Noise-induced Cochlear Synaptopathy and Signal Processing Disorders

Chen, Hengchao; Shi, Lijuan; Liu, Lijie; Yin, Shankai; Aiken, Steven J.; Wang, Jian

doi:10.1016/j.neuroscience.2018.09.026

Cited by 35 publications

(28 citation statements)

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“…It has been widely accepted that noise may induced damage on IHCs and SGNs in the cochlea [17], including synaptopathy, which is one of the main reasons of HHL. Increasing evidence has shown that exposure to even a single dose of high-intensity noise can generate a substantial degree of cochlear synaptopathy [2,18].…”

Section: Discussionmentioning

confidence: 99%

“…In animal studies showing the temporary elevation in hearing thresholds caused by noise exposure, there may be reduced neural responses in an adaptive way, and theoretically the HHL-like state quickly recovers. It has been known that after a single, brief noise exposure, the damaged and the totally destroyed synapses can be partially repaired, but the repaired synapses are functionally abnormal [17]. The mechanism underlying noise induced threshold elevation and hearing recovery is closely related to IHC functions, especially cochlear synapse plasticity.…”

Section: Discussionmentioning

confidence: 99%

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Hidden hearing loss is associated with loss of ribbon synapses of cochlea inner hair cells

et al. 2021

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This study aimed to observe the changes in the cochlea ribbon synapses after repeated exposure to moderate-to-high intensity noise. Guinea pigs received 95 dB SPL white noise exposure 4 hours a day for consecutive 7 days (we regarded it a medium-term and moderate-intensity noise, or MTMI noise). Animals were divided into 4 groups: Control, 1DPN (1-day post noise), 1WPN (1-week post noise), and 1MPN (1-month post noise). Auditory function analysis by ABR and CAP recordings, as well as ribbon synapse morphological analyses by immunohistochemistry (Ctbp2 and PSD95 staining) were performed one day, one week, and one month after noise exposure. After MTMI noise exposure, the amplitudes of auditory brainstem response (ABR) I and III waves were suppressed. The compound action potential (CAP) threshold was elevated, and CAP amplitude was reduced in the 1DPN group. No apparent changes in hair cell shape, arrangement or number were observed, but the number of ribbon synapse was reduced. The 1WPN and 1MPN groups showed that part of ABR and CAP changes recovered, as well as the synapse number. The defects in cochlea auditory function and synapse changes were observed mainly in the high-frequency region. Together, repeated exposure in MTMI noise can cause hidden hearing loss, which is partially reversible after leaving the noise environment; and MTMI noise induced hidden hearing loss is associated with inner hair cell ribbon synapses.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Hidden hearing loss is associated with loss of ribbon synapses of cochlea inner hair cells

et al. 2021

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“…This group of auditory never fibers has a high threshold, larger dynamic range and is therefore critical for coding sound at higher intensity levels and against a background noise (Liberman, 1978(Liberman, , 1980Liberman and Kiang, 1984;Tsuji and Liberman, 1997;Taberner and Liberman, 2005;Liberman et al, 2011). Second, the interrupted synapses can be partially re-established (Shi et al, 2013(Shi et al, , 2015aKaur et al, 2019;Kim et al, 2019), but the repaired synapses have been found to have coding deficits (Shi et al, 2015a(Shi et al, , 2016Song et al, 2016;Chen et al, 2019a). Since the noise-induced synaptic damage, or synaptopathy, can be established by noise without causing hearing loss defined by a threshold shift per se, noise-induced hidden hearing loss has been used as an umbrella term to reflect the functional deficits at suprathreshold levels (Moser and Starr, 2016;Plack et al, 2016;Song et al, 2016;Kobel et al, 2017;Liberman and Kujawa, 2017;Liberman, 2017;Lobarinas et al, 2017;Chen et al, 2019a).…”

Section: Introductionmentioning

confidence: 99%

Pre-exposure to Lower-Level Noise Mitigates Cochlear Synaptic Loss Induced by High-Level Noise

Fan

Zhang

Wang

et al. 2020

Front. Syst. Neurosci.

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The auditory sensory organs appear to be less damaged by exposure to high-level noise that is presented after exposure to non-traumatizing low-level noise. This phenomenon is known as the toughening or conditioning effect. Functionally, it is manifested by a reduced threshold shift, and morphologically by a reduced hair cell loss. However, it remains unclear whether prior exposure to toughening noise can mitigate the synaptic loss induced by exposure to damaging noise. Since the cochlear afferent synapse between the inner hair cells and primary auditory neurons has been identified as a novel site involved in noise-induced cochlear damage, we were interested in assessing whether this synapse can be toughened. In the present study, the synaptic loss was induced by a damaging noise exposure (106 dB SPL) and compared across Guinea pigs who had and had not been previously exposed to a toughening noise (85 dB SPL). Results revealed that the toughening noise heavily reduced the synaptic loss observed 1 day after exposure to the damaging noise. Although it was significant, the protective effect of the toughening noise on permanent synaptic loss was much smaller. Compared with cases in the control group without noise exposure, coding deficits were seen in both toughened groups, as reflected in the compound action potential (CAP) by signals with amplitude modulation. In general, the pre-exposure to the toughening noise resulted in a significantly reduced synaptic loss by the high-level noise. However, this morphological protection was not accompanied by a robust functional benefit.

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“… 17 Expression of BDNF and NT-3 also differ; as the animal matures, BDNF expression diminishes to almost undetectable levels in rodents, while NT-3 is maintained throughout its lifetime. 18 In addition, BDNF and NT-3 differentially regulate calcium (Ca 2+ ) and potassium (K + ) currents, 19 - 21 control dendritic morphogenesis 22 - 24 and repair inner hair cell-to-SG neuronal synapses, 25 , 26 all of which are critical for normal hearing. However, aberrant neurotrophin signaling results in the spatial remodeling of the tonotopic axis in the cochlea and subsequent hearing loss, 27 , 28 while synaptic repair via neurotrophins provides a novel therapeutic approach for peripheral insult.…”

Section: Introductionmentioning

confidence: 99%

Effects of Neurotrophin-3 on Intrinsic Neuronal Properties at a Central Auditory Structure

Takahashi

Sanchez

2020

J Exp Neurosci

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Neurotrophins, a class of growth factor proteins that control neuronal proliferation, morphology, and apoptosis, are found ubiquitously throughout the nervous system. One particular neurotrophin (NT-3) and its cognate tyrosine receptor kinase (TrkC) have recently received attention as a possible therapeutic target for synaptopathic sensorineural hearing loss. Additionally, research shows that NT-3-TrkC signaling plays a role in establishing the sensory organization of frequency topology (ie, tonotopic order) in the cochlea of the peripheral inner ear. However, the neurotrophic effects of NT-3 on central auditory properties are unclear. In this study we examined whether NT-3-TrkC signaling affects the intrinsic electrophysiological properties at a first-order central auditory structure in chicken, known as nucleus magnocellularis (NM). Here, the expression pattern of specific neurotrophins is well known and tightly regulated. By using whole-cell patch-clamp electrophysiology, we show that NT-3 application to brainstem slices does not affect intrinsic properties of high-frequency neuronal regions but had robust effects for low-frequency neurons, altering voltage-dependent potassium functions, action potential repolarization kinetics, and passive membrane properties. We suggest that NT-3 may contribute to the precise establishment and organization of tonotopy in the central auditory pathway by playing a specialized role in regulating the development of intrinsic neuronal properties of low-frequency NM neurons.

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Noise-induced Cochlear Synaptopathy and Signal Processing Disorders

Cited by 35 publications

References 100 publications

Hidden hearing loss is associated with loss of ribbon synapses of cochlea inner hair cells

Hidden hearing loss is associated with loss of ribbon synapses of cochlea inner hair cells

Pre-exposure to Lower-Level Noise Mitigates Cochlear Synaptic Loss Induced by High-Level Noise

Effects of Neurotrophin-3 on Intrinsic Neuronal Properties at a Central Auditory Structure

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