. Calculation of the free energy of transfer from the threshold concentrations for the n-alcohols suggests that they undergo partition into a hydrophobic environment such as is found in lipid bilayers. Lanthanum chloride, which inhibited lingual nerve responses to hydrophilic compounds, presumably by blocking their diffusion across tight junctions, did not inhibit responses to these non-electrolytes. At high concentrations, hexanol acted as an anaesthetic in that the lingual nerve no longer responded to thermal and chemical stimuli whereas ethanol, which only increased lingual nerve activity, did not inhibit those responses. Epithelial transport, as indicated by the short-circuit current (Isc) measured across tongues bathed in symmetrical solutions of Krebs-Henseleit buffer, was reversibly inhibited by ethanol, hexanol, octanol, phenyl ethanol and menthol. The stimulus concentration necessary to inhibit 50% of the Isc decreased with increasing octanol:water partition coefficient.(ABSTRACT TRUNCATED AT 250 WORDS)

Full Text

Duke Authors

Cited Authors

  • Simon, SA; Sostman, AL

Published Date

  • 1991

Published In

Volume / Issue

  • 36 / 11

Start / End Page

  • 805 - 813

PubMed ID

  • 1722391

Pubmed Central ID

  • 1722391

International Standard Serial Number (ISSN)

  • 0003-9969

Language

  • eng

Conference Location

  • England