scholarly journals The Impacts of Noise Exposure on the Middle Ear Muscle Reflex in a Veteran Population

2021 ◽  
Author(s):  
Naomi Bramhall ◽  
Kelly M. Reavis ◽  
M. Patrick Feeney ◽  
Sean Kampel
Keyword(s):  
Animal Models ◽  
Middle Ear ◽  
Noise Exposure ◽  
Outer Hair Cell ◽  
Auditory Brainstem ◽  
Nerve Fibers ◽  
Intensity Level ◽  
Physiological Indicators ◽  
Brainstem Response ◽  
Muscle Reflex

Noise-induced cochlear synaptopathy, the loss of the synaptic connections between inner hair cells and afferent auditory nerve fibers, has been demonstrated in multiple animal models, including non-human primates. However, given that synaptopathy can only be confirmed with post-mortem temporal bone analysis, it has been difficult to determine whether noise-induced synaptopathy occurs in humans. Human studies of noise-induced synaptopathy using physiological indicators identified in animal models (auditory brainstem response [ABR] wave I amplitude, the envelope following response [EFR], and the middle ear muscle reflex [MEMR]) have yielded mixed findings. Differences in the population studied may have contributed to the differing results. For example, due to differences in the intensity level of the noise exposure, noise-induced synaptopathy may be easier to detect in a military Veteran population than in populations with recreational noise exposure. We previously demonstrated a reduction in ABR wave I amplitude and EFR magnitude for young Veterans with normal audiograms reporting high levels of noise exposure compared to non-Veteran controls. In this report, we expand on the previous analysis in the same population to determine if MEMR magnitude is similarly reduced. The results of the statistical analysis, although not conventionally statistically significant, suggest a reduction in mean MEMR magnitude for Veterans reporting high noise exposure compared with non-Veteran controls. In addition, the MEMR appears relatively insensitive to subclinical outer hair cell dysfunction and is not well correlated with ABR and EFR measurements. When combined with our previous ABR and EFR findings in the same population, these results suggest that noise-induced synaptopathy occurs in humans. In addition, the findings indicate that the MEMR may be a good candidate for non-invasive diagnosis of cochlear synaptopathy/deafferentation and that the MEMR may reflect the integrity of different neural populations than the ABR and EFR.

scholarly journals Auditory Brainstem Response Altered in Humans With Noise Exposure Despite Normal Outer Hair Cell Function

2017 ◽  
Vol 38 (1) ◽  
pp. e1-e12 ◽  
Author(s):  
Naomi F. Bramhall ◽  
Dawn Konrad-Martin ◽  
Garnett P. McMillan ◽  
Susan E. Griest
Keyword(s):  
Hair Cell ◽  
Auditory Brainstem Response ◽  
Noise Exposure ◽  
Outer Hair Cell ◽  
Cell Function ◽  
Auditory Brainstem ◽  
Brainstem Response

scholarly journals An antibody to RGMa promotes regeneration of cochlear synapses after noise exposure

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jerome Nevoux ◽  
Mihaela Alexandru ◽  
Thomas Bellocq ◽  
Lei Tanaka ◽  
Yushi Hayashi ◽  
...  
Keyword(s):  
Hair Cells ◽  
Noise Exposure ◽  
Auditory Brainstem ◽  
Afferent Input ◽  
Nerve Fibers ◽  
Auditory Neuropathy ◽  
Axonal Guidance ◽  
Inner Hair Cell ◽  
Inner Hair Cells ◽  
Brainstem Response

AbstractAuditory neuropathy is caused by the loss of afferent input to the brainstem via the components of the neural pathway comprising inner hair cells and the first order neurons of the spiral ganglion. Recent work has identified the synapse between cochlear primary afferent neurons and sensory hair cells as a particularly vulnerable component of this pathway. Loss of these synapses due to noise exposure or aging results in the pathology identified as hidden hearing loss, an initial stage of cochlear dysfunction that goes undetected in standard hearing tests. We show here that repulsive axonal guidance molecule a (RGMa) acts to prevent regrowth and synaptogenesis of peripheral auditory nerve fibers with inner hair cells. Treatment of noise-exposed animals with an anti-RGMa blocking antibody regenerated inner hair cell synapses and resulted in recovery of wave-I amplitude of the auditory brainstem response, indicating effective reversal of synaptopathy.

scholarly journals Envelope Following Response Measurements in Young Veterans Are Consistent With Noise-Induced Cochlear Synaptopathy

2020 ◽  
Author(s):  
Naomi Bramhall ◽  
Garnett McMillan ◽  
Sean Kampel
Keyword(s):  
Animal Models ◽  
Otoacoustic Emissions ◽  
Animal Studies ◽  
Noise Exposure ◽  
Auditory Brainstem ◽  
Auditory Nerve Fiber ◽  
Auditory Thresholds ◽  
Distortion Product ◽  
Brainstem Response ◽  
Envelope Following Response

Animal studies have demonstrated that noise exposure can lead to the loss of the synapses between the inner hair cells and their afferent auditory nerve fiber targets without impacting auditory thresholds. Although several non-invasive physiological measures appear to be sensitive to cochlear synaptopathy in animal models, including auditory brainstem response (ABR) wave I amplitude, the envelope following response (EFR), and the middle ear muscle reflex (MEMR), human studies of these measures in samples that are expected to vary in terms of the degree of noise-induced synaptopathy have resulted in mixed findings. One possible explanation for the differing results is that synaptopathy risk is lower for recreational noise exposure than for occupational or military noise exposure. The goal of this analysis was to determine if EFR magnitude and ABR wave I amplitude are reduced among young Veterans with a history of military noise exposure compared with non-Veteran controls with minimal noise exposure. EFRs and ABRs were obtained in a sample of young (19-35 years) Veterans and non-Veterans with normal audiograms and robust distortion product otoacoustic emissions (DPOAEs). Mean EFR magnitudes and ABR wave I amplitudes were reduced for Veterans compared with non-Veteran controls. These findings replicate previous ABR wave I amplitude results in young Veterans and are consistent with animal models of noise-induced cochlear synaptopathy.

Use of Solid Lipid Nanoparticles for the Treatment of Acute Acoustic Stress-Induced Cochlea Damage

2020 ◽  
Vol 20 (12) ◽  
pp. 7412-7418
Author(s):  
Ningning Wang ◽  
Xian Gao ◽  
Min Li ◽  
Yongtuan Li ◽  
Minghong Sun
Keyword(s):  
Solid Lipid Nanoparticles ◽  
Guinea Pigs ◽  
Noise Exposure ◽  
Outer Hair Cell ◽  
Lipid Nanoparticles ◽  
Auditory Brainstem ◽  
Drug Bioavailability ◽  
Solid Lipid ◽  
Cell Counts ◽  
Brainstem Response

To study the effects of drug delivery using solid lipid nanoparticles in the treatment of acute noise exposure-induced cochlea damage. The solid lipid nanoparticles (SLNs) were used as carriers to effectively encapsulate the drug clozapine, improve drug stability in the carrier system, and increase drug bioavailability in vivo. Solid lipid nanoparticles carrying clozapine were produced by ultrasonic technology. The clozapine solution or sulphate SLN was administered though intratympanic or intravenous injection on the first day of noise exposure Guinea pigs were exposed to 110 dB sound pressure level (SPL) noise (2 h per day with center frequencies of 0.25–4.0 kHz for 4 days). After noise exposure, the guinea pigs were subjected to auditory brainstem response (ABR) threshold measurements. Reactive oxygen species (ROS) levels were detected in the cochlea by electron spin resonance (ESR), and outer hair cell counts (OHCs) were obtained using silver nitrate (AgNO3). SLN particles carrying clozapine exhibited protective effects on the cochlea. The threshold shift and ROS production in treated animals, especially in animals treated with clozapine SLN through intraperitoneal injection, were significantly lower than those in untreated animals.

scholarly journals Outer Hair Cell Function is Normal in βV Spectrin Knockout Mice

2021 ◽  
Author(s):  
Michael C. Stankewich ◽  
Jun-Ping Bai ◽  
Paul R. Stabach ◽  
Saaim Khan ◽  
Lei Song ◽  
...  
Keyword(s):  
Hair Cell ◽  
Otoacoustic Emissions ◽  
Outer Hair Cell ◽  
Cell Function ◽  
Auditory Brainstem ◽  
Nerve Fibers ◽  
Outer Hair Cells ◽  
Neuronal Structure ◽  
Efferent Nerve ◽  
Brainstem Response

ABSTRACTReports have proposed a putative role for βV spectrin in outer hair cells (OHCs) of the cochlea. In an ongoing investigation of the role of the cytoskeleton in electromotility, we tested mice with a targeted exon deletion of βV spectrin (Spnb5), and unexpectedly find that Spnb5(-/-) animals’ auditory thresholds are unaffected. Similarly, these mice have normal OHC electromechanical activity (otoacoustic emissions) and non-linear capacitance. Moreover, Spnb5 mRNA is undetectable in the organ of Corti or OHCs. In contrast, magnitudes of auditory brainstem response (ABR) peak 1-amplitudes are significantly reduced. Evidence of a synaptopathy was absent with normal hair cell CtBP-2 counts. In Spnb5(-/-) mice, the number of afferent and efferent nerve fibers is decreased. Taken together, these data establish that βV spectrin is important for hearing, affecting neuronal structure and function. Significantly, these data exclude βV spectrin as functionally important to OHCs as has been previously suggested.

scholarly journals An Antibody to RGMa Promotes Regeneration of Cochlear Synapses after Noise Exposure

2020 ◽  
Author(s):  
Jerome Nevoux ◽  
Mihaela Alexandru ◽  
Thomas Bellocq ◽  
Lei Tanaka ◽  
Yushi Hayashi ◽  
...  
Keyword(s):  
Hair Cells ◽  
Noise Exposure ◽  
Auditory Brainstem ◽  
Afferent Input ◽  
Nerve Fibers ◽  
Auditory Neuropathy ◽  
Axonal Guidance ◽  
Inner Hair Cell ◽  
Inner Hair Cells ◽  
Brainstem Response

SUMMARYAuditory neuropathy is caused by the loss of afferent input to the brainstem via the components of the neural pathway comprising inner hair cells and the first order neurons of the spiral ganglion. Recent work has identified the synapse between cochlear primary afferent neurons and sensory hair cells as a particularly vulnerable component of this pathway. Loss of these synapses due to noise exposure or aging results in the pathology identified as hidden hearing loss, an initial stage of cochlear dysfunction that goes undetected in standard hearing tests. We show here that repulsive axonal guidance molecule a (RGMa) acts to prevent regrowth and synaptogenesis of peripheral auditory nerve fibers with inner hair cells. Treatment of noise-exposed animals with an anti-RGMa blocking antibody regenerated inner hair cell synapses and resulted in recovery of wave-I amplitude of the auditory brainstem response, indicating effective reversal of synaptopathy.

Glutathione Ester But Not Glutathione Protects Against Cisplatin-Induced Ototoxicity in a Rat Model

2003 ◽  
Vol 14 (03) ◽  
pp. 124-133 ◽  
Author(s):  
Kathleen C.M. Campbell ◽  
Deb L. Larsen ◽  
Robert P. Meech ◽  
Leonard P. Rybak ◽  
Larry F. Hughes
Keyword(s):  
Auditory Brainstem Response ◽  
Outer Hair Cell ◽  
Tone Burst ◽  
Auditory Brainstem ◽  
Control Group ◽  
Brainstem Response ◽  
Group A ◽  
Direct Administration ◽  
Response Thresholds ◽  
Para Determinar

Glutathione (GSH) provides an important antioxidant and detoxification pathway. We tested to determine if direct administration of GSH or GSH ester could reduce cisplatin- (CDDP) induced ototoxicity. We tested eight groups of five rats each: a control group, a group receiving 16 mg/kg ip CDDP infused over 30 minutes, and six groups receiving either GSH or GSH ester at 500, 1000, or 1500 mg/kg intraperitoneally 30 minutes prior to 16 mg/kg CDDP. Auditory brainstem response thresholds were measured for click and tone-burst stimuli at baseline and 3 days later. Outer hair cell (OHC) loss was measured for the apical, middle and basal turns. The 500 mg/kg GSH ester reduced hearing loss and OHC loss, but protection decreased as dosage increased, suggesting possible toxicity. GSH was not significantly protective. The best GSH ester protection was less than we have previously reported with D-methionine. El glutatión (GSH) brinda una importante vía antioxidante y de cetoxificación. Realizamos una prueba para determinar si la administración directa de GSH o del éster de GSH podía reducir la ototoxicidad inducida por cisplatino (CDDP). Hicimos una evaluación en ocho grupos de cinco ratas cada uno: un grupo control, un grupo que recibió CDDP intraperitoneal a 16 mg/kg en una ínfusión durante 30 minutos y seis grupos que recibieron intraperitonealmente GSH o el éster de GSH a 500, 1000 o 1500 mg/kg, 30 minutos antes del CDDP a 16 mg/kg. Se midieron umbrales de respuestas auditivas del tallo cerebral tanto para clicks como para bursts tonales, al inicio y 3 días después. La pérdida de células ciliadas externas (OHC) fue establecida a nivel de las vueltas apical, media y basal. La dosis de 500 mg/kg de éster de GSH redujo la hipoacusia y la pérdida de OHC, pero la protección disminuyó conforme la dosis se incrementó, sugiriendo una posible toxicidad. EL GSH no resultó significativamente protector. El mejor efecto protector del éster de GSH fue menor que el previamente reportado con D-Metionina.

Effects of noise exposure on neonatal auditory brainstem response thresholds in pregnant guinea pigs at different gestational periods

2016 ◽  
Vol 43 (1) ◽  
pp. 78-86
Author(s):  
Chihiro Morimoto ◽  
Kazuhiko Nario ◽  
Tadashi Nishimura ◽  
Ryota Shimokura ◽  
Hiroshi Hosoi ◽  
...  
Keyword(s):  
Auditory Brainstem Response ◽  
Guinea Pigs ◽  
Noise Exposure ◽  
Auditory Brainstem ◽  
Brainstem Response ◽  
Response Thresholds
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