Differential effects of pannexins on noise-induced hearing loss

2016 ◽  
Vol 473 (24) ◽  
pp. 4665-4680 ◽  
Author(s):  
Julia M. Abitbol ◽  
John J. Kelly ◽  
Kevin Barr ◽  
Ashley L. Schormans ◽  
Dale W. Laird ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Noise Exposure ◽  
Morphological Changes ◽  
Cell Types ◽  
Auditory Pathway ◽  
Auditory Brainstem ◽  
Vital Role ◽  
Noise Induced Hearing Loss ◽  
Loud Noise ◽  
Brainstem Response

Hearing loss, including noise-induced hearing loss, is highly prevalent and severely hinders an individual's quality of life, yet many of the mechanisms that cause hearing loss are unknown. The pannexin (Panx) channel proteins, Panx1 and Panx3, are regionally expressed in many cell types along the auditory pathway, and mice lacking Panx1 in specific cells of the inner ear exhibit hearing loss, suggesting a vital role for Panxs in hearing. We proposed that Panx1 and/or Panx3 null mice would exhibit severe hearing loss and increased susceptibility to noise-induced hearing loss. Using the auditory brainstem response, we surprisingly found that Panx1−/− and Panx3−/− mice did not harbor hearing or cochlear nerve deficits. Furthermore, while Panx1−/− mice displayed no protection against loud noise-induced hearing loss, Panx3−/− mice exhibited enhanced 16- and 24-kHz hearing recovery 7 days after a loud noise exposure (NE; 12 kHz tone, 115 dB sound pressure level, 1 h). Interestingly, Cx26, Cx30, Cx43, and Panx2 were up-regulated in Panx3−/− mice compared with wild-type and/or Panx1−/− mice, and assessment of the auditory tract revealed morphological changes in the middle ear bones of Panx3−/− mice. It is unclear if these changes alone are sufficient to provide protection against loud noise-induced hearing loss. Contrary to what we expected, these data suggest that Panx1 and Panx3 are not essential for baseline hearing in mice tested, but the therapeutic targeting of Panx3 may prove protective against mid-high-frequency hearing loss caused by loud NE.

Comparing the electrophysiological effects of traumatic noise exposure between rodents

2022 ◽  
Author(s):  
Lenneke Kiefer ◽  
Lisa Koch ◽  
Melisa Merdan-Desik ◽  
Bernhard H. Gaese ◽  
Manuela Nowotny
Keyword(s):  
Hearing Loss ◽  
Noise Exposure ◽  
Temporal Dynamics ◽  
Auditory Pathway ◽  
Auditory Brainstem ◽  
Individual Variability ◽  
Rodent Species ◽  
Waveform Analysis ◽  
Auditory Brainstem Responses ◽  
Noise Induced Hearing Loss

Noise-induced hearing deficits are important health problems in the industrialized world. As the underlying physiological dysfunctions are not well understood, research in suitable animal models is urgently needed. Three rodent species (Mongolian gerbil, rat and mouse) were studied to compare the temporal dynamics of noise-induced hearing loss after identical procedures of noise exposure. Auditory brainstem responses (ABRs) were measured before, during and up to eight weeks after noise exposure for threshold determination and ABR waveform analysis. Trauma induction with stepwise increasing sound pressure level was interrupted by five interspersed ABR measurements. Comparing short- and long-term dynamics underlying the following noise-induced hearing loss revealed diverging time courses between the three species. Hearing loss occurred early on during noise exposure in all three rodent species at or above trauma frequency. Initial noise level (105 dB SPL) was most effective in rats while the delayed level-increase to 115 dB SPL affected mice much stronger. Induced temporary threshold shifts in rats and mice were larger in animals with lower pre-trauma ABR thresholds. The increase in activity (gain) along the auditory pathway was derived by comparing the amplitudes of short- and long-latency ABR waveform components. Directly after trauma, significant effects were found for rats (decreasing gain) and mice (increasing gain) while gerbils revealed high individual variability in gain changes. Taken together, our comparative study revealed pronounced species-specific differences in the development of noise-induced hearing loss and the related processing along the auditory pathway.

scholarly journals Effect of Phlorofucofuroeckol A and Dieckol Extracted from Ecklonia cava on Noise-induced Hearing Loss in a Mouse Model

Marine Drugs ◽  
2021 ◽  
Vol 19 (8) ◽  
pp. 443
Author(s):  
Hyunjun Woo ◽  
Min-Kyung Kim ◽  
Sohyeon Park ◽  
Seung-Hee Han ◽  
Hyeon-Cheol Shin ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Noise Exposure ◽  
Radical Scavenging ◽  
Threshold Shift ◽  
Ecklonia Cava ◽  
Control Group ◽  
Noise Induced Hearing Loss ◽  
Antioxidant Agents ◽  
Brainstem Response

One of the well-known causes of hearing loss is noise. Approximately 31.1% of Americans between the ages of 20 and 69 years (61.1 million people) have high-frequency hearing loss associated with noise exposure. In addition, recurrent noise exposure can accelerate age-related hearing loss. Phlorofucofuroeckol A (PFF-A) and dieckol, polyphenols extracted from the brown alga Ecklonia cava, are potent antioxidant agents. In this study, we investigated the effect of PFF-A and dieckol on the consequences of noise exposure in mice. In 1,1-diphenyl-2-picrylhydrazyl assay, dieckol and PFF-A both showed significant radical-scavenging activity. The mice were exposed to 115 dB SPL of noise one single time for 2 h. Auditory brainstem response(ABR) threshold shifts 4 h after 4 kHz noise exposure in mice that received dieckol were significantly lower than those in the saline with noise group. The high-PFF-A group showed a lower threshold shift at click and 16 kHz 1 day after noise exposure than the control group. The high-PFF-A group also showed higher hair cell survival than in the control at 3 days after exposure in the apical turn. These results suggest that noise-induced hair cell damage in cochlear and the ABR threshold shift can be alleviated by dieckol and PFF-A in the mouse. Derivatives of these compounds may be applied to individuals who are inevitably exposed to noise, contributing to the prevention of noise-induced hearing loss with a low probability of adverse effects.

scholarly journals Deletion of Oncomodulin Gives Rise to Early Progressive Cochlear Dysfunction in C57 and CBA Mice

2021 ◽  
Vol 13 ◽  
Author(s):  
Leslie K. Climer ◽  
Aubrey J. Hornak ◽  
Kaitlin Murtha ◽  
Yang Yang ◽  
Andrew M. Cox ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Cell Function ◽  
Otoacoustic Emission ◽  
Cell Types ◽  
Auditory Brainstem ◽  
Outer Hair Cells ◽  
Distortion Product Otoacoustic Emission ◽  
Distortion Product ◽  
Age Related ◽  
Brainstem Response

Ca2+ signaling is a major contributor to sensory hair cell function in the cochlea. Oncomodulin (OCM) is a Ca2+ binding protein (CaBP) preferentially expressed in outer hair cells (OHCs) of the cochlea and few other specialized cell types. Here, we expand on our previous reports and show that OCM delays hearing loss in mice of two different genetic backgrounds: CBA/CaJ and C57Bl/6J. In both backgrounds, genetic disruption of Ocm leads to early progressive hearing loss as measured by auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE). In both strains, loss of Ocm reduced hearing across lifetime (hearing span) by more than 50% relative to wild type (WT). Even though the two WT strains have very different hearing spans, OCM plays a considerable and similar role within their genetic environment to regulate hearing function. The accelerated age-related hearing loss (ARHL) of the Ocm KO illustrates the importance of Ca2+ signaling in maintaining hearing health. Manipulation of OCM and Ca2+ signaling may reveal important clues to the systems of function/dysfunction that lead to ARHL.

scholarly journals Noise Exposure and Hearing Threshold Profile among Zumba Fitness Regulars in Kuantan, Pahang, Malaysia

2020 ◽  
Vol 19 (2) ◽  
Author(s):  
Razali A ◽  
Othman MS ◽  
Rahman MS ◽  
Misaridin NFI
Keyword(s):  
Hearing Loss ◽  
Noise Exposure ◽  
Hearing Threshold ◽  
Sound Level ◽  
Hearing Level ◽  
Noise Induced Hearing Loss ◽  
Loud Noise ◽  
Abnormal Pattern ◽  
Level Meter ◽  
Hearing System

INTRODUCTION: Recreational noise exposure has become a major threat to the hearing system, and this includes exposure to loud noise during group exercises such as Zumba Fitness, where loud music plays an important role. This study aimed to assess the noise exposure and hearing threshold profile among Zumba Fitness regulars in Kuantan, Malaysia. MATERIALS AND METHODS: Noise exposure and hearing profile threshold were measured during Zumba Fitness sessions at a fitness studio in Kuantan, Malaysia from 24th June 2014 to 12th August 2014. Noise exposure was measured using a noise dosimeter for one hour of Zumba Fitness session with a total of nine sessions run by three different instructors while sound level pressure was taken using a sound level meter during ambient, peak session and during cooling down. Thirty participants answered questionnaires and underwent pure tone diagnostic audiometry test at a local clinic for hearing threshold documentation. RESULTS: Some areas of the hall posed higher risks of causing noise-induced hearing loss especially near the amplifiers. There were periods when the hearing level exceeded 115 dBA. Early abnormal pattern could be observed in the hearing profiles of some of the participants to suggest preliminary hearing problems. CONCLUSION: Zumba Fitness regulars have a risk of developing noise-induced hearing loss and preventive steps should be properly addressed as NIHL is permanent and irreversible.

scholarly journals Effect of Specific Retinoic Acid Receptor Agonists on Noise-Induced Hearing Loss

2019 ◽  
Vol 16 (18) ◽  
pp. 3428 ◽  
Author(s):  
Sang Hyun Kwak ◽  
Gi-Sung Nam ◽  
Seong Hoon Bae ◽  
Jinsei Jung
Keyword(s):  
Hearing Loss ◽  
Retinoic Acid ◽  
Noise Exposure ◽  
Retinoic Acid Receptor ◽  
Protective Effects ◽  
Noise Induced Hearing Loss ◽  
Acid Receptor ◽  
Significant Difference ◽  
Brainstem Response ◽  
Selective Agonists

Noise is one of the most common causes of hearing loss in industrial countries. There are many studies about chemical agents to prevent noise-induced hearing loss (NIHL). However, there is no commercially available drug yet. Retinoic acid is an active metabolite of Vitamin A; it has an anti-apoptic role in NIHL. This study aims to verify the differences among selective agonists of retinoic acid receptors (RARs) in NIHL. All-trans retinoic acid (ATRA), AM80 (selective retinoic acid receptor α agonist), AC261066 (Selective retinoic acid receptor β1 agonist), and CD1530 (Selective retinoic acid λ agonist) were injected to 6–7 weeks old CJ5BL/6 mice before noise (110 dB for 3 h) exposure. In the auditory brainstem response test pre-, post 1, 3, and 7 days after noise exposure, not only ATRA but all kinds of selective RAR agonists showed protective effects in hearing threshold and wave I amplitude. Though there was no significant difference in the level of protective effects between agonists, α agonist showed the most prominent effect in preserving hearing function as well as outer hair cells after noise exposure. In conclusion, selective agonists of RAR demonstrate comparable protective effects against NIHL to retinoic acid. Given that these selective RAR agonists have less side effects than retinoic acid, they may be promising potential drugs against NIHL.

scholarly journals Effects of D-methionine in mice with noise-induced hearing loss mice

2019 ◽  
Vol 47 (8) ◽  
pp. 3874-3885 ◽  
Author(s):  
Yanru Wang ◽  
Yan Qu ◽  
Xuzhen Chen ◽  
Pu Zhang ◽  
Dan Su ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Basement Membrane ◽  
Mouse Model ◽  
Hair Cells ◽  
Noise Exposure ◽  
Stria Vascularis ◽  
Connexin 26 ◽  
Noise Induced Hearing Loss ◽  
Expression Levels ◽  
Brainstem Response

Objective To study the effects of D-methionine in a mouse model of noise-induced hearing loss (NIHL). Methods We investigated changes in auditory function and microscopic cochlear structure in a mouse model of NIHL, and carried out 4-hydroxynonenal (4-HNE) immunostaining and terminal deoxynucleotidyl transferase dUTP nick-end labeling, and examined expression levels of connexins 26 and 30 by western blot. Results The auditory brainstem response threshold was significantly increased by noise exposure. Noise exposure also damaged the inner and particularly the outer hair cells in the cochlear basement membrane, while histochemistry demonstrated only scattered loss of hair cells in the basement membrane in mice treated with D-methionine before or after noise exposure. D-methionine inhibited apoptosis in the cochlear basement membrane, stria vascularis, and spiral ligament. 4-HNE expression in the basement membrane, stria vascularis, and spiral collateral ligament was increased by noise exposure, but this increase was attenuated by D-methionine. Connexin 26 and connexin 30 expression levels were reduced by noise exposure, and this effect was similarly attenuated by D-methionine administered either before or after noise exposure. Conclusion D-methionine administered before or after noise exposure could rescue NIHL by protecting cochlear morphology, inhibiting apoptosis, and maintaining connexin 26 and 30 expression.

Work-Related, Noise-Induced Hearing Loss: Evaluation Including Evoked Potential Audiometry

1994 ◽  
Vol 110 (2) ◽  
pp. 177-184 ◽  
Author(s):  
David M. Barrs ◽  
Lisa K. Althoff ◽  
Wesley W. O. Krueger ◽  
James E. Olsson
Keyword(s):  
Hearing Loss ◽  
High Frequency ◽  
Auditory Brainstem ◽  
Noise Induced Hearing Loss ◽  
Work Related ◽  
Middle Latency Response ◽  
Behavioral Thresholds ◽  
Valuable Adjunct ◽  
Brainstem Response ◽  
Magnetic Resonance Scanning

This article reviews the evaluation of 246 workers (492 ears) who underwent otologic and audiologic testing as part of a worker's compensation claim for work-related, noise-induced hearing loss. Tinnitus was present in 58% of the patients, but was rarely a major symptom. Other otologic symptoms or a history of ear disease were virtually nonexistent. Standard audiometry showed a downsloping, high-frequency sensorineural hearing loss in 85% of the ears tested, with only 37% having a characteristic “noise notch” at 4000 or 6000 hertz. Asymmetric hearing loss was not uncommon, with 48 patients (20%) undergoing magnetic resonance scanning, all of whom showed no central lesion responsible for the loss. Proven malingering was surprisingly uncommon (9%). In this study, evoked response audiometry was a valuable adjunct to confirm behavioral thresholds in the evaluation of possible work-related, noise-induced hearing loss. The middle latency response was more effective than the auditory brainstem response as a result of the high-frequency steepness of the audiometric curve.

scholarly journals The DNA methylation inhibitor RG108 protects against noise-induced hearing loss

2021 ◽  
Author(s):  
Zhiwei Zheng ◽  
Shan Zeng ◽  
Chang Liu ◽  
Wen Li ◽  
Liping Zhao ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Hearing Loss ◽  
Dna Methyltransferase ◽  
Noise Exposure ◽  
Auditory Brainstem ◽  
Auditory Brainstem Responses ◽  
Dna Methyltransferase 1 ◽  
Noise Induced Hearing Loss ◽  
Threshold Elevation ◽  
Whole Mount

Abstract Background Noise-induced hearing loss represents a commonly diagnosed type of hearing disability, severely impacting the quality of life of individuals. The current work is aimed at assessing the effects of DNA methylation on noise-induced hearing loss. Methods Blocking DNA methyltransferase 1 (DNMT1) activity with a selective inhibitor RG108 or silencing DNMT1 with siRNA was used in this study. Auditory brainstem responses were measured at baseline and 2 days after trauma in mice to assess auditory functions. Whole-mount immunofluorescent staining and confocal microcopy of mouse inner ear specimens were performed to analyze noise-induced damage in cochleae and the auditory nerve at 2 days after noise exposure. Results The results showed that noise exposure caused threshold elevation of auditory brainstem responses and cochlear hair cell loss. Whole-mount cochlea staining revealed a reduction in the density of auditory ribbon synapses between inner hair cells and spiral ganglion neurons. Inhibition of DNA methyltransferase activity via a non-nucleoside specific pharmacological inhibitor, RG108, or silencing of DNA methyltransferase-1 with siRNA significantly attenuated ABR threshold elevation, hair cell damage, and the loss of auditory synapses. Conclusions This study suggests that inhibition of DNMT1 ameliorates noise-induced hearing loss and indicates that DNMT1 may be a promising therapeutic target. Graphical abstract

scholarly journals The Physiological Bases of Hidden Noise-Induced Hearing Loss: Protocol for a Functional Neuroimaging Study (Preprint)

2017 ◽  
Author(s):  
Rebecca Susan Dewey ◽  
Deborah A Hall ◽  
Hannah Guest ◽  
Garreth Prendergast ◽  
Christopher J Plack ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Noise Exposure ◽  
Functional Neuroimaging ◽  
Nerve Fibers ◽  
High Threshold ◽  
Hearing Level ◽  
Noise Induced Hearing Loss ◽  
Brainstem Response ◽  
Neuroimaging Study ◽  
Hidden Hearing Loss

BACKGROUND Rodent studies indicate that noise exposure can cause permanent damage to synapses between inner hair cells and high-threshold auditory nerve fibers, without permanently altering threshold sensitivity. These demonstrations of what is commonly known as hidden hearing loss have been confirmed in several rodent species, but the implications for human hearing are unclear. OBJECTIVE Our Medical Research Council–funded program aims to address this unanswered question, by investigating functional consequences of the damage to the human peripheral and central auditory nervous system that results from cumulative lifetime noise exposure. Behavioral and neuroimaging techniques are being used in a series of parallel studies aimed at detecting hidden hearing loss in humans. The planned neuroimaging study aims to (1) identify central auditory biomarkers associated with hidden hearing loss; (2) investigate whether there are any additive contributions from tinnitus or diminished sound tolerance, which are often comorbid with hearing problems; and (3) explore the relation between subcortical functional magnetic resonance imaging (fMRI) measures and the auditory brainstem response (ABR). METHODS Individuals aged 25 to 40 years with pure tone hearing thresholds ≤20 dB hearing level over the range 500 Hz to 8 kHz and no contraindications for MRI or signs of ear disease will be recruited into the study. Lifetime noise exposure will be estimated using an in-depth structured interview. Auditory responses throughout the central auditory system will be recorded using ABR and fMRI. Analyses will focus predominantly on correlations between lifetime noise exposure and auditory response characteristics. RESULTS This paper reports the study protocol. The funding was awarded in July 2013. Enrollment for the study described in this protocol commenced in February 2017 and was completed in December 2017. Results are expected in 2018. CONCLUSIONS This challenging and comprehensive study will have the potential to impact diagnostic procedures for hidden hearing loss, enabling early identification of noise-induced auditory damage via the detection of changes in central auditory processing. Consequently, this will generate the opportunity to give personalized advice regarding provision of ear defense and monitoring of further damage, thus reducing the incidence of noise-induced hearing loss.

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