Loss of synaptic ribbons is an early cause in ROS-induced acquired sensorineural hearing loss

Kurasawa, Shunkou; Mohri, Hiroaki; Tabuchi, Keiji; Ueyama, Takehiko

doi:10.1016/j.nbd.2023.106280

Cited by 8 publications

(2 citation statements)

References 41 publications

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“…Glutamate excitotoxicity due to acoustic overstimulation contributes to the disruption of IHC synaptic ribbons, which occurs early after noise exposure [31]. Kurasawa et al reported that ROS lead to the degeneration of IHC synaptic ribbons with a decreased expression of Piccolo 1-a major component of synaptic ribbons [32]. ROS have been demonstrated to be one of the causes of cochlear synaptopathy in acquired sensorineural hearing loss.…”

Section: Discussionmentioning

confidence: 99%

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C-Phycocyanin Attenuates Noise-Induced Cochlear Synaptopathy via the Inhibition of Oxidative Stress and Intercellular Adhesion Molecule-1 in the Cochlea

Lin,

Shih,

Lin

et al. 2024

IJMS

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The synapses between inner hair cells (IHCs) and spiral ganglion neurons (SGNs) are the most vulnerable structures in the noise-exposed cochlea. Cochlear synaptopathy results from the disruption of these synapses following noise exposure and is considered the main cause of poor speech understanding in noisy environments, even when audiogram results are normal. Cochlear synaptopathy leads to the degeneration of SGNs if damaged IHC-SGN synapses are not promptly recovered. Oxidative stress plays a central role in the pathogenesis of cochlear synaptopathy. C-Phycocyanin (C-PC) has antioxidant and anti-inflammatory activities and is widely utilized in the food and drug industry. However, the effect of the C-PC on noise-induced cochlear damage is unknown. We first investigated the therapeutic effect of C-PC on noise-induced cochlear synaptopathy. In vitro experiments revealed that C-PC reduced the H2O2-induced generation of reactive oxygen species in HEI-OC1 auditory cells. H2O2-induced cytotoxicity in HEI-OC1 cells was reduced with C-PC treatment. After white noise exposure for 3 h at a sound pressure of 118 dB, the guinea pigs intratympanically administered 5 μg/mL C-PC exhibited greater wave I amplitudes in the auditory brainstem response, more IHC synaptic ribbons and more IHC-SGN synapses according to microscopic analysis than the saline-treated guinea pigs. Furthermore, the group treated with C-PC had less intense 4-hydroxynonenal and intercellular adhesion molecule-1 staining in the cochlea compared with the saline group. Our results suggest that C-PC improves cochlear synaptopathy by inhibiting noise-induced oxidative stress and the inflammatory response in the cochlea.

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Section: Discussionmentioning

confidence: 99%

“…These findings demonstrated that C-PC can attenuate noise-induced cochlear synaptopathy by scavenging ROS and inhibiting ICAM-1. Excessive ROS formation is one main cause of noise-induced damage to IHC synaptic ribbons [32]. Therefore, the antioxidant activity of C-PC plays a crucial role in the protection of IHC-SGN synapses.…”

Section: Discussionmentioning

confidence: 99%