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.

Changes in the spatiotemporal pattern of spontaneous activity across a cortical column after noise trauma

2021 ◽  
Author(s):  
Vinay Parameshwarappa ◽  
Laurent Pezard ◽  
Arnaud Jean Norena
Keyword(s):  
Hearing Loss ◽  
Spontaneous Activity ◽  
Local Field ◽  
Local Field Potentials ◽  
Spatiotemporal Pattern ◽  
Noise Induced Hearing Loss ◽  
Field Potentials ◽  
Cortical Column ◽  
Cortical Layers ◽  
Noise Trauma

In the auditory modality, noise trauma has often been used to investigate cortical plasticity as it causes cochlear hearing loss. One limitation of these past studies, however, is that the effects of noise trauma have been mostly documented at the granular layer, which is the main cortical recipient of thalamic inputs. Importantly, the cortex is composed of six different layers each having its own pattern of connectivity and specific role in sensory processing. The present study aims at investigating the effects of acute and chronic noise trauma on the laminar pattern of spontaneous activity in primary auditory cortex of the anesthetized guinea pig. We show that spontaneous activity is dramatically altered across cortical layers after acute and chronic noise-induced hearing loss. First, spontaneous activity was globally enhanced across cortical layers, both in terms of firing rate and amplitude of spike-triggered average of local field potentials. Second, current source density on (spontaneous) spike-triggered average of local field potentials indicates that current sinks develop in the supra- and infragranular layers. These latter results suggest that supragranular layers become a major input recipient and that the propagation of spontaneous activity over a cortical column is greatly enhanced after acute and chronic noise-induced hearing loss. We discuss the possible mechanisms and functional implications of these changes.

scholarly journals Noise-induced hyperactivity in the inferior colliculus: its relationship with hyperactivity in the dorsal cochlear nucleus

2012 ◽  
Vol 108 (4) ◽  
pp. 976-988 ◽  
Author(s):  
N. F. Manzoor ◽  
F. G. Licari ◽  
M. Klapchar ◽  
R. L. Elkin ◽  
Y. Gao ◽  
...  
Keyword(s):  
Spontaneous Activity ◽  
Inferior Colliculus ◽  
Cochlear Nucleus ◽  
Time Course ◽  
Noise Exposure ◽  
Dorsal Cochlear Nucleus ◽  
Control Group ◽  
Before And After ◽  
Intense Noise ◽  
And Control

Intense noise exposure causes hyperactivity to develop in the mammalian dorsal cochlear nucleus (DCN) and inferior colliculus (IC). It has not yet been established whether the IC hyperactivity is driven by hyperactivity from extrinsic sources that include the DCN or instead is maintained independently of this input. We have investigated the extent to which IC hyperactivity is dependent on input from the contralateral DCN by comparing recordings of spontaneous activity in the IC of noise-exposed and control hamsters before and after ablation of the contralateral DCN. One group of animals was binaurally exposed to intense sound (10 kHz, 115 dB SPL, 4 h), whereas the control group was not. Both groups were studied electrophysiologically 2–3 wk later by first mapping spontaneous activity along the tonotopic axis of the IC to confirm induction of hyperactivity. Spontaneous activity was then recorded at a hyperactive IC locus over two 30-min periods, one with DCNs intact and the other after ablation of the contralateral DCN. In a subset of animals, activity was again mapped along the tonotopic axis after the time course of the activity was recorded before and after DCN ablation. Following recordings, the brains were fixed, and histological evaluations were performed to assess the extent of DCN ablation. Ablation of the DCN resulted in major reductions of IC hyperactivity. Levels of postablation activity in exposed animals were similar to the levels of activity in the IC of control animals, indicating an almost complete loss of hyperactivity in exposed animals. The results suggest that hyperactivity in the IC is dependent on support from extrinsic sources that include and may even begin with the DCN. This finding does not rule out longer term compensatory or homeostatic adjustments that might restore hyperactivity in the IC over time.

scholarly journals Changes in microRNA Expression in the Cochlear Nucleus and Inferior Colliculus after Acute Noise-Induced Hearing Loss

2020 ◽  
Vol 21 (22) ◽  
pp. 8792
Author(s):  
Sohyeon Park ◽  
Seung Hee Han ◽  
Byeong-Gon Kim ◽  
Myung-Whan Suh ◽  
Jun Ho Lee ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Inferior Colliculus ◽  
Neural Plasticity ◽  
Cochlear Nucleus ◽  
Organ Of Corti ◽  
Auditory Pathway ◽  
Noise Induced Hearing Loss ◽  
Candidate Mirnas ◽  
Central Auditory Pathway

Noise-induced hearing loss (NIHL) can lead to secondary changes that induce neural plasticity in the central auditory pathway. These changes include decreases in the number of synapses, the degeneration of auditory nerve fibers, and reorganization of the cochlear nucleus (CN) and inferior colliculus (IC) in the brain. This study investigated the role of microRNAs (miRNAs) in the neural plasticity of the central auditory pathway after acute NIHL. Male Sprague–Dawley rats were exposed to white band noise at 115 dB for 2 h, and the auditory brainstem response (ABR) and morphology of the organ of Corti were evaluated on days 1 and 3. Following noise exposure, the ABR threshold shift was significantly smaller in the day 3 group, while wave II amplitudes were significantly larger in the day 3 group compared to the day 1 group. The organ of Corti on the basal turn showed evidence of damage and the number of surviving outer hair cells was significantly lower in the basal and middle turn areas of the hearing loss groups relative to controls. Five and three candidate miRNAs for each CN and IC were selected based on microarray analysis and quantitative reverse transcription PCR (RT-qPCR). The data confirmed that even short-term acoustic stimulation can lead to changes in neuroplasticity. Further studies are needed to validate the role of these candidate miRNAs. Such miRNAs may be used in the early diagnosis and treatment of neural plasticity of the central auditory pathway after acute NIHL.

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.

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.

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