The role of transient receptor potential vanilloid-1 on neural responses to acids by the chorda tympani, glossopharyngeal and superior laryngeal nerves in mice.
The transient receptor potential vanilloid-1 (TRPV1) receptor acts as a polymodal nociceptor activated by capsaicin, heat, and acid. TRPV1, which is expressed in sensory neurons innervating the oral cavity, is associated with an oral burning sensation in response to spicy food containing capsaicin. However, little is known about the involvement of TRPV1 in responses to acid stimuli in either the gustatory system or the general somatosensory innervation of the oropharynx. To test this possibility, we recorded electrophysiological responses to several acids (acetic acid, citric acid and HCl) and other taste stimuli from the mouse chorda tympani, glossopharyngeal and superior laryngeal nerves, and compared potential effects of iodo-resiniferatoxin (I-RTX), a potent TRPV1 antagonist, on chemical responses of the three nerves. The results indicated that in the chorda tympani nerve, I-RTX (1-100 nM) did not affect responses to acids, sucrose and quinine HCl, but reduced responses to NaCl (I-RTX at concentrations of 10 and 100 nM) and KCl and NH(4)Cl (100 nM). In contrast, in the glossopharyngeal nerve, I-RTX significantly suppressed responses to all acids and salts, but not to sucrose and quinine HCl. Responses to acetic acid were suppressed by I-RTX even at 0.1 nM concentration. The superior laryngeal nerve responded in a concentration-dependent manner to acetic acid, citric acid, HCl, KCl, NH(4)Cl and monosodium l-glutamate. The responses to acetic acid, but not to the other stimuli, were significantly inhibited by I-RTX. These results suggested that TRPV1 may be involved in the mechanism for responses to acids presented to the posterior oral cavity and larynx. This high degree of responsiveness to acetic acid may account for the oral burning sensation, known as a flavor characteristic of vinegar.
Arai
T
T
Section of Oral Neuroscience, Graduate School of Dental Sciences, Kyushu University, Higashi-ku, Fukuoka, Japan.
Ohkuri
T
T
Yasumatsu
K
K
Kaga
T
T
Ninomiya
Y
Y
D019342:Acetic Acid; D000143:Acids; D000818:Animals; D002814:Chorda Tympani Nerve / Q000187:drug effects / Q000502:physiology*; D019343:Citric Acid; D004224:Diterpenes / Q000494:pharmacology; D005260:Female; D005503:Food Additives; D005930:Glossopharyngeal Nerve / Q000187:drug effects / Q000502:physiology*; D006851:Hydrochloric Acid; D007823:Laryngeal Nerves / Q000187:drug effects / Q000502:physiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D011803:Quinine; D012492:Salts; D012970:Sodium Glutamate; D013395:Sucrose; D013549:Sweetening Agents; D050916:TRPV Cation Channels / Q000037:antagonists & inhibitors / Q000378:metabolism*; D013649:Taste / Q000502:physiology
D000143:Acids; D004224:Diterpenes; D005503:Food Additives; D012492:Salts; D013549:Sweetening Agents; D050916:TRPV Cation Channels; C493921:TRPV1 protein, mouse; C468130:iodoresiniferatoxin; D019343:Citric Acid; D013395:Sucrose; D011803:Quinine; D019342:Acetic Acid; D006851:Hydrochloric Acid; D012970:Sodium Glutamate