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Effect of Nicotine on Chorda Tympani Responses to Salty and Sour Stimuli

¹Department of Physiology, Virginia Commonwealth University; and ²Philip Morris USA, Richmond, Virginia

Submitted 31 March 2007; accepted in final form 29 June 2007

The effect of nicotine on the benzamil (Bz)-insensitive (transient receptor potential vanilloid-1 variant cation channel, TRPV1t) and the Bz-sensitive (epithelial Na⁺ channel, ENaC) salt taste receptors and sour taste was investigated by monitoring intracellular Na⁺ and H⁺ activity (pH_i) in polarized fungiform taste receptor cells (TRCs) and the chorda tympani (CT) nerve responses to NaCl, KCl, and HCl. CT responses in Sprague–Dawley rats and both wildtype and TRPV1 knockout (KO) mice were recorded in the presence and absence of agonists [resiniferatoxin (RTX) and elevated temperature] and an antagonist (SB-366791) of TRPV1t, the ENaC blocker (Bz), and varying apical pH (pH_o). At concentrations <0.015 M, nicotine enhanced and at >0.015 M, it inhibited CT responses to KCl and NaCl. Nicotine produced maximum enhancement in the Bz-insensitive NaCl CT response at pH_o between 6 and 7. RTX and elevated temperature increased the sensitivity of the CT response to nicotine in salt-containing media, and SB-366791 inhibited these effects. TRPV1 KO mice demonstrated no Bz-insensitive CT response to NaCl and no sensitivity to nicotine, RTX, and elevated temperature. We conclude that nicotine modulates salt responses by direct interaction with TRPV1t. At pH_o >8, the apical membrane permeability of nicotine was increased significantly, resulting in increase in TRC pH_i and volume, activation of ENaC, and enhancement of the Bz-sensitive NaCl CT response. At pH_o >8, nicotine also inhibited the phasic component of the HCl CT response. We conclude that the effects of nicotine on ENaC and the phasic HCl CT response arise from increases in TRC pH_i and volume.

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