ArticleJournal of the Association for Research in Otolaryngology : JARO2019
Rapamycin Protects Spiral Ganglion Neurons from Gentamicin-Induced Degeneration In Vitro.
Article in Journal of the Association for Research in Otolaryngology : JARO, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Biohybrid cochlear implants: neural interfaces, regenerative pathways, and translational benchmarks.Journal of neuroengineering and rehabilitation · 2026Review
- Autophagy in Sensorineural Hearing Loss: Jekyll or Hyde?International journal of molecular sciences · 2026Review
- The mTOR Pathway in Hearing Disorders: Mechanistic Links to Aging, Regeneration, and Neurodegeneration.Molecular neurobiology · 2026Review
- Protective Effects of (-)-Butaclamol Against Gentamicin-Induced Ototoxicity: In Vivo and In Vitro Approaches.International journal of molecular sciences · 2025Article
- Experimental and clinical tests of FDA-approved kinase inhibitors for the treatment of neurological disorders (update 2024).Exploration of drug science · 2025Article
- Article
- Activated tissue-resident macrophages contribute to hair cell insults in noise-induced hearing loss in mice.Communications biology · 2024Article
- A Low Dose of Rapamycin Promotes Hair Cell Differentiation by Enriching SOX2Journal of the Association for Research in Otolaryngology : JARO · 2024Article
- The cochlea is built to last a lifetime.Hearing research · 2023Review
- FDA-Approved Kinase Inhibitors in Preclinical and Clinical Trials for Neurological Disorders.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Cellular autophagy, the compelling roles in hearing function and dysfunction.Frontiers in cellular neuroscience · 2022Review
- PRDX1 activates autophagy via the PTEN-AKT signaling pathway to protect against cisplatin-induced spiral ganglion neuron damage.Autophagy · 2021Article
- Review
- mTOR Signaling in the Inner Ear as Potential Target to Treat Hearing Loss.International journal of molecular sciences · 2021Review
- Programmed cell death pathways in hearing loss: A review of apoptosis, autophagy and programmed necrosis.Cell proliferation · 2020Review
- Low-dose rapamycin-induced autophagy in cochlear outer sulcus cells.Laryngoscope investigative otolaryngology · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gentamicin, one of the most widely used aminoglycoside antibiotics, is known to have toxic effects on the inner ear. Taken up by cochlear hair cells and spiral ganglion neurons (SGNs), gentamicin induces the accumulation of reactive oxygen species (ROS) and initiates apoptosis or programmed cell death, resulting in a permanent and irreversible hearing loss. Since the survival of SGNs is specially required for cochlear implant, new procedures that prevent SGN cell loss are crucial to the success of cochlear implantation. ROS modulates the activity of the mammalian target of rapamycin (mTOR) signaling pathway, which mediates apoptosis or autophagy in cells of different organs. However, whether mTOR signaling plays an essential role in the inner ear and whether it is involved in the ototoxic side effects of gentamicin remain unclear. In the present study, we found that gentamicin induced apoptosis and cell loss of SGNs in vivo and significantly decreased the density of SGN and outgrowth of neurites in cultured SGN explants. The phosphorylation levels of ribosomal S6 kinase and elongation factor 4E binding protein 1, two critical kinases in the mTOR complex 1 (mTORC1) signaling pathway, were modulated by gentamicin application in the cochlea. Meanwhile, rapamycin, a specific inhibitor of mTORC1, was co-applied with gentamicin to verify the role of mTOR signaling. We observed that the density of SGN and outgrowth of neurites were significantly increased by rapamycin treatment. Our finding suggests that mTORC1 is hyperactivated in the gentamicin-induced degeneration of SGNs, and rapamycin promoted SGN survival and outgrowth of neurites.
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