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 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.

Molecular and Structural Changes in the Cochlear Nucleus in Response to Hearing Loss

2018 ◽  
pp. 142-162
Author(s):  
Maria E. Rubio
Keyword(s):  
Hearing Loss ◽  
Cochlear Nucleus ◽  
Structural Changes ◽  
Auditory Pathway ◽  
The United States ◽  
Cellular Mechanisms ◽  
Auditory Experience ◽  
Central Auditory Pathway ◽  
The Brain

Hearing loss is the third most common health problem in the United States. It can affect the quality of life and relationships. About 48 million Americans have lost some hearing. Age, illness, and genetics contribute to the generation of hearing loss. During development, auditory synaptic circuitries are highly plastic and able to adapt to fluctuations in auditory experience. Whether this is so for mature auditory nerve synapses and circuitries within nuclei along the central auditory pathway is less understood. Daily fluctuations in auditory experience can lead to hearing deficits, including hearing loss and/or deafness, Therefore, understanding the cellular mechanisms that occur in mature central auditory synaptic circuitries that lead and/or contribute to hearing loss is important. This chapter focuses on published studies using animal models describing structural and molecular changes that occur in the cochlear nucleus in response to hearing loss, the first gateway of sound processing in the brain.

Hearing Loss of a Central Type Secondary to Anoxic Anoxia

1976 ◽  
Vol 85 (6) ◽  
pp. 826-832 ◽  
Author(s):  
Kazumi Makishima ◽  
Roger B. Katz ◽  
James B. Snow
Keyword(s):  
Hearing Loss ◽  
Auditory Cortex ◽  
Inferior Colliculus ◽  
Guinea Pigs ◽  
Auditory Pathway ◽  
Threshold Sensitivity ◽  
Central Type ◽  
Acoustic Stimuli ◽  
Central Auditory Pathway ◽  
Relative Vulnerability

The effect of anoxic anoxia on the threshold sensitivity and amplitude of the responses from the auditory cortex, inferior colliculus and cochlea to acoustic stimuli in guinea pigs was studied. Decay of the amplitude of the responses from the auditory cortex and the inferior colliculus occurs faster and is more severe than that of the cochlea. Recovery of the amplitude of the responses is slower at the auditory cortex and the inferior colliculus than at the cochlea. Loss of auditory threshold sensitivity in anoxic anoxia is most prominent at the auditory cortex. The loss of sensitivity at the inferior colliculus is the next most severe. The loss of sensitivity at the cochlea is negligible. The relative vulnerability of the central auditory pathway to anoxic anoxia as compared to the end organ is demonstrated.

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.

The role of middle ear muscles in the development of resistance to noise induced hearing loss

1994 ◽  
Vol 74 (1-2) ◽  
pp. 22-28 ◽  
Author(s):  
Donald Henderson ◽  
Malini Subramaniam ◽  
Martin Papazian ◽  
Vlasta P. Spongr
Keyword(s):  
Hearing Loss ◽  
Middle Ear ◽  
Noise Induced Hearing Loss ◽  
Development Of Resistance

scholarly journals Multiphoton NAD(P)H FLIM reveals metabolic changes in individual cell types of the intact cochlea upon sensorineural hearing loss

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Paromita Majumder ◽  
Thomas S. Blacker ◽  
Lisa S. Nolan ◽  
Michael R. Duchen ◽  
Jonathan E. Gale
Keyword(s):  
Oxidative Stress ◽  
Hearing Loss ◽  
Cell Model ◽  
Organ Of Corti ◽  
Cell Types ◽  
Fluorescence Lifetime Imaging ◽  
Noise Induced Hearing Loss ◽  
Label Free ◽  
Age Related ◽  
The Individual

AbstractAn increasing volume of data suggests that changes in cellular metabolism have a major impact on the health of tissues and organs, including in the auditory system where metabolic alterations are implicated in both age-related and noise-induced hearing loss. However, the difficulty of access and the complex cyto-architecture of the organ of Corti has made interrogating the individual metabolic states of the diverse cell types present a major challenge. Multiphoton fluorescence lifetime imaging microscopy (FLIM) allows label-free measurements of the biochemical status of the intrinsically fluorescent metabolic cofactors NADH and NADPH with subcellular spatial resolution. However, the interpretation of NAD(P)H FLIM measurements in terms of the metabolic state of the sample are not completely understood. We have used this technique to explore changes in metabolism associated with hearing onset and with acquired (age-related and noise-induced) hearing loss. We show that these conditions are associated with altered NAD(P)H fluorescence lifetimes, use a simple cell model to confirm an inverse relationship between τbound and oxidative stress, and propose such changes as a potential index of oxidative stress applicable to all mammalian cell types.

scholarly journals Noise Induced Hearing Loss and Tinnitus—New Research Developments and Remaining Gaps in Disease Assessment, Treatment, and Prevention

2020 ◽  
Vol 10 (10) ◽  
pp. 732
Author(s):  
Tang-Chuan Wang ◽  
Ta-Yuan Chang ◽  
Richard Tyler ◽  
Ying-Ju Lin ◽  
Wen-Miin Liang ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Neural Plasticity ◽  
Noise Exposure ◽  
Disease Assessment ◽  
Noise Induced Hearing Loss ◽  
Ongoing Research ◽  
Adaptive Changes ◽  
Treatment And Prevention ◽  
Underlying Mechanisms ◽  
New Research

Long-term noise exposure often results in noise induced hearing loss (NIHL). Tinnitus, the generation of phantom sounds, can also result from noise exposure, although understanding of its underlying mechanisms are limited. Recent studies, however, are shedding light on the neural processes involved in NIHL and tinnitus, leading to potential new and innovative treatments. This review focuses on the assessment of NIHL, available treatments, and development of new pharmacologic and non-pharmacologic treatments based on recent studies of central auditory plasticity and adaptive changes in hearing. We discuss the mechanisms and maladaptive plasticity of NIHL, neuronal aspects of tinnitus triggers, and mechanisms such as tinnitus-associated neural changes at the cochlear nucleus underlying the generation of tinnitus after noise-induced deafferentation. We include observations from recent studies, including our own studies on associated risks and emerging treatments for tinnitus. Increasing knowledge of neural plasticity and adaptive changes in the central auditory system suggest that NIHL is preventable and transient abnormalities may be reversable, although ongoing research in assessment and early detection of hearing difficulties is still urgently needed. Since no treatment can yet reverse noise-related damage completely, preventative strategies and increased awareness of hearing health are essential.

Effects of L-Baclofen and D-Baclofen on the Auditory System: A Study of Click-Evoked Potentials from the Inferior Colliculus in the Rat

1995 ◽  
Vol 104 (5) ◽  
pp. 399-404 ◽  
Author(s):  
William S. Szczepaniak ◽  
Aage R. Møller
Keyword(s):  
Inferior Colliculus ◽  
Cochlear Nucleus ◽  
Auditory Pathway ◽  
Detectable Effect ◽  
Potential Treatment ◽  
Racemic Form ◽  
System A ◽  
Auditory Disorders ◽  
Severe Tinnitus ◽  
Second Peak

The drug baclofen is a potential treatment for severe tinnitus, but its action in relieving tinnitus is not known. Baclofen is available as an approved drug only in racemic form with about equal content of the two enantiomers. In the present paper we show that l-baclofen causes a considerable (40.7%) suppression of the amplitude of the second peak in the click-evoked response from the cochlear nucleus. Bipolar recordings from the external nucleus of the inferior colliculus showed that l-baclofen caused a reduction in the amplitude of three or four distinct peaks in this response. d-Baclofen had no detectable effect on the response from the cochlear nucleus, and had only a slight effect on one component of the response from the external nucleus of the inferior colliculus. The demonstrated effect of l-baclofen on excitation in the ascending auditory pathway indicates that this drug may be a potential treatment for hyperactive auditory disorders such as tinnitus and hyperacusis.

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