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TRPA1 activation in non-sensory supporting cells contributes to regulation of cochlear sensitivity after acoustic trauma.

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.

SUBMITTER: Velez-Ortega AC

PROVIDER: S-EPMC10313773 | biostudies-literature | 2023 Jun

REPOSITORIES: biostudies-literature

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TRPA1 activation in non-sensory supporting cells contributes to regulation of cochlear sensitivity after acoustic trauma.

Vélez-Ortega A Catalina AC Stepanyan Ruben R Edelmann Stephanie E SE Torres-Gallego Sara S Park Channy C Marinkova Desislava A DA Nowacki Joshua S JS Sinha Ghanshyam P GP Frolenkov Gregory I GI

Nature communications 20230630 1

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 Ca<sup>2+</sup> responses, which propagate across the organ of Corti and cause long-lasting contractions of pillar and Deiters' cells. Caged Ca<sup>2+</sup> experiments demonstrated that, similar to Deiters' cells, pillar cells als ...[more]

PMID: 37391431

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Project description:It is critical for hearing that the descending cochlear efferent system provides a negative feedback to hair cells to regulate hearing sensitivity and protect hearing from noise. The medial olivocochlear (MOC) efferent nerves project to outer hair cells (OHCs) to regulate OHC electromotility, which is an active cochlear amplifier and can increase hearing sensitivity. Here, we report that the MOC efferent nerves also could innervate supporting cells (SCs) in the vicinity of OHCs to regulate hearing sensitivity. MOC nerve fibers are cholinergic, and acetylcholine (ACh) is a primary neurotransmitter. Immunofluorescent staining showed that MOC nerve endings, presynaptic vesicular acetylcholine transporters (VAChTs), and postsynaptic ACh receptors were visible at SCs and in the SC area. Application of ACh in SCs could evoke a typical inward current and reduce gap junctions (GJs) between them, which consequently enhanced the direct effect of ACh on OHCs to shift but not eliminate OHC electromotility. This indirect, GJ-mediated inhibition had a long-lasting influence. In vivo experiments further demonstrated that deficiency of this GJ-mediated efferent pathway decreased the regulation of active cochlear amplification and compromised the protection against noise. In particular, distortion product otoacoustic emission (DPOAE) showed a delayed reduction after noise exposure. Our findings reveal a new pathway for the MOC efferent system via innervating SCs to control active cochlear amplification and hearing sensitivity. These data also suggest that this SC GJ-mediated efferent pathway may play a critical role in long-term efferent inhibition and is required for protection of hearing from noise trauma.NEW & NOTEWORTHY The cochlear efferent system provides a negative feedback to control hair cell activity and hearing sensitivity and plays a critical role in noise protection. We reveal a new efferent control pathway in which medial olivocochlear efferent fibers have innervations with cochlear supporting cells to control their gap junctions, therefore regulating outer hair cell electromotility and hearing sensitivity. This supporting cell gap junction-mediated efferent control pathway is required for the protection of hearing from noise.

Dataset Information

TRPA1 activation in non-sensory supporting cells contributes to regulation of cochlear sensitivity after acoustic trauma.

Publications

TRPA1 activation in non-sensory supporting cells contributes to regulation of cochlear sensitivity after acoustic trauma.

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