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| Poster #284 Identifying mechanisms of astringency transduction |
| Mikaéla Murph1, Anisa Seenauth1, Keylin Escobar2, Yalda Moayedi1 1New York University College of Dentistry, New York, NY, United States 2Columbia University, New York, NY, United States |
Astringency is defined as a dry, rough, and puckering sensation that is associated with phenolic compounds, known as tannins, that are present in many plant-based foods. Astringency sensation depends on the activation of trigeminal neurons, suggesting that transduction depends on somatosensation rather than taste. Chemosensory and mechanical mechanisms of phenolic compound transduction have been proposed, with evidence supporting both mechanisms. Using a combination of calcium imaging and brief access preference testing behavioral assays, our data suggests that a mechanosensory subpopulation of trigeminal neurons are activated directly by tannic acid through chemotransduction, providing a potential mechanism for astringency sensation. Preliminary in vivo calcium imaging suggests that trigeminal mechanosensory neurons that respond to tannic acid are responsive to stroking but not pressure, a response profile that is highly represented by a subpopulation of trigeminal neurons labelled by Vglut3. We found that 40% of Vglut3lineage neurons respond to tannic acid in vivo, suggesting that Vglut3lineage neurons may be involved in transduction of tannic acid. Through in vitro calcium imaging we have found that tannic acid responsive neurons are enriched in the Vglut3lineage subpopulation and respond in the absence of mucosa and saliva, indicating that epithelial intermediates are not required for astringency transduction. Our behavior assays show that while astringency aversion is only mildly affected by olfaction and taste, selective inhibition of Vglut3lineage neurons reduces aversion to tannic acid. Collectively, our results suggest a role for Vglut3lineage neurons in astringency transduction and sensation. |