Coding deficits in hidden hearing loss induced by noise: the nature and impacts

Song, Qiang; Shen, Pei‐Hong; Li, Xiaowei; Shi, Lijuan; Liu, Lijie; Wang, Jiping; Zhong, Yu; Stephen, Kegan; Aiken, Steven J.; Yin, Shankai; Wang, Jian

doi:10.1038/srep25200

Cited by 101 publications

(118 citation statements)

References 32 publications

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“…In both mice (Liberman et al, 2015) and guinea pigs (Furman et al, 2013; Song et al, 2016), surviving ribbons in noise-damaged regions were often larger than normal. Surviving ribbons were also hypertrophied in the noise-exposed macaques (see Fig.…”

Section: Resultsmentioning

confidence: 99%

Noise-induced cochlear synaptopathy in rhesus monkeys ( Macaca mulatta )

et al. 2017

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Cochlear synaptopathy can result from various insults, including acoustic trauma, aging, ototoxicity, or chronic conductive hearing loss. For example, moderate noise exposure in mice can destroy up to ∼50% of synapses between auditory nerve fibers (ANFs) and inner hair cells (IHCs) without affecting outer hair cells (OHCs) or thresholds, because the synaptopathy occurs first in high-threshold ANFs. However, the fiber loss likely impairs temporal processing and hearing-in-noise, a classic complaint of those with sensorineural hearing loss. Non-human primates appear to be less vulnerable to noise-induced hair-cell loss than rodents, but their susceptibility to synaptopathy has not been studied. Because establishing a non-human primate model may be important in the development of diagnostics and therapeutics, we examined cochlear innervation and the damaging effects of acoustic overexposure in young adult rhesus macaques. Anesthetized animals were exposed bilaterally to narrow-band noise centered at 2 kHz at various sound-pressure levels for 4 hrs. Cochlear function was assayed for up to 8 weeks following exposure via auditory brainstem responses (ABRs) and otoacoustic emissions (OAEs). A moderate loss of synaptic connections (mean of 12-27% in the basal half of the cochlea) followed temporary threshold shifts (TTS), despite minimal hair-cell loss. A dramatic loss of synapses (mean of 50-75% in the basal half of the cochlea) was seen on IHCs surviving noise exposures that produced permanent threshold shifts (PTS) and widespread hair-cell loss. Higher noise levels were required to produce PTS in macaques compared to rodents, suggesting that primates are less vulnerable to hair-cell loss. However, the phenomenon of noise-induced cochlear synaptopathy in primates is similar to that seen in rodents.

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Section: Resultsmentioning

confidence: 99%

Noise-induced cochlear synaptopathy in rhesus monkeys ( Macaca mulatta )

et al. 2017

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“…However, comparable noise-exposure studies in guinea pigs have suggested that, after an initial reduction in the number of presynaptic ribbons, the synapse count may largely recover (Liu et al., 2012, Shi et al., 2013). It appears as though these synapses are reformed to some degree, but although they are present, their coding properties are functionally abnormal, both in their amplitude and latency profiles (Song et al., 2016). These studies suggest clear differences in the manifestation of cochlear synaptopathy in the guinea pig compared to the mouse and they also report ribbon damage to high-SR units as well as the more widely demonstrated loss of low-SR fibers.…”

Section: Discussionmentioning

confidence: 99%

Effects of noise exposure on young adults with normal audiograms I: Electrophysiology

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et al. 2017

Hearing Research

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Noise-induced cochlear synaptopathy has been demonstrated in numerous rodent studies. In these animal models, the disorder is characterized by a reduction in amplitude of wave I of the auditory brainstem response (ABR) to high-level stimuli, whereas the response at threshold is unaffected. The aim of the present study was to determine if this disorder is prevalent in young adult humans with normal audiometric hearing. One hundred and twenty six participants (75 females) aged 18–36 were tested. Participants had a wide range of lifetime noise exposures as estimated by a structured interview. Audiometric thresholds did not differ across noise exposures up to 8 kHz, although 16-kHz audiometric thresholds were elevated with increasing noise exposure for females but not for males. ABRs were measured in response to high-pass (1.5 kHz) filtered clicks of 80 and 100 dB peSPL. Frequency-following responses (FFRs) were measured to 80 dB SPL pure tones from 240 to 285 Hz, and to 80 dB SPL 4 kHz pure tones amplitude modulated at frequencies from 240 to 285 Hz (transposed tones). The bandwidth of the ABR stimuli and the carrier frequency of the transposed tones were chosen to target the 3–6 kHz characteristic frequency region which is usually associated with noise damage in humans. The results indicate no relation between noise exposure and the amplitude of the ABR. In particular, wave I of the ABR did not decrease with increasing noise exposure as predicted. ABR wave V latency increased with increasing noise exposure for the 80 dB peSPL click. High carrier-frequency (envelope) FFR signal-to-noise ratios decreased as a function of noise exposure in males but not females. However, these correlations were not significant after the effects of age were controlled. The results suggest either that noise-induced cochlear synaptopathy is not a significant problem in young, audiometrically normal adults, or that the ABR and FFR are relatively insensitive to this disorder in young humans, although it is possible that the effects become more pronounced with age.

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“…Noise-induced synaptopathy in guinea pigs requires higher sound levels than in mice and long-term degeneration of spiral ganglion cells is less pronounced (Lin et al., 2011). In stark contrast with mouse data, guinea pig synapses damaged by noise appear largely repairable (Liu et al., 2012, Shi et al., 2013), leading to only transient changes in the distribution of spontaneous rates among AN fibers (Song et al., 2016). Early indications from a macaque model suggest that primates may exhibit even greater resistance to noise-induced synaptopathy (Burton et al., 2016).…”

Section: Discussionmentioning

confidence: 99%

Tinnitus with a normal audiogram: Relation to noise exposure but no evidence for cochlear synaptopathy

et al. 2017

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In rodents, exposure to high-level noise can destroy synapses between inner hair cells and auditory nerve fibers, without causing hair cell loss or permanent threshold elevation. Such “cochlear synaptopathy” is associated with amplitude reductions in wave I of the auditory brainstem response (ABR) at moderate-to-high sound levels. Similar ABR results have been reported in humans with tinnitus and normal audiometric thresholds, leading to the suggestion that tinnitus in these cases might be a consequence of synaptopathy. However, the ABR is an indirect measure of synaptopathy and it is unclear whether the results in humans reflect the same mechanisms demonstrated in rodents. Measures of noise exposure were not obtained in the human studies, and high frequency audiometric loss may have impacted ABR amplitudes. To clarify the role of cochlear synaptopathy in tinnitus with a normal audiogram, we recorded ABRs, envelope following responses (EFRs), and noise exposure histories in young adults with tinnitus and matched controls. Tinnitus was associated with significantly greater lifetime noise exposure, despite close matching for age, sex, and audiometric thresholds up to 14 kHz. However, tinnitus was not associated with reduced ABR wave I amplitude, nor with significant effects on EFR measures of synaptopathy. These electrophysiological measures were also uncorrelated with lifetime noise exposure, providing no evidence of noise-induced synaptopathy in this cohort, despite a wide range of exposures. In young adults with normal audiograms, tinnitus may be related not to cochlear synaptopathy but to other effects of noise exposure.

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Coding deficits in hidden hearing loss induced by noise: the nature and impacts

Cited by 101 publications

References 32 publications

Noise-induced cochlear synaptopathy in rhesus monkeys ( Macaca mulatta )

Noise-induced cochlear synaptopathy in rhesus monkeys ( Macaca mulatta )

Effects of noise exposure on young adults with normal audiograms I: Electrophysiology

Tinnitus with a normal audiogram: Relation to noise exposure but no evidence for cochlear synaptopathy

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