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Chem Senses. 2014 Jul;39(6):471-87. doi: 10.1093/chemse/bju014. Epub 2014 Apr 9.

Astringency is a trigeminal sensation that involves the activation of G protein-coupled signaling by phenolic compounds.

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Department of Cell Physiology, Ruhr University Bochum, Universitätsstr. 150, D-44780 Bochum, Germany, Leibniz Research Centre for Working Environment and Human Factors (IfADo), Ardeystr. 67, D-44139 Dortmund, Germany,
Department of Cell Physiology, Ruhr University Bochum, Universitätsstr. 150, D-44780 Bochum, Germany.
Food Chemistry and Molecular Sensory Science, Technical University of Munich, Lise-Meitner-Str. 34, D-85354 Freising, Germany.
Institute for Biology II, RWTH-Aachen University, Worringer Weg 1, D-52074 Aachen, Germany.
General Food Technology, Technical University of Munich, Gregor-Mendel-Str. 2, D-85350 Freising-Weihenstephan, Germany.
Institute of Neuro- and Sensory Physiology, Medical Faculty, University of Düsseldorf, Universitätsstr. 1, D-40225 Düsseldorf, Germany.
Department of Otorhinolaryngology, St. Elisabeth Hospital, Ruhr University Bochum, Bleichstraße 15, D-44787 Bochum, Germany.
Molecular Neurosciences, Department of Psychiatry and Psychotherapy, University of Regensburg, Universitätsstr. 84, D-93053 Regensburg, Germany.
Symrise AG, Ingredient Research Flavor & Nutrition, Mühlenfeldstr. 1, PO Box 1253, D-37603 Holzminden, Germany and.
Department of Community Dentistry and Behavioral Science, College of Dentistry, University of Florida, 1395 Center Drive, PO Box 103628, Gainesville, FL 32610-3628, USA.


Astringency is an everyday sensory experience best described as a dry mouthfeel typically elicited by phenol-rich alimentary products like tea and wine. The neural correlates and cellular mechanisms of astringency perception are still not well understood. We explored taste and astringency perception in human subjects to study the contribution of the taste as well as of the trigeminal sensory system to astringency perception. Subjects with either a lesion or lidocaine anesthesia of the Chorda tympani taste nerve showed no impairment of astringency perception. Only anesthesia of both the lingual taste and trigeminal innervation by inferior alveolar nerve block led to a loss of astringency perception. In an in vitro model of trigeminal ganglion neurons of mice, we studied the cellular mechanisms of astringency perception. Primary mouse trigeminal ganglion neurons showed robust responses to 8 out of 19 monomeric phenolic astringent compounds and 8 polymeric red wine polyphenols in Ca(2+) imaging experiments. The activating substances shared one or several galloyl moieties, whereas substances lacking the moiety did not or only weakly stimulate responses. The responses depended on Ca(2+) influx and voltage-gated Ca(2+) channels, but not on transient receptor potential channels. Responses to the phenolic compound epigallocatechin gallate as well as to a polymeric red wine polyphenol were inhibited by the Gαs inactivator suramin, the adenylate cyclase inhibitor SQ, and the cyclic nucleotide-gated channel inhibitor l-cis-diltiazem and displayed sensitivity to blockers of Ca(2+)-activated Cl(-) channels.


TRP channels; calcium imaging; capsaicin; chemesthesis; epigallocatechin gallate; hemiageusia

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