Noise induced reversible changes of cochlear ribbon synapses contribute to temporary hearing loss in mice

Abstract

Conclusion: Noise exposure can cause a decline in cochlear ribbon synapses and result in consequent hearing loss. The reduction of synaptic puncta appears reversible and may contribute to hearing restoration in mice after noise exposure. Objective: To detect whether noise induced reversible changes of cochlear ribbon synapses contribute to temporary hearing loss in C57BL/6J mice. Methods: The mice were assigned randomly to five groups and exposed to white noise at 110 dB SPL for 2 h except the control group. ABR thresholds were acquired before noise exposure (control), immediately following exposure (Day 0), or on Days 4, 7, or 14 after noise exposure. Light microscopy, scanning emission microscopy, and whole mounts examination was utilized to study whether there is morphology change of outer hair cells (OHC), inner hair cells (IHC), or spiral ganglion cells (SGN) due to the 110 dB white noise. Moreover, experimental approaches, including immunostaining and confocal microcopy, were used to detect whether ribbon synapses were the primary targets of noise-induced temporary hearing loss. Result: Exposure to 110 dB white noise for 2 h induced TTS in mice, with the maximal ABR threshold elevations seen on the 4^th day after noise exposure. There were no significant morphological changes in the cochlea. Paralleled changes of pre-synaptic ribbons in both the number and post-synaptic density (PSDs) during this noise exposure were detected. The number of pre-synaptic ribbon, post-synaptic density (PSDs), and co-localized puncta correlated with the shifts of ABR thresholds. Moreover, a complete recovery of ABR thresholds and synaptic puncta was seen on the 14^th day after the noise stimulations.

Keywords:

• Noise exposure
• hearing impairment
• ribbon synapse plasticity
• inner hair cell

Acknowledgments

This work was supported by grants from the National Basic Research Program of China (973Program) (2012CB967900; 2012CB967901) and the National Natural Science Foundation of China (NSFC) (31040038). Additionally, this work was supported by grants from the China Postdoctoral Science Foundation (201003779; 20100470103), and Beijing Natural Science Foundation (5122040).

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.