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 Tinnitus and Auditory Perception After a History of Noise Exposure: Relationship to Auditory Brainstem Response Measures

2017 ◽  
Author(s):  
Naomi Bramhall
Keyword(s):  
Speech Perception ◽  
Confidence Interval ◽  
Hair Cell ◽  
Auditory Nerve ◽  
Auditory Brainstem Response ◽  
Auditory Perception ◽  
Noise Exposure ◽  
Auditory Brainstem ◽  
Distortion Product ◽  
Brainstem Response

ObjectivesDetermine whether auditory brainstem response (ABR) wave I amplitude is associated with measures of auditory perception in young people with normal distortion product otoacoustic emissions (DPOAEs) and varying levels of noise exposure history.DesignTinnitus, loudness tolerance, and speech perception ability were measured in 31 young military Veterans and 43 non-Veterans (19-35 years of age) with normal pure tone thresholds and DPOAEs. Speech perception was evaluated in quiet using NU-6 word lists and in background noise using the words in noise (WIN) test. Loudness discomfort levels were measured using 1, 3, 4, and 6 kHz pulsed pure tones. DPOAEs and ABRs were collected in each participant to assess outer hair cell (OHC) and auditory nerve function. ResultsThe probability of reporting tinnitus in this sample increased by a factor of 2.0 per 0.1 µV decrease in ABR wave I amplitude (90% Bayesian confidence interval = 1.2 to 4.2) for males and by a factor of 2.2 (90% confidence interval = 1.1 to 5.1) for females after adjusting for sex and DPOAE level. No apparent relationship was found between wave I amplitude and either loudness tolerance or speech perception in quiet or noise.ConclusionsReduced ABR wave I amplitude was associated with a markedly increased risk of tinnitus, even after adjusting for DPOAEs and sex. In contrast, wave III and V amplitudes had little effect on tinnitus risk. This suggests that changes in peripheral input at the level of the inner hair cell (IHC) or auditory nerve may lead to increases in central gain that give rise to the perception of tinnitus. Although the extent of synaptopathy in the study participants cannot be measured directly, these findings are consistent with the prediction that tinnitus may be a perceptual consequence of cochlear synaptopathy.

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.

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.

scholarly journals Prevention of acquired sensorineural hearing loss in mice by in vivo Htra2 gene editing

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Xi Gu ◽  
Daqi Wang ◽  
Zhijiao Xu ◽  
Jinghan Wang ◽  
Luo Guo ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Protective Effect ◽  
Hair Cell ◽  
Sensorineural Hearing Loss ◽  
Auditory Brainstem Response ◽  
Gene Editing ◽  
Auditory Brainstem ◽  
Sensorineural Hearing ◽  
Brainstem Response

Abstract Background Aging, noise, infection, and ototoxic drugs are the major causes of human acquired sensorineural hearing loss, but treatment options are limited. CRISPR/Cas9 technology has tremendous potential to become a new therapeutic modality for acquired non-inherited sensorineural hearing loss. Here, we develop CRISPR/Cas9 strategies to prevent aminoglycoside-induced deafness, a common type of acquired non-inherited sensorineural hearing loss, via disrupting the Htra2 gene in the inner ear which is involved in apoptosis but has not been investigated in cochlear hair cell protection. Results The results indicate that adeno-associated virus (AAV)-mediated delivery of CRISPR/SpCas9 system ameliorates neomycin-induced apoptosis, promotes hair cell survival, and significantly improves hearing function in neomycin-treated mice. The protective effect of the AAV–CRISPR/Cas9 system in vivo is sustained up to 8 weeks after neomycin exposure. For more efficient delivery of the whole CRISPR/Cas9 system, we also explore the AAV–CRISPR/SaCas9 system to prevent neomycin-induced deafness. The in vivo editing efficiency of the SaCas9 system is 1.73% on average. We observed significant improvement in auditory brainstem response thresholds in the injected ears compared with the non-injected ears. At 4 weeks after neomycin exposure, the protective effect of the AAV–CRISPR/SaCas9 system is still obvious, with the improvement in auditory brainstem response threshold up to 50 dB at 8 kHz. Conclusions These findings demonstrate the safe and effective prevention of aminoglycoside-induced deafness via Htra2 gene editing and support further development of the CRISPR/Cas9 technology in the treatment of non-inherited hearing loss as well as other non-inherited diseases.

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

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.

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