TRPA1 activation in non-sensory supporting cells contributes to regulation of cochlear sensitivity after acoustic trauma.
| Title: | TRPA1 activation in non-sensory supporting cells contributes to regulation of cochlear sensitivity after acoustic trauma. |
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| Authors: | Vélez-Ortega AC; Department of Physiology, College of Medicine, University of Kentucky, Lexington, KY, 40536, USA. catavelezo@uky.edu.; Stepanyan R; Department of Physiology, College of Medicine, University of Kentucky, Lexington, KY, 40536, USA.; Department of Otolaryngology, Case Western Reserve University, Cleveland, OH, 44106, USA.; Edelmann SE; Department of Physiology, College of Medicine, University of Kentucky, Lexington, KY, 40536, USA.; Torres-Gallego S; Department of Physiology, College of Medicine, University of Kentucky, Lexington, KY, 40536, USA.; Park C; Department of Head & Neck Surgery, David Geffen School of Medicine, UCLA, Los Angeles, CA, 90095, USA.; Marinkova DA; Department of Physiology, College of Medicine, University of Kentucky, Lexington, KY, 40536, USA.; Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR, 72205, USA.; Nowacki JS; Department of Physiology, College of Medicine, University of Kentucky, Lexington, KY, 40536, USA.; Sinha GP; Department of Physiology, College of Medicine, University of Kentucky, Lexington, KY, 40536, USA.; Department of Anesthesiology and Perioperative Medicine, University of Pittsburgh, Pittsburgh, PA, 15261, USA.; Frolenkov GI; Department of Physiology, College of Medicine, University of Kentucky, Lexington, KY, 40536, USA. Gregory.Frolenkov@uky.edu. |
| Source: | Nature communications [Nat Commun] 2023 Jun 30; Vol. 14 (1), pp. 3871. Date of Electronic Publication: 2023 Jun 30. |
| Publication Type: | Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
| Language: | English |
| Journal Info: | Publisher: Nature Pub. Group Country of Publication: England NLM ID: 101528555 Publication Model: Electronic Cited Medium: Internet ISSN: 2041-1723 (Electronic) Linking ISSN: 20411723 NLM ISO Abbreviation: Nat Commun Subsets: MEDLINE |
| Imprint Name(s): | Original Publication: [London] : Nature Pub. Group |
| MeSH Terms: | TRPA1 Cation Channel*/genetics ; Hearing Loss, Noise-Induced*; Animals ; Mice ; Cochlea ; Epithelial Cells ; Evoked Potentials, Auditory, Brain Stem ; Labyrinth Supporting Cells |
| Abstract: | TRPA1 channels are expressed in nociceptive neurons, where they detect noxious stimuli, and in the mammalian cochlea, where their function is unknown. Here we show that TRPA1 activation in the supporting non-sensory Hensen's cells of the mouse cochlea causes prolonged Ca2+ responses, which propagate across the organ of Corti and cause long-lasting contractions of pillar and Deiters' cells. Caged Ca2+ experiments demonstrated that, similar to Deiters' cells, pillar cells also possess Ca2+-dependent contractile machinery. TRPA1 channels are activated by endogenous products of oxidative stress and extracellular ATP. Since both these stimuli are present in vivo after acoustic trauma, TRPA1 activation after noise may affect cochlear sensitivity through supporting cell contractions. Consistently, TRPA1 deficiency results in larger but less prolonged noise-induced temporary shift of hearing thresholds, accompanied by permanent changes of latency of the auditory brainstem responses. We conclude that TRPA1 contributes to the regulation of cochlear sensitivity after acoustic trauma.; (© 2023. The Author(s).) |
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| Grant Information: | S10 RR027400 United States RR NCRR NIH HHS; R01 DC014658 United States DC NIDCD NIH HHS; R01 DC009434 United States DC NIDCD NIH HHS |
| Substance Nomenclature: | 0 (TRPA1 Cation Channel); 0 (Trpa1 protein, mouse) |
| Entry Date(s): | Date Created: 20230630 Date Completed: 20230707 Latest Revision: 20231117 |
| Update Code: | 20260130 |
| PubMed Central ID: | PMC10313773 |
| DOI: | 10.1038/s41467-023-39589-w |
| PMID: | 37391431 |
| Database: | MEDLINE |
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't