ArticleJournal of the Association for Research in Otolaryngology : JARO2026
A Diphtheria Toxin-Induced Mouse Model of Auditory Neuropathy: From Cochlear Synaptopathy to Neuronal Degeneration.
Article in Journal of the Association for Research in Otolaryngology : JARO, 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
purposeAuditory neuropathy (AN) is a hearing disorder that is often overlooked due to its hidden cochlear activity and hearing loss profiles. Diphtheria toxin (DT) is commonly used to induce deafness in conditional gene knockout mouse models, but its ototoxic targets in wild-type animals remain controversial. This study aimed to characterize the pathogenic effects of DT on the cochlea of wild-type mice and establish a reliable model of AN.
methodsAdult CBA/CaJ mice of both sexes (n = 81) were administered by DT for three consecutive days. AN was confirmed by electrophysiological profiles: abnormal auditory brainstem response (ABR) with preserved distortion product otoacoustic emissions (DPOAE), followed by histopathological evaluation of the cochlear auditory pathway.
resultsDT induced a characteristic AN-characteristic hearing loss in mice. It initiated with ribbon synapse degeneration in inner hair cells (IHCs) within 24 h, coinciding with a significant reduction in ABR amplitude peak I. By post-injection day 3, extensive damage was observed, including IHC loss, degeneration of type I spiral ganglion neurons (SGNs), and demyelination of their axons. Despite a minimal loss of OHCs (~ 2.1%), OHC function remained intact as evidenced by DPOAE. A progressive degeneration of SGNs and demyelination of axons persisted over the 21-day observation period.
conclusionOur findings demonstrate that DT selectively targets the IHCs and type I afferent pathway in wild-type mice, resulting in a progressive AN- characteristic pathology. This study establishes a mouse model of AN that can serve as a basis for further investigation into the mechanisms underlying similar pathologies.
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