Dynamics of cochlear synaptopathy after acoustic overexposure
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Recent work shows that acoustic overexposures causing only transient threshold elevation, and no hair cell loss, nevertheless can cause irreversible loss of the synapses between inner hair cells and cochlear nerve fibers (Kujawa and Liberman 2009). This cochlear synaptopathy, which is selective for the subset of sensory fibers with high thresholds and low spontaneous rates (Furman et al. 2013), appeared fully developed at 24-h post-exposure and showed no recovery by 8 weeks. However, prior studies of this synaptopathy counted only pre-synaptic ribbons, did not examine post-exposure times less than 24 h, and did not analyze the spatial patterns of degeneration around the hair cell circumference. Here, we immunostained for pre-synaptic ribbons, post-synaptic terminals and glutamate receptor patches, as well as the hair cell cytoplasm in noise-exposed and control mice to address the dynamics and spatial organization of the synaptopathic process as a function of post-exposure time from 0 h to 2 weeks. Our analysis showed that the loss of synaptic elements is nearly complete immediately after the 2-h exposure, that there is a reversible downregulation of gluR expression in the peripheral terminals which may be part of a protective mechanism, that there may be reversible reorganization of synaptic locations immediately after exposure, and that the spatial patterns are consistent with the idea that low-SR fibers are mainly found on the modiolar face of the hair cell and are the most vulnerable to noise-induced degeneration.
Keywordsauditory nerve inner ear synaptic ribbon glutamate receptor
This research was supported by grants from the NIDCD: R01 DC 0188 and P30 DC 05209.
Conflict of Interest
The authors have no financial conflicts of interest to declare.
- Fried MP, Dudek SE, Bohne BA (1976) Basal turn cochlear lesions following exposure to low-frequency noise. Trans Am Acad Ophthalmol Tolaryngol 82:285–298Google Scholar
- Kujawa SG, Micucci S, Liberman MC (2011) Noise-induced primary neural degeneration: effects of spectrum, duration, intensity and survival. In: Midwinter Meeting of the Association for Research in Otolaryngology, p 56Google Scholar
- Liberman MC, Kiang NY (1978) Acoustic trauma in cats. Cochlear pathology and auditory-nerve activity. Acta Otolaryngol 358:1–63Google Scholar
- Liberman MC, Mulroy MJ (1982) Acute and chronic effects of acoustic trauma: cochlear pathology and auditory nerve pathophysiology. In: New perspectives on noise-induced hearing loss (Hamernik RP, Henderson D, Salvi R, eds), pp 105–136.Google Scholar
- Matsubara A, Laake JH, Davanger S, Usami S, Ottersen OP (1996) Organization of AMPA receptor subunits at a glutamate synapse: a quantitative immunogold analysis of hair cell synapses in the rat organ of Corti. J Neurosci : Off J Soc Neurosci 16:4457–4467Google Scholar
- Narayan SS, Ruggero MA (2000) Basilar membrane mechanics at the hook region of the chinchilla cochlea. In: Recent developments in auditory mechanics (Wada H, Takasaka T, Ikeda K, Ohyama K, Koike T, eds), pp 95–101: World Scientific Press.Google Scholar
- Schmiedt RA, Schulte BA (1992) Physiologic and histopathologic changes in quiet- and noise-aged gerbil cochleas. In: Dancer AL, Henderson D, Salvi RJ, Hamernik RP (eds) Noise induced hearing loss. Mosby, St. Louis, pp 246–258Google Scholar