Neural and infranuclear region changes in outer hair cells in acoustically exposed rabbits

Omata, Takeo; Omata, Eriko; Hj, Wilhelms; Schätzle, W.

doi:10.1007/bf00714495

Cited by 5 publications

(4 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The observation in Chrna9L9ЈT KI mice of an increase in synaptic counts after noise exposure, is intriguing. In the ears of unexposed WT mice, synaptic counts show a spatial distribution from base to apex: the number of ribbon synapses per IHC peaks at the medial region, where the cochlea is most sensitive to sound (Meyer et al, 2009). However, in Chrna9L9ЈT KI mice, this distribution is lost: synaptic counts were comparable to those in WT mice at low-and high-frequency regions, except in the middle turn where a significant reduction was observed.…”

Section: Ohc Function and Efferent Innervation Pattern After Noise Exmentioning

confidence: 87%

“…However, recent work by Lauer (2017) with Chrna9 KO mice did not find accelerated onset of hearing loss up to 15 months of age. Considering that MOC neurons regulate several aspects of auditory processing like the dynamic range of hearing and detection of relevant auditory signals in background noise (Maison et al, 2001;Guinan, 2011), we propose that the interruption in synaptic communication between MOC terminals and OHCs after acoustic trauma contributes, together with cochlear synaptopathy, to the reported symptoms of HHL.…”

Section: Noise-induced Degeneration Of Moc Terminalsmentioning

confidence: 99%

“…Hair cell count showed no loss of IHCs or OHCs in the different genotypes in control and exposed groups (data not shown). To analyze the IHC-auditory nerve fiber synapses, organ of Corti whole-mounts were immunostained with antibodies against CtBP2-Ribeye, a critical protein present at the presynaptic ribbon (Khimich et al, 2005), and GluA2 AMPA-type glutamate receptors, which are expressed at the postsynaptic afferent terminal (Matsubara et al, 1996;. IHC-afferent synapses were identified by colocalization of a pair of CtBP2/GluA2 puncta at the base of the IHC .…”

Section: Noise-induced Cochlear Synaptopathy In Mice With Different Lmentioning

confidence: 99%

See 2 more Smart Citations

Enhancement of the Medial Olivocochlear System Prevents Hidden Hearing Loss

et al. 2018

View full text Add to dashboard Cite

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.

show abstract

Section: Ohc Function and Efferent Innervation Pattern After Noise Exmentioning

confidence: 87%

Section: Noise-induced Degeneration Of Moc Terminalsmentioning

confidence: 99%

Section: Noise-induced Cochlear Synaptopathy In Mice With Different Lmentioning

confidence: 99%

See 1 more Smart Citation

Enhancement of the Medial Olivocochlear System Prevents Hidden Hearing Loss

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Damage of ipsilateral side efferent nerve endings from noise was proven by a study using electron microscopy. [12,23] The damage consisted of several ultrastructural alterations including a reduction in the number of synaptic vesicles at the presynaptic membrane, as well as swollen mitochondria in the efferent terminals. These morphological changes of ipsilateral efferent nerve degeneration after noise exposure also could be applied to contralateral side efferent nerve endings even in plugged condition in our study.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2014

View full text Add to dashboard Cite

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.

show abstract