Age-Related and Noise-Induced Hearing Loss

2018 ◽  
pp. 162-188
Author(s):  
Ruili Xie ◽  
Tessa-Jonne F. Ropp ◽  
Michael R. Kasten ◽  
Paul B. Manis
Keyword(s):  
Hearing Loss ◽  
Auditory Nerve ◽  
Transmitter Release ◽  
Time Course ◽  
Functional Change ◽  
Noise Induced Hearing Loss ◽  
Nerve Activity ◽  
Auditory Periphery ◽  
Age Related ◽  
Age Related Hearing Loss

Hearing loss generally occurs in the auditory periphery but leads to changes in the central auditory system. Noise-induced hearing loss (NIHL) and age-related hearing loss (ARHL) affect neurons in the ventral cochlear nucleus (VCN) at both the cellular and systems levels. In response to a decrease in auditory nerve activity associated with hearing loss, the large synaptic endings of the auditory nerve, the endbulbs of Held, undergo simplification of their structure and the volume of the postsynaptic bushy neurons decreases. A major functional change shared by NIHL and ARHL is the development of asynchronous transmitter release at endbulb synapses during periods of high afferent firing. Compensatory adjustements in transmitter release, including changes in release probability and quantal content, have also been reported. The excitability of the bushy cells undergoes subtle changes in the long-term, although short-term, reversible changes in excitability may also occur. These changes are not consistently observed across all models of hearing loss, suggesting that the time course of hearing loss, and potential developmental effects, may influence endbulb transmission in multiple ways. NIHL can alter the representation of the loudness of tonal stimuli by VCN neurons and is accompanied by changes in spontaneous activity in VCN neurons. However, little is known about the representation of more complex stimuli. The relationship between mechanistic changes in VCN neurons with noise-induced or age-related hearing loss, the accompanying change in sensory coding, and the reversibility of changes with the reintroduction of auditory nerve activity are areas that deserve further thoughtful exploration.

scholarly journals Synaptic Transmission at the Cochlear Nucleus Endbulb Synapse During Age-Related Hearing Loss in Mice

2005 ◽  
Vol 94 (3) ◽  
pp. 1814-1824 ◽  
Author(s):  
Yong Wang ◽  
Paul B. Manis
Keyword(s):  
Hearing Loss ◽  
Synaptic Transmission ◽  
Cochlear Nucleus ◽  
Auditory Nerve ◽  
High Frequency ◽  
Nerve Activity ◽  
Synaptic Release ◽  
Endbulb Of Held ◽  
Age Related ◽  
Age Related Hearing Loss

Age-related hearing loss (AHL) typically starts from high-frequency regions of the cochlea and over time invades lower-frequency regions. During this progressive hearing loss, sound-evoked activity in spiral ganglion cells is reduced. DBA mice have an early onset of AHL. In this study, we examined synaptic transmission at the endbulb of Held synapse between auditory nerve fibers and bushy cells in the anterior ventral cochlear nucleus (AVCN). Synaptic transmission in hearing-impaired high-frequency areas of the AVCN was altered in old DBA mice. The spontaneous miniature excitatory postsynaptic current (mEPSC) frequency was substantially reduced (about 60%), and mEPSCs were significantly slower (about 115%) and smaller (about 70%) in high-frequency regions of old (average age 45 days) DBA mice compared with tonotopically matched regions of young (average age 22 days) DBA mice. Moreover, synaptic release probability was about 30% higher in high-frequency regions of young DBA than that in old DBA mice. Auditory nerve–evoked EPSCs showed less rectification in old DBA mice, suggesting recruitment of GluR2 subunits into the AMPA receptor complex. No similar age-related changes in synaptic release or EPSCs were found in age-matched, normal hearing young and old CBA mice. Taken together, our results suggest that auditory nerve activity plays a critical role in maintaining normal synaptic function at the endbulb of Held synapse after the onset of hearing. Auditory nerve activity regulates both presynaptic (release probability) and postsynaptic (receptor composition and kinetics) function at the endbulb synapse after the onset of hearing.

Medical-Legal Assessment of Hearing Loss

1995 ◽  
Vol 112 (5) ◽  
pp. P75-P75
Author(s):  
Robert A. Dobie
Keyword(s):  
Hearing Loss ◽  
Time Course ◽  
Noise Induced Hearing Loss ◽  
Educational Objectives ◽  
Legal Assessment ◽  
Epidemiologic Data ◽  
Age Related ◽  
Exposure History ◽  
Age Related Hearing Loss

Educational objectives: To understand the epidemiology of noise-induced hearing loss (NIHL) and age-related hearing loss (ARHL), including time course, interactions, and importance of occupational and nonoccupational exposure history; to use clinical and epidemiologic data and principles to diagnose NIHL and ARHL; and to estimate the relative contributions of each in individual cases.

scholarly journals Noise-induced and age-related hearing loss:  new perspectives and potential therapies

F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 927 ◽  
Author(s):  
M Charles Liberman
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Sensorineural Hearing Loss ◽  
Hair Cells ◽  
Auditory Nerve ◽  
Cell Loss ◽  
Sensorineural Hearing ◽  
Hair Cell Loss ◽  
Age Related ◽  
Age Related Hearing Loss

The classic view of sensorineural hearing loss has been that the primary damage targets are hair cells and that auditory nerve loss is typically secondary to hair cell degeneration. Recent work has challenged that view. In noise-induced hearing loss, exposures causing only reversible threshold shifts (and no hair cell loss) nevertheless cause permanent loss of >50% of the synaptic connections between hair cells and the auditory nerve. Similarly, in age-related hearing loss, degeneration of cochlear synapses precedes both hair cell loss and threshold elevation. This primary neural degeneration has remained a “hidden hearing loss” for two reasons: 1) the neuronal cell bodies survive for years despite loss of synaptic connection with hair cells, and 2) the degeneration is selective for auditory nerve fibers with high thresholds. Although not required for threshold detection when quiet, these high-threshold fibers are critical for hearing in noisy environments. Research suggests that primary neural degeneration is an important contributor to the perceptual handicap in sensorineural hearing loss, and it may be key to the generation of tinnitus and other associated perceptual anomalies. In cases where the hair cells survive, neurotrophin therapies can elicit neurite outgrowth from surviving auditory neurons and re-establishment of their peripheral synapses; thus, treatments may be on the horizon.

scholarly journals Biased Auditory Nerve Central Synaptopathy Exacerbates Age-related Hearing Loss

2020 ◽  
Author(s):  
Meijian Wang ◽  
Chuangeng Zhang ◽  
Shengyin Lin ◽  
Yong Wang ◽  
Benjamin J. Seicol ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Auditory Processing ◽  
Auditory Nerve ◽  
Spiral Ganglion ◽  
Central Auditory Processing ◽  
Endbulb Of Held ◽  
Age Related ◽  
Central Synapses ◽  
Ganglion Neurons ◽  
Age Related Hearing Loss

SUMMARYSound information is transmitted from the cochlea to the brain by different subtypes of spiral ganglion neurons (SGN), which show varying degrees of vulnerbility under pathological conditions. It remains unclear how information from these SGNs reassemble among target neurons in the cochlear nucleus (CN) at the auditory nerve (AN) central synapses, and how different synapses change during hearing loss. Combining immunohistochemistry with electrophysiology, we investigated the giant endbulb of Held synapses and their postsynaptic bushy neurons in mice under normal hearing and age-related hearing loss (ARHL). We found that calretinin-expressing and non-calretinin-expressing endbulbs converge at continuously different ratios onto bushy neurons with varying physiological properties. Endbulbs degenerate during ARHL, and the degeneration is more severe in non-calretinin-expressing synapses, which correlates with a gradual decrease in neuronal subpopulation predominantly innervated by these inputs. Our findings suggest that biased AN central synaptopathy and shifted CN neuronal composition underlie reduced auditory input and altered central auditory processing during ARHL.

scholarly journals Functional Change in the Caudal Pontine Reticular Nucleus Induced by Age-Related Hearing Loss

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Ning Zhao ◽  
Ana’am Alkharabsheh ◽  
Fei Xu ◽  
Wei Sun
Keyword(s):  
Hearing Loss ◽  
Neural Plasticity ◽  
High Frequency ◽  
Acoustic Startle ◽  
Low Frequency ◽  
Functional Change ◽  
Reticular Nucleus ◽  
Age Related ◽  
Loudness Level ◽  
Age Related Hearing Loss

Increased acoustic startle responses (ASR), which represent reduced uncomfortable loudness level in humans, have been reported in middle-aged C57BL/6J mice with sensorineural hearing loss. Although neural plasticity changes in the central auditory system after the peripheral lesions were suggested to underlie this phenomenon, the neurological cause of exaggerated ASR is still not clear. In this study, the local field potentials and firing rates of the caudal pontine reticular nucleus (PnC), which plays a major role in the ASR pathway, were recorded in 2-month- and 6-month-old C57BL/6 J mice. Consistent with our previous studies, the amplitude of ASR increased, and the threshold of ASR decreased in the 6-month-old mice after developing 20–40 dB hearing loss. The PnC response induced by high-frequency stimuli (>20 kHz) decreased in the 6-month group, whereas the PnC response induced by low-frequency stimuli (<12 kHz) showed a significant increase in the 6-month group compared to the 2-month group. The enhancement of PnC response is similar to the ASR increase found in the 6-month-old C57 mice. Our results suggest that the high-frequency hearing loss caused an increase in PnC sensitivity in the C57 mice which may enhance ASRs.

scholarly journals Biased auditory nerve central synaptopathy is associated with age‐related hearing loss

2021 ◽  
Author(s):  
Meijian Wang ◽  
Chuangeng Zhang ◽  
Shengyin Lin ◽  
Yong Wang ◽  
Benjamin J. Seicol ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Auditory Nerve ◽  
Age Related ◽  
Age Related Hearing Loss

scholarly journals D-Stellate Neurons of the Ventral Cochlear Nucleus Decrease in Auditory Nerve-Evoked Activity during Age-Related Hearing Loss

2019 ◽  
Vol 9 (11) ◽  
pp. 302
Author(s):  
Yong Wang ◽  
Meijian Wang ◽  
Ruili Xie
Keyword(s):  
Hearing Loss ◽  
Cochlear Nucleus ◽  
Auditory Nerve ◽  
Inhibitory Neurons ◽  
Membrane Properties ◽  
Patch Clamp Technique ◽  
Age Related ◽  
Underlying Mechanisms ◽  
Age Related Hearing Loss ◽  
Intrinsic Membrane Properties

Age-related hearing loss (ARHL) is associated with weakened inhibition in the central auditory nervous system including the cochlear nucleus. One of the main inhibitory neurons of the cochlear nucleus is the D-stellate neuron, which provides extensive glycinergic inhibition within the local neural network. It remains unclear how physiological activities of D-stellate neurons change during ARHL and what are the underlying mechanisms. Using in vitro whole-cell patch clamp technique, we studied the intrinsic membrane properties of D-stellate neurons, the changes of their firing properties, and the underlying mechanisms in CBA/CaJ mice at the ages of 3–4 months (young), 17–19 months (middle age), and 27–33 months (aged). We found that the intrinsic membrane properties of D-stellate neurons were unchanged among these three age groups. However, these neurons showed decreased firing rate with age in response to sustained auditory nerve stimulation. Further investigation showed that auditory nerve-evoked excitatory postsynaptic currents (EPSCs) were significantly reduced in strength with age. These findings suggest that D-stellate neurons receive weakened synaptic inputs from the auditory nerve and decreased sound driven activity with age, which are expected to reduce the overall inhibition and enhance the central gain in the cochlear nucleus during ARHL.

FBXO3 Downregulation Attenuates Noise-induced Hearing Loss by Suppressing ATG10 Degradation and Activating Autophagy

2020 ◽  
Author(s):  
Fan Ye ◽  
Bi Lin ◽  
Lian Fang
Keyword(s):  
Hearing Loss ◽  
Noise Exposure ◽  
Underlying Mechanism ◽  
Noise Induced Hearing Loss ◽  
Age Related ◽  
Rat Cochlea ◽  
Model Treatment ◽  
Ear Injury ◽  
Age Related Hearing Loss

Abstract Noise induced hearing loss (NIHL) is a kind of hearing impairment, which is next to the age-related hearing loss. More and more evidences have verified that overproduction of reactive oxygen species is a common pathologic phenomenon of different inner ear injury including NIHL, and autophagy contributes to attenuate NIHL by reducing oxidative stress. However, the underlying mechanism by which noise exposure causes autophagy activation remains unclear. In this study, we found that NIHL was accompanied by autophagy in the rat cochlea. Furthermore, twelve common genes were found at the GEO datasets GSE85290 and GSE8342, and E3 ubiquitination ligase FBXO3 was confirmed significantly reduced in NIHL rat cochlea. Next, we demonstrated that FBXO3 can directly binding with autophagy-related protein 10 (ATG10), which is necessary for the initiation of autophagy, and mediate its degradation. In vivo animal model treatment with rapamycin, an autophagy activator, significantly reduced the NIHL. Based on these data, we confirmed that FBXO3 played an important role in autophagy caused by NIHL, may be a potential target of NIHL treatment.

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