Noise-Induced Cochlear Synaptopathy and Ribbon Synapse Regeneration: Repair Process and Therapeutic Target

Wang, Jian; Yin, Shankai; Chen, Hengchao; Shi, Lijuan

doi:10.1007/978-981-13-6123-4_3

Cited by 13 publications

(7 citation statements)

References 105 publications

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“…Ribbon synapses are vital structures between inner HC and SGNs, which are the primary synaptic structures in the sound conduction pathway and play an important role in sound signal transmission [ 30 – 32 ]. Previous studies have shown that ribbon synapses are highly sensitive to noise in the cochlea [ 33 – 35 ]. Here, we found that SS-induced tinnitus did not cause the elevations of hearing threshold or cause loss of cochlear HCs.…”

Section: Discussionmentioning

confidence: 99%

Loss of Cochlear Ribbon Synapse Is a Critical Contributor to Chronic Salicylate Sodium Treatment-Induced Tinnitus without Change Hearing Threshold

Zhang

Peng

et al. 2020

Neural Plasticity

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Tinnitus is a common auditory disease worldwide; it is estimated that more than 10% of all individuals experience this hearing disorder during their lifetime. Tinnitus is sometimes accompanied by hearing loss. However, hearing loss is not acquired in some other tinnitus generations. In this study, we injected adult rats with salicylate sodium (SS) (200 mg/kg/day for 10 days) and found no significant hearing threshold changes at 2, 4, 8, 12, 14, 16, 20, or 24 kHz (all p>0.05). Tinnitus was confirmed in the treated rats via Behaviour Testing of Acoustic Startle Response (ASR) and Gap Prepulse Inhibition Test of Acoustic Startle Reflex (GPIAS). A immunostaining study showed that there is significant loss of anti-CtBP2 puncta (a marker of cochlear inner hair cell (HC) ribbon synapses) in treated animals in apical, middle, and basal turns (all p<0.05). The ABR wave I amplitudes were significantly reduced at 4, 8, 12, 14, 16, and 20 kHz (all p<0.05). No significant losses of outer HCs, inner HCs, or HC cilia were observed (all p>0.05). Thus, our study suggests that loss of cochlear inner HC ribbon synapse after SS exposure is a contributor to the development of tinnitus without changing hearing threshold.

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Section: Discussionmentioning

confidence: 99%

Loss of Cochlear Ribbon Synapse Is a Critical Contributor to Chronic Salicylate Sodium Treatment-Induced Tinnitus without Change Hearing Threshold

Zhang

Peng

et al. 2020

Neural Plasticity

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“…A previous study showed that excitatory receptors activated by released glutamate and glycine are responsible for noise trauma‐induced impairment of cochleae, [ 38 ] so neural cell line maybe suitable for deafness drug screening. To further study noise‐induced neuropathy, we mimicked noise‐induced hearing loss in vitro by exposing Neuro‐2a cells, a mouse neuroblastoma (neural crest‐derived) cell line, to glutamate excitotoxicity, which causes cell death.…”

Section: Resultsmentioning

confidence: 99%

Personalized Porous Gelatin Methacryloyl Sustained‐Release Nicotinamide Protects Against Noise‐Induced Hearing Loss

Feng,

Dong,

Song

et al. 2024

Advanced Science

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There are no Food and Drug Administration‐approved drugs for treating noise‐induced hearing loss (NIHL), reflecting the absence of clear specific therapeutic targets and effective delivery strategies. Noise trauma is demonstrated results in nicotinamide adenine dinucleotide (NAD+) downregulation and mitochondrial dysfunction in cochlear hair cells (HCs) and spiral ganglion neurons (SGNs) in mice, and NAD+ boosted by nicotinamide (NAM) supplementation maintains cochlear mitochondrial homeostasis and prevents neuroexcitatory toxic injury in vitro and ex vivo, also significantly ameliorated NIHL in vivo. To tackle the limited drug delivery efficiency due to sophisticated anatomical barriers and unique clearance pathway in ear, personalized NAM‐encapsulated porous gelatin methacryloyl (PGMA@NAM) are developed based on anatomy topography of murine temporal bone by micro‐computed tomography and reconstruction of round window (RW) niche, realizing hydrogel in situ implantation completely, NAM sustained‐release and long‐term auditory preservation in mice. This study strongly supports personalized PGMA@NAM as NIHL protection drug with effective inner ear delivery, providing new inspiration for drug‐based treatment of NIHL.

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“…The treatment modalities for blast-induced hearing loss involving cochlear synaptopathy or stereociliary bundle disruption can be applied to other types of SNHL with the same underlying pathology. As mentioned above, our blast-induced hearing loss models also represented cochlear synaptopathy, which is a good target for SNHL treatment 42 . Recent studies have revealed that neurotrophin-3 43 and Rho-associated coiled-coil containing protein kinase inhibitor 44 confer protective or regenerative effects against the loss of ribbon synapses after inner ear damage.…”

Section: Discussionmentioning

confidence: 99%

Effect of shock wave power spectrum on the inner ear pathophysiology in blast-induced hearing loss

Kimura

Mizutari

Kurioka

et al. 2021

Sci Rep

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Blast exposure can induce various types of hearing impairment, including permanent hearing loss, tinnitus, and hyperacusis. Herein, we conducted a detailed investigation of the cochlear pathophysiology in blast-induced hearing loss in mice using two blasts with different characteristics: a low-frequency dominant blast generated by a shock tube and a high-frequency dominant shock wave generated by laser irradiation (laser-induced shock wave). The pattern of sensorineural hearing loss (SNHL) was low-frequency- and high-frequency-dominant in response to the low- and high-frequency blasts, respectively. Pathological examination revealed that cochlear synaptopathy was the most frequent cochlear pathology after blast exposure, which involved synapse loss in the inner hair cells without hair cell loss, depending on the power spectrum of the blast. This pathological change completely reflected the physiological analysis of wave I amplitude using auditory brainstem responses. Stereociliary bundle disruption in the outer hair cells was also dependent on the blast’s power spectrum. Therefore, we demonstrated that the dominant frequency of the blast power spectrum was the principal factor determining the region of cochlear damage. We believe that the presenting models would be valuable both in blast research and the investigation of various types of hearing loss whose pathogenesis involves cochlear synaptopathy.

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Noise-Induced Cochlear Synaptopathy and Ribbon Synapse Regeneration: Repair Process and Therapeutic Target

Cited by 13 publications

References 105 publications

Loss of Cochlear Ribbon Synapse Is a Critical Contributor to Chronic Salicylate Sodium Treatment-Induced Tinnitus without Change Hearing Threshold

Loss of Cochlear Ribbon Synapse Is a Critical Contributor to Chronic Salicylate Sodium Treatment-Induced Tinnitus without Change Hearing Threshold

Personalized Porous Gelatin Methacryloyl Sustained‐Release Nicotinamide Protects Against Noise‐Induced Hearing Loss

Effect of shock wave power spectrum on the inner ear pathophysiology in blast-induced hearing loss

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