ArticleMolecular neurobiology2013
Cochlear inner hair cell ribbon synapse is the primary target of ototoxic aminoglycoside stimuli.
Article in Molecular neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 84 citations in OpenAlex.
- TRPV4 mediates aminoglycoside trafficking and ototoxicity without compromising antimicrobial efficacy.Cell death discovery · 2026Article
- TNF-α impairs the stria vascularis by inducing pericyte apoptosis via the NF-κB pathway in gentamicin-induced hearing loss.Journal of neuroinflammation · 2026Article
- Combined Effects of Low-Dose Kanamycin and Noise Exposure on Auditory Brainstem Response and Cochlear Microphonic Potential in Guinea Pigs.Iranian journal of child neurology · 2026Article
- Hair cell loss - cause or consequence of hearing loss?Frontiers in cell and developmental biology · 2026Review
- Impact of repeated intranasal gentamicin irrigation on auditory brainstem evoked potentials in rats.Experimental brain research · 2024Article
- The human OPA1Cellular and molecular life sciences : CMLS · 2024Article
- ROS-induced oxidative stress and mitochondrial dysfunction: a possible mechanism responsible for noise-induced ribbon synaptic damage.American journal of translational research · 2024Article
- Mechanisms and Impact of Aminoglycoside-Induced Vestibular Deficits.American journal of audiology · 2023Review
- Aminoglycosides-Related Ototoxicity: Mechanisms, Risk Factors, and Prevention in Pediatric Patients.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Wideband Acoustic Reflex Measurement.Seminars in hearing · 2023Review
- c-Myb protects cochlear hair cells from cisplatin-induced damage via the PI3K/Akt signaling pathway.Cell death discovery · 2022Article
- Putative COVID-19 therapies imatinib, lopinavir, ritonavir, and ivermectin cause hair cell damage: A targeted screen in the zebrafish lateral line.Frontiers in cellular neuroscience · 2022Article
- Multiple Sevoflurane Exposures During the Neonatal Period Cause Hearing Impairment and Loss of Hair Cell Ribbon Synapses in Adult Mice.Frontiers in neuroscience · 2022Article
- Telmisartan Attenuates Kanamycin-Induced Ototoxicity in Rats.International journal of molecular sciences · 2021Article
- [Research progress in auditory center plasticity and tinnitus mechanism].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2021Review
- Functional Impacts of Aminoglycoside Treatment on Speech Perception and Extended High-Frequency Hearing Loss in a Pediatric Cystic Fibrosis Cohort.American journal of audiology · 2021Article
- Wideband Acoustic Reflex Growth in Adults With Cystic Fibrosis.American journal of audiology · 2021Article
- Mechanisms of Aminoglycoside- and Cisplatin-Induced Ototoxicity.American journal of audiology · 2021Review
- Generation and characterization of a P2rx2 V60L mouse model for DFNA41.Human molecular genetics · 2021Article
- Activity-Dependent Neurodegeneration and Neuroplasticity of Auditory Neurons Following Conductive Hearing Loss in Adult Mice.Cellular and molecular neurobiology · 2021Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ribbon synapses of inner hair cells (IHCs) play an important role in sound encoding and neurotransmitter release. However, it remains unclear whether IHC ribbon synapse plasticity can be interrupted by ototoxic aminoglycoside stimuli. Here, we report that quantitative changes in the number of IHC ribbon synapses and hearing loss occur in response to gentamicin treatment in mice. Using 3D reconstruction, we were able to calculate the number of IHC ribbon synapses after ototoxic gentamicin exposure. Mice were injected intraperitoneally with a low dose of gentamicin (100 mg/kg) once a day for 14 days. Double immunostaining was used to identify IHC ribbon synapses; histopathology and scanning electron microscopy were used to observe the morphology of cochlear hair cells and spiral ganglion neurons (SGNs), the hearing threshold shifts were recorded by auditory brainstem response examinations. Our study shows that the maximal number of IHC ribbon synapses appeared at the 7th day after treatment, followed by a significant reduction after the 7th day regardless of ongoing treatment. Correspondingly, the maximal elevation of hearing threshold was observed at the 7th day after treatment. Meanwhile, additional cochlear components included OHCs, IHCs, and SGNs were unaffected, suggesting that IHC ribbon synapses are more susceptible to ototoxic aminoglycoside stimulation. Our study indicated that quantitative changes in the number of IHC ribbon synapses is critical response to lower dose of ototoxic stimulation, and may contribute to moderate hearing loss. Additionally, our data indcated that ribbon synaptic plasticity may require the quantitative changes to play self-protective role adapted to ototoxic aminoglycoside stimuli.
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