Medial olivocochlear efferent terminals are protected by sound conditioning

Canlon, Barbara; Fransson, Anette; Viberg, Agneta

doi:10.1016/s0006-8993(99)02091-0

Cited by 18 publications

(9 citation statements)

References 27 publications

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“…One signature of cochlear synaptopathy observed in HHL in mice is a reduction of ABR peak 1 amplitudes without permanent changes in ABR thresholds (Kujawa and Liberman, 2009). This peak represents the summed sound-evoked spike activity at the first synapse between IHCs and afferent nerve fibers (Buchwald and Huang, 1975;Antoli-Candela and Kiang, 1978). As shown in Figure 2, a and c, a large reduction in amplitudes was observed at 11.33, 16, and 22.65 kHz in WT mice 1 d after acoustic trauma (Friedman test: df ϭ 2, p ϭ 0.048 at 11.33 kHz; p ϭ 0.026 at 16 kHz; and p ϭ 0.018 at 22.65 kHz), which did not completely recover after 7 d (Friedman test: df ϭ 2, p ϭ 0.048 at 16 kHz; and p ϭ 0.003 at 22.65 kHz).…”

Section: Auditory Function In Mice With Different Degrees Of Efferentmentioning

confidence: 99%

Enhancement of the Medial Olivocochlear System Prevents Hidden Hearing Loss

et al. 2018

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Cochlear synaptopathy produced by exposure to noise levels that cause only transient auditory threshold elevations is a condition that affects many people and is believed to contribute to poor speech discrimination in noisy environments. These functional deficits in hearing, without changes in sensitivity, have been called hidden hearing loss (HHL). It has been proposed that activity of the medial olivocochlear (MOC) system can ameliorate acoustic trauma effects. Here we explore the role of the MOC system in HHL by comparing the performance of two different mouse models: an α9 nicotinic receptor subunit knock-out (KO; KO), which lacks cholinergic transmission between efferent neurons and hair cells; and a gain-of-function knock-in (KI;' KI) carrying an α9 point mutation that leads to enhanced cholinergic activity. Animals of either sex were exposed to sound pressure levels that in wild-type produced transient cochlear threshold shifts and a decrease in neural response amplitudes, together with the loss of ribbon synapses, which is indicative of cochlear synaptopathy. Moreover, a reduction in the number of efferent contacts to outer hair cells was observed. In KO ears, noise exposure produced permanent auditory threshold elevations together with cochlear synaptopathy. In contrast, the' KI was completely resistant to the same acoustic exposure protocol. These results show a positive correlation between the degree of HHL prevention and the level of cholinergic activity. Notably, enhancement of the MOC feedback promoted new afferent synapse formation, suggesting that it can trigger cellular and molecular mechanisms to protect and/or repair the inner ear sensory epithelium. Noise overexposure is a major cause of a variety of perceptual disabilities, including speech-in-noise difficulties, tinnitus, and hyperacusis. Here we show that exposure to noise levels that do not cause permanent threshold elevations or hair cell death can produce a loss of cochlear nerve synapses to inner hair cells as well as degeneration of medial olivocochlear (MOC) terminals contacting the outer hair cells. Enhancement of the MOC reflex can prevent both types of neuropathy, highlighting the potential use of drugs that increase α9α10 nicotinic cholinergic receptor activity as a pharmacotherapeutic strategy to avoid hidden hearing loss.

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Section: Auditory Function In Mice With Different Degrees Of Efferentmentioning

confidence: 99%

Enhancement of the Medial Olivocochlear System Prevents Hidden Hearing Loss

et al. 2018

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“…Although the MOC-R decreased after conditioning, it is not yet known how much of this decrement was due to the diminished MEM-R observed at 1 day postconditioning. It is unlikely that this decrease was due to a lack of MOC efferent terminals because Canlon et al (1999) reported earlier that sound-conditioning likely protected these nerve endings. Brown et al (1998) observed slight changes in MOC discharge rates in cells with best frequency responses about 1 2 oct above the conditioning-frequency band, nevertheless, these changes in MOC discharge rates observed for sedated guinea pigs were not reflected in greater MOC-R strengths in either the alert rabbit of the current study, or the awake guinea pig (Peng et al, 2007).…”

Section: Discussionmentioning

confidence: 94%

“…However, when compared with the frequency range and magnitude of the frequency-related protection, these authors concluded that protection from sound-conditioning could not be completely explained by strengthening the MOC-R. Yet, using synaptophysin immunoreactivity as a marker for the medial olivocochlear (MOC) system, Canlon et al (1999) showed that sound-conditioning significantly reduced noiseinduced injury to MOC nerve terminals, thus, suggesting that the conditioning procedure might protect efferent-nerve terminals from morphological damage due to overexposure. However, in contrast to the earlier Kujawa and Liberman (1999) findings, results from a more recent investigation suggested that long-term sound-conditioning decreased MOC-R strength in alert guinea pigs thereby increasing DPOAE magnitudes (Peng et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Influence of sound-conditioning on noise-induced susceptibility of distortion-product otoacoustic emissions

Luebke

Stagner

Martin

et al. 2015

The Journal of the Acoustical Society of America

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Cochlear damage caused by loud sounds can be attenuated by "sound-conditioning" methods. The amount of adaptation for distortion product otoacoustic emissions (DPOAEs) measured in alert rabbits previously predicted an ear's susceptibility to a subsequent noise exposure. The present study investigated if sound-conditioning influenced the robustness of such DPOAE adaptation, and if such conditioning elicited more protection by increasing the amount of DPOAE adaptation. Toward this end, rabbits were divided into two study groups: (1) experimental animals exposed to a sound-conditioning protocol, and (2) unconditioned control animals. After base-line measures, all rabbits were exposed to an overstimulation paradigm consisting of an octave band noise, and then re-assessed 3 weeks post-exposure to determine permanent changes in DPOAEs. A major result was that prior sound-conditioning protected reductions in DPOAE levels by an average of 10-15 dB. However, DPOAE adaptation decreased with sound-conditioning, so that such conditioning was no longer related to noise-induced reductions in DPOAEs. Together, these findings suggest that sound-conditioning affected neural pathways other than those that likely mediate DPOAE adaptation (e.g., medial olivocochlear efferent and/or middle-ear muscle reflexes).

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“…Synaptophysin, an intrinsic membrane protein of synaptic vesicles, is present in the efferent synaptic terminals of neurons innervating both the inner and OHCs in a variety of species and have been used to show damage of efferent nerve from noise in several papers. [14,15] α-synuclein, synaptic proteins widely expressed within central nervous system, is known to be localized to the efferent auditory synapses below OHCs and we recently demonstrated reduction of α-synuclein in old C57 mice and suggested its role as a possible cause of early-onset presbycusis. [15,16] In this study, we investigated its change in NIHL and inferred its role from results.…”

Section: Introductionmentioning

confidence: 86%

Protective effect of unilateral and bilateral ear plugs on noise-induced hearing loss: Functional and morphological evaluation in animal model

et al. 2014

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The aim of the following study is to evaluate immediate protective effect of ear plug from noise morphologically and functionally. An 1-month aged 29 male C57BL/6 mice. Subjects were divided into four groups as normal control(G1), bilaterally plugged group (G2), unilaterally plugged group (G3) and noise control group (G4) and later 3 groups were exposed to 110 sound pressure level white noise for 60 min. Immediately after noise exposure, audiologic tests were performed and cochlear morphology and expression levels of a-synuclein in the cochlea were investigated. There were no functional changes in G2 and plugged ears of G3 after noise exposure, whereas unplugged ears of G3 and G4 showed significant hearing loss. In morphological study, there were a significant degeneration of the organ of Corti and mean number and diameter of efferent buttons, in unplugged ears of G3 and G4. Plugged ears of G3 also showed mild changes in morphological study. Reduction of a-synuclein was observed at the efferent terminals or cochlear extracts after noise exposure. The protective effect of ear plug on noise exposure was proven morphologically and functionally in the animal model of noise-induced hearing loss. Further study on cellular or ultrastructural level with ear plug will be needed to reveal more precise mechanism.

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Medial olivocochlear efferent terminals are protected by sound conditioning

Cited by 18 publications

References 27 publications

Enhancement of the Medial Olivocochlear System Prevents Hidden Hearing Loss

Enhancement of the Medial Olivocochlear System Prevents Hidden Hearing Loss

Influence of sound-conditioning on noise-induced susceptibility of distortion-product otoacoustic emissions

Protective effect of unilateral and bilateral ear plugs on noise-induced hearing loss: Functional and morphological evaluation in animal model

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