scholarly journals Acute and long-term circuit-level effects in the auditory cortex after sound trauma

2020 ◽  
Author(s):  
Marcus Jeschke ◽  
Max F.K. Happel ◽  
Konstantin Tziridis ◽  
Patrick Krauss ◽  
Achim Schilling ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Auditory Cortex ◽  
Noise Exposure ◽  
Temporal Evolution ◽  
Current Source ◽  
Sensory Receptor ◽  
Mongolian Gerbils ◽  
Noise Induced Hearing Loss ◽  
Hearing Impairments

AbstractHarmful environmental sounds are a prevailing source for chronic hearing impairments, including noise induced hearing loss, hyperacusis, or tinnitus. How these symptoms are related to pathophysiological damage to the sensory receptor epithelia and its effects along the auditory pathway, such as functional reorganizations in the auditory cortex (ACx), have been documented in numerous studies. An open question concerns the temporal evolution of maladaptive changes after damage and their manifestation in the balance between afferent thalamocortical input and corticocortical input to the ACx.To address this, we investigated the loci of plastic reorganizations across the tonotopic axis of the auditory cortex of male Mongolian gerbils (Meriones unguiculatus) acutely after a sound trauma and after several weeks. We used a laminar residual current-source density analysis to dissociate adaptations of intracolumnar input and horizontally relayed corticocortical input to synaptic populations across cortical layers in ACx. A pure tone-based sound trauma caused acute changes of subcortical inputs and corticocortical inputs at all tonotopic regions, particularly showing a broad elimination of tone-evoked inputs at tonotopic regions with a pre-trauma best frequency between 2-8 kHz. At other cortical sites, the overall columnar activity acutely decreased, while relative contributions of lateral corticocortical inputs increased. After 4-6 weeks, cortical activity to the altered sensory inputs showed a general increase of local thalamocortical input reaching levels higher than before the trauma. Hence, our results suggest a detailed mechanism for overcompensation of altered frequency input in the auditory cortex that relies on a changing balancing of thalamocortical and intracortical input and is confined to the spectral neighborhood of the trauma frequency.Significance statementHarmful noise exposure is a major anthropogenic cause of hearing disorders and is becoming an ever-increasing burden for human health and society. Damage to the sensory epithelia elicited by harmful sounds can subsequently lead to chronic hearing loss, hyperacusis or tinnitus. We still lack an understanding of the pathophysiological plastic processes and their evolution, particularly at the circuit level of the auditory cortex (ACx), which is fundamentally involved in auditory perception. We demonstrate that plastic changes in ACx after noise induced hearing loss (NIHL) occur over several weeks, and that changes in intracortical functional connectivity compensate the acute effects in the deafferentiated subcortical inputs. Such long-term changes may underlie the temporal evolution of hearing impairments or phantom sounds after NIHL.

scholarly journals Acute and Long-Term Circuit-Level Effects in the Auditory Cortex After Sound Trauma

2021 ◽  
Vol 14 ◽  
Author(s):  
Marcus Jeschke ◽  
Max F. K. Happel ◽  
Konstantin Tziridis ◽  
Patrick Krauss ◽  
Achim Schilling ◽  
...  
Keyword(s):  
Auditory Cortex ◽  
Current Source ◽  
Auditory Pathway ◽  
Meriones Unguiculatus ◽  
Sensory Receptor ◽  
Mongolian Gerbils ◽  
Hearing Impairments ◽  
Density Analysis ◽  
Acute Changes ◽  
Open Question

Harmful environmental sounds are a prevailing source of chronic hearing impairments, including noise induced hearing loss, hyperacusis, or tinnitus. How these symptoms are related to pathophysiological damage to the sensory receptor epithelia and its effects along the auditory pathway, have been documented in numerous studies. An open question concerns the temporal evolution of maladaptive changes after damage and their manifestation in the balance of thalamocortical and corticocortical input to the auditory cortex (ACx). To address these issues, we investigated the loci of plastic reorganizations across the tonotopic axis of the auditory cortex of male Mongolian gerbils (Meriones unguiculatus) acutely after a sound trauma and after several weeks. We used a residual current-source density analysis to dissociate adaptations of intracolumnar input and horizontally relayed corticocortical input to synaptic populations across cortical layers in ACx. A pure tone-based sound trauma caused acute changes of subcortical inputs and corticocortical inputs at all tonotopic regions, particularly showing a broad reduction of tone-evoked inputs at tonotopic regions around the trauma frequency. At other cortical sites, the overall columnar activity acutely decreased, while relative contributions of lateral corticocortical inputs increased. After 4–6 weeks, cortical activity in response to the altered sensory inputs showed a general increase of local thalamocortical input reaching levels higher than before the trauma. Hence, our results suggest a detailed mechanism for overcompensation of altered frequency input in the auditory cortex that relies on a changing balance of thalamocortical and intracortical input and along the frequency gradient of the cortical tonotopic map.

scholarly journals Acute and Long-Term Effects of Noise Exposure on the Neuronal Spontaneous Activity in Cochlear Nucleus and Inferior Colliculus Brain Slices

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Moritz Gröschel ◽  
Jana Ryll ◽  
Romy Götze ◽  
Arne Ernst ◽  
Dietmar Basta
Keyword(s):  
Hearing Loss ◽  
Spontaneous Activity ◽  
Inferior Colliculus ◽  
Cochlear Nucleus ◽  
Noise Exposure ◽  
Brain Slices ◽  
Noise Induced Hearing Loss ◽  
Long Term Effects ◽  
Noise Trauma

Noise exposure leads to an immediate hearing loss and is followed by a long-lasting permanent threshold shift, accompanied by changes of cellular properties within the central auditory pathway. Electrophysiological recordings have demonstrated an upregulation of spontaneous neuronal activity. It is still discussed if the observed effects are related to changes of peripheral input or evoked within the central auditory system. The present study should describe the intrinsic temporal patterns of single-unit activity upon noise-induced hearing loss of the dorsal and ventral cochlear nucleus (DCN and VCN) and the inferior colliculus (IC) in adult mouse brain slices. Recordings showed a slight, but significant, elevation in spontaneous firing rates in DCN and VCN immediately after noise trauma, whereas no differences were found in IC. One week postexposure, neuronal responses remained unchanged compared to controls. At 14 days after noise trauma, intrinsic long-term hyperactivity in brain slices of the DCN and the IC was detected for the first time. Therefore, increase in spontaneous activity seems to develop within the period of two weeks, but not before day 7. The results give insight into the complex temporal neurophysiological alterations after noise trauma, leading to a better understanding of central mechanisms in noise-induced hearing loss.

MicroRNAs in Noise-Induced Hearing Loss and their Regulation by Oxidative Stress and Inflammation

2020 ◽  
Vol 21 (12) ◽  
pp. 1216-1224
Author(s):  
Fatemeh Forouzanfar ◽  
Samira Asgharzade
Keyword(s):  
Oxidative Stress ◽  
Hearing Loss ◽  
Hair Cell ◽  
Noise Exposure ◽  
Cell Damage ◽  
Sensory Cells ◽  
Noise Induced Hearing Loss ◽  
Irreversible Damage ◽  
Open Access Journals

Noise exposure (NE) has been recognized as one of the causes of sensorineural hearing loss (SNHL), which can bring about irreversible damage to sensory hair cells in the cochlea, through the launch of oxidative stress pathways and inflammation. Accordingly, determining the molecular mechanism involved in regulating hair cell apoptosis via NE is essential to prevent hair cell damage. However, the role of microRNAs (miRNAs) in the degeneration of sensory cells of the cochlea during NE has not been so far uncovered. Thus, the main purpose of this study was to demonstrate the regulatory role of miRNAs in the oxidative stress pathway and inflammation induced by NE. In this respect, articles related to noise-induced hearing loss (NIHL), oxidative stress, inflammation, and miRNA from various databases of Directory of Open Access Journals (DOAJ), Google Scholar, PubMed; Library, Information Science & Technology Abstracts (LISTA), and Web of Science were searched and retrieved. The findings revealed that several studies had suggested that up-regulation of miR-1229-5p, miR-451a, 185-5p, 186 and down-regulation of miRNA-96/182/183 and miR-30b were involved in oxidative stress and inflammation which could be used as biomarkers for NIHL. There was also a close relationship between NIHL and miRNAs, but further research is required to prove a causal association between miRNA alterations and NE, and also to determine miRNAs as biomarkers indicating responses to NE.

Noise Exposure and Hearing Disorders

2017 ◽  
Author(s):  
David C. Byrne ◽  
Thais C. Morata
Keyword(s):  
Hearing Loss ◽  
Noise Exposure ◽  
Hearing Protection ◽  
Noise Induced Hearing Loss ◽  
Hearing Disorders ◽  
Industrial Noise ◽  
Significant Impairment ◽  
Protection Devices ◽  
The Impact ◽  
Occupational Hearing Loss

Exposure to industrial noise and the resulting effect of occupational hearing loss is a common problem in nearly all industries. This chapter describes industrial noise exposure, its assessment, and hearing disorders that result from overexposure to noise. Beginning with the properties of sound, noise-induced hearing loss and other effects of noise exposure are discussed. The impact of hearing disorders and the influence of other factors on hearing loss are described. Typically, noise-induced hearing loss develops slowly, and usually goes unnoticed until a significant impairment has occurred. Fortunately, occupational hearing loss is nearly always preventable. Therefore, this chapter gives particular attention to recommendations for measures to prevent occupational hearing loss such as engineering noise controls and hearing protection devices.

scholarly journals Contributions and limitations of using machine learning to predict noise-induced hearing loss

2021 ◽  
Author(s):  
Feifan Chen ◽  
Zuwei Cao ◽  
Emad M. Grais ◽  
Fei Zhao
Keyword(s):  
Machine Learning ◽  
Hearing Loss ◽  
Roc Curve ◽  
Prediction Error ◽  
Noise Exposure ◽  
Model Construction ◽  
Support Vector ◽  
Exposure Level ◽  
Noise Induced Hearing Loss ◽  
Current Review

Abstract Purpose Noise-induced hearing loss (NIHL) is a global issue that impacts people’s life and health. The current review aims to clarify the contributions and limitations of applying machine learning (ML) to predict NIHL by analyzing the performance of different ML techniques and the procedure of model construction. Methods The authors searched PubMed, EMBASE and Scopus on November 26, 2020. Results Eight studies were recruited in the current review following defined inclusion and exclusion criteria. Sample size in the selected studies ranged between 150 and 10,567. The most popular models were artificial neural networks (n = 4), random forests (n = 3) and support vector machines (n = 3). Features mostly correlated with NIHL and used in the models were: age (n = 6), duration of noise exposure (n = 5) and noise exposure level (n = 4). Five included studies used either split-sample validation (n = 3) or ten-fold cross-validation (n = 2). Assessment of accuracy ranged in value from 75.3% to 99% with a low prediction error/root-mean-square error in 3 studies. Only 2 studies measured discrimination risk using the receiver operating characteristic (ROC) curve and/or the area under ROC curve. Conclusion In spite of high accuracy and low prediction error of machine learning models, some improvement can be expected from larger sample sizes, multiple algorithm use, completed reports of model construction and the sufficient evaluation of calibration and discrimination risk.

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.

Field Monitoring of Otoacoustic Emissions During Noise Exposure: Pilot Study in Controlled Environment

2017 ◽  
Vol 26 (3S) ◽  
pp. 352-368 ◽  
Author(s):  
Vincent Nadon ◽  
Annelies Bockstael ◽  
Dick Botteldooren ◽  
Jérémie Voix
Keyword(s):  
Hearing Loss ◽  
Pilot Study ◽  
Otoacoustic Emissions ◽  
Ambient Noise ◽  
Noise Exposure ◽  
High Temporal Resolution ◽  
Noise Induced Hearing Loss ◽  
Conservation Programs ◽  
Hearing Conservation ◽  
Hearing Status

Purpose In spite of all the efforts to implement workplace hearing conservation programs, noise-induced hearing loss remains the leading cause of disability for North American workers. Nonetheless, an individual's susceptibility to noise-induced hearing loss can be estimated by monitoring changes in hearing status in relation to the level of ambient noise exposure. The purpose of this study was to validate an approach that could improve workplace hearing conservation practices. The approach was developed using a portable and robust system designed for noisy environments and consisted of taking continuous measurements with high temporal resolution of the health status of the inner ear using otoacoustic emissions (OAEs). Method A pilot study was conducted in a laboratory, exposing human subjects to industrial noise recordings at realistic levels. In parallel, OAEs were measured periodically using the designed OAE system as well as with a commercially available OAE system, used as a reference. Results Variations in OAE levels were analyzed and discussed along with the limitations of the reference and designed systems. Conclusions This study demonstrates that the monitoring of an individual's OAEs could be useful in monitoring temporary changes in hearing status induced by exposure to ambient noise and could be considered as a new tool for effective hearing conservation programs in the workplace.

scholarly journals Primed to die: an investigation of the genetic mechanisms underlying noise-induced hearing loss and cochlear damage in homozygous Foxo3-knockout mice

2021 ◽  
Vol 12 (7) ◽  
Author(s):  
Holly J. Beaulac ◽  
Felicia Gilels ◽  
Jingyuan Zhang ◽  
Sarah Jeoung ◽  
Patricia M. White
Keyword(s):  
Oxidative Stress ◽  
Hearing Loss ◽  
Noise Exposure ◽  
Multiphoton Microscopy ◽  
Cell Loss ◽  
Outer Hair Cells ◽  
Noise Induced Hearing Loss ◽  
Knock Out ◽  
Cell Death Pathway ◽  
Cochlear Damage

AbstractThe prevalence of noise-induced hearing loss (NIHL) continues to increase, with limited therapies available for individuals with cochlear damage. We have previously established that the transcription factor FOXO3 is necessary to preserve outer hair cells (OHCs) and hearing thresholds up to two weeks following mild noise exposure in mice. The mechanisms by which FOXO3 preserves cochlear cells and function are unknown. In this study, we analyzed the immediate effects of mild noise exposure on wild-type, Foxo3 heterozygous (Foxo3+/−), and Foxo3 knock-out (Foxo3−/−) mice to better understand FOXO3’s role(s) in the mammalian cochlea. We used confocal and multiphoton microscopy to examine well-characterized components of noise-induced damage including calcium regulators, oxidative stress, necrosis, and caspase-dependent and caspase-independent apoptosis. Lower immunoreactivity of the calcium buffer Oncomodulin in Foxo3−/− OHCs correlated with cell loss beginning 4 h post-noise exposure. Using immunohistochemistry, we identified parthanatos as the cell death pathway for OHCs. Oxidative stress response pathways were not significantly altered in FOXO3’s absence. We used RNA sequencing to identify and RT-qPCR to confirm differentially expressed genes. We further investigated a gene downregulated in the unexposed Foxo3−/− mice that may contribute to OHC noise susceptibility. Glycerophosphodiester phosphodiesterase domain containing 3 (GDPD3), a possible endogenous source of lysophosphatidic acid (LPA), has not previously been described in the cochlea. As LPA reduces OHC loss after severe noise exposure, we treated noise-exposed Foxo3−/− mice with exogenous LPA. LPA treatment delayed immediate damage to OHCs but was insufficient to ultimately prevent their death or prevent hearing loss. These results suggest that FOXO3 acts prior to acoustic insult to maintain cochlear resilience, possibly through sustaining endogenous LPA levels.

scholarly journals Comparative analysis of the potential and actual risk of noise-induced hearing loss in employees of “noise” industries

2021 ◽  
Vol 100 (9) ◽  
pp. 947-952
Author(s):  
Elena A. Preobrazhenskaia ◽  
Anna V. Sukhova ◽  
Elena N. Kriuchkova
Keyword(s):  
Hearing Loss ◽  
Potential Risk ◽  
Noise Exposure ◽  
Calculated Data ◽  
Risk Groups ◽  
Epidemiological Studies ◽  
Noise Induced Hearing Loss ◽  
Actual Risk ◽  
Real Risk ◽  
Processing Plants

Introduction. The high incidence of noise-induced hearing loss (NIHL) makes it possible to attribute the problem of prevention and prediction of the risk of NIHL to the number of socially significant ones. The aim of the study is to conduct a comparative assessment of the potential risk of hearing loss caused by noise according to GOST R ISO 1999-2017, and the actual risk of NIHL in workers of “noise” industries according to epidemiological research. Materials and methods. The calculation of the potential risk of hearing loss according to GOST R ISO 1999-2017 included assessing age, noise and total hearing loss at noise exposure with 85, 90, 95 and 100 dBA. The actual risk of NIHL was evaluated on survey data of 600 miners and 600 workers of processing plants. Results. The calculation of the probable risk according to GOST R ISO 1999-2017 and the assessment of the actual risk according to epidemiological studies showed that the risk of NIHL depends on both noise exposure and age. As the levels of noise affecting an employee increase, the risk of an NIHL becomes more determined by the effect of noise. At noise levels 85, 90 and 95 dBA, the probable risk calculated under GOST R ISO 1999-2017 coincides with the actual risk established according to epidemiological studies. At the same time, for miners exposed to high-intensity noise 100 dBА, the real risk was not as high as could be assumed from the calculated data. Conclusion. The results obtained allow stating that the GOST ISO 1999-2017 standard with a high degree of potential risk allows predicting the group risk of hearing loss due to noise exposure, to quantify the degree of risk and can be used for the formation of risk groups for NIHL and the development of programs for the preservation of hearing.

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