Acidic stimuli activates two distinct pathways in taste receptor cells from rat fungiform papillae

• Published in: Brain research Vol. 923; no. 1; pp. 58 - 70
• Main Authors: Liu, Lieju, Simon, S.A
• Format: Journal Article
• Language: English
• Published: London Elsevier B.V 27.12.2001; Amsterdam Elsevier; New York, NY
• Subjects: Acid Sensing Ion Channels; Acids - pharmacology; Adjuvants, Immunologic - pharmacology; Amiloride - pharmacology; Animals; Biological and medical sciences; Bitter taste; Calcium - metabolism; Capsaicin - analogs & derivatives; Capsaicin - pharmacology; Chemoreceptor Cells - drug effects; Chemoreceptor Cells - physiology; Cholera Toxin - pharmacology; Diuretics - pharmacology; Dose-Response Relationship, Drug; Female; Fundamental and applied biological sciences. Psychology; GTP-Binding Proteins - metabolism; Male; Membrane Proteins; Nerve Tissue Proteins; Olfactory system and olfaction. Gustatory system and gustation; papillae (fungiform); Pertussis Toxin; Proton sensor; Protons; Rats; Rats, Sprague-Dawley; Receptors, Drug - genetics; Receptors, Drug - metabolism; Reverse Transcriptase Polymerase Chain Reaction; Sodium Channels - genetics; Sodium Channels - metabolism; Sour taste; Stimulation, Chemical; Tachyphylaxis - physiology; Taste - physiology; Taste Buds - metabolism; Taste transduction; Vertebrates: nervous system and sense organs; Virulence Factors, Bordetella - pharmacology; Sour taste; Proton sensor; Bitter taste; Taste transduction; Vertebrata; Tongue; Mammalia; Fungiform papilla; Rat; Gustation; Rodentia; Sensory receptor; Gustatory receptor; Chemical stimulus; Acid flavour
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(01)03190-0

A sour taste sensation may be produced when acidic stimuli interact with taste receptor cells (TRCs) on the dorsal surface of the tongue. We have searched for pathways in TRCs that may be activated by acidic stimuli using RT-PCR and changes in intracellular calcium (Ca 2+ I) induced by acidic stimuli in rat fungiform papillae. RT-PCR revealed the presence of proton-gated subunits ASIC-β and VR1. Ca 2+ imaging measurements of the TRCs revealed two distinct responses to acidic stimuli: Ca 2+ i was increased in 9% (28/308; Type I) and was decreased in 39% (121/308; Type II). Neither of these responses was affected by the removal of extracellular Ca 2+, indicating that the changes arise from the release and sequestration of Ca 2+ from intracellular stores. These responses were also not inhibited by the vanilloid receptor antagonist, capsazepine, suggesting they do not arise from the activation of vanilloid receptors. The Type I, but not the Type II response was inhibited by amiloride. Dose–response measurements for Types I and II responses yielded pH 50% of 4.8 and 4.9, respectively. Type II responses were inhibited by pertussis toxin, suggesting G-protein involvement. TRCs that exhibit Type II responses could also be activated by quinine (which increased Ca 2+ I) thus suggesting a mechanism by which the addition of acid may be suppressive to other chemical stimuli.