ArticleFrontiers in molecular neuroscience2026
The aryl hydrocarbon receptor is expressed in non-sensory cells in the cochlea and regulates hair cell survival.
Article in Frontiers in molecular neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Damage or loss of hair cells, the sensory cells for hearing, is caused by ototoxic drugs or acoustic trauma, and results in permanent hearing loss because the adult cochlea lacks regenerative capacity. Therefore, identifying pathways that regulate hair cell survival is critical. Here we investigate a novel pathway, aryl hydrocarbon receptor (AhR) signaling in the cochlea. We demonstrate for the first time, the expression pattern of AhR in the cochlea under physiological conditions and after exposure to neomycin or noise. Under physiological conditions, AhR was strongly expressed in glia surrounding spiral ganglion neurons with low expression in the organ of Corti. Following neomycin treatment or noise exposure, AhR expression increased in supporting cells suggesting a dynamic response to hair cell injury. This hair cell to supporting cell communication is mediated in part by purinergic signaling, since treatment with ATP mimicked the effect of neomycin, and treatment with the purinergic antagonist suramin eliminated AhR upregulation. In addition, deletion of
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