scholarly journals Physiological changes throughout the ear due to age and noise - a longitudinal study

2021 ◽  
Author(s):  
Alix Blockley ◽  
Daisy Ogle ◽  
Charlie Woodrow ◽  
Fernando Montealegre-Zapata ◽  
Ben Warren
Keyword(s):  
Hearing Loss ◽  
Auditory Nerve ◽  
Noise Exposure ◽  
Schistocerca Gregaria ◽  
Membrane Resistance ◽  
Resting Potential ◽  
Auditory Neurons ◽  
Electrophysiological Properties ◽  
Age Related ◽  
Transduction Current

Biological and mechanical systems, whether by their overuse or their aging, will inevitably fail. Hearing provides a poignant example of this with noise-induced and age-related hearing loss. Hearing loss is not unique to humans, however, and is experienced by all animals in the face of wild and eclectic differences in ear morphology and operation. Here we exploited the high throughput and accessible tympanal ear of the desert locust, Schistocerca gregaria (mixed sex) to rigorously quantify changes in the auditory system due to noise exposure (3 kHz pure tone at 126 dB SPL) and age. We analysed tympanal dispalcements, morphology of the auditory Mullers organ and measured activity of the auditory nerve, the transduction current and electrophysiological properties of individual auditory receptors. We found that noise mildly and transiently changes tympanal displacements, decreases both the width of the auditory nerve and the transduction current recorded from individual auditory neurons. Whereas age, but not noise, decreases the number of auditory neurons and increases their resting potential. Multiple other properties of Mullers organ were unaffected by either age or noise including: the number of supporting cells in Mullers organ or the nerve, membrane resistance and capacitance of the auditory neurons. The sound-evoked activity of the auditory nerve decreased as a function of age and this decrease was exacerbated by noise, with the largest difference during the middle of their life span. This middle-aged deafness pattern of hearing loss mirrors that found for humans exposed to noise early in their life.

scholarly journals IGF-1 Haploinsufficiency Causes Age-Related Chronic Cochlear Inflammation and Increases Noise-Induced Hearing Loss

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1686
Author(s):  
Adelaida M. Celaya ◽  
Lourdes Rodríguez-de la Rosa ◽  
Jose M. Bermúdez-Muñoz ◽  
José M. Zubeldia ◽  
Carlos Romá-Mateo ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Inflammatory Cytokines ◽  
Noise Exposure ◽  
Sensorineural Deafness ◽  
Serum Levels ◽  
Genetic Syndromes ◽  
Expression Ratio ◽  
Postnatal Maturation ◽  
Age Related ◽  
Underlying Mechanisms

Insulin-like growth factor 1 (IGF-1) deficiency is an ultrarare syndromic human sensorineural deafness. Accordingly, IGF-1 is essential for the postnatal maturation of the cochlea and the correct wiring of hearing in mice. Less severe decreases in human IGF-1 levels have been associated with other hearing loss rare genetic syndromes, as well as with age-related hearing loss (ARHL). However, the underlying mechanisms linking IGF-1 haploinsufficiency with auditory pathology and ARHL have not been studied. Igf1-heterozygous mice express less Igf1 transcription and have 40% lower IGF-1 serum levels than wild-type mice. Along with ageing, IGF-1 levels decreased concomitantly with the increased expression of inflammatory cytokines, Tgfb1 and Il1b, but there was no associated hearing loss. However, noise exposure of these mice caused increased injury to sensory hair cells and irreversible hearing loss. Concomitantly, there was a significant alteration in the expression ratio of pro- and anti-inflammatory cytokines in Igf1+/− mice. Unbalanced inflammation led to the activation of the stress kinase JNK and the failure to activate AKT. Our data show that IGF-1 haploinsufficiency causes a chronic subclinical proinflammatory age-associated state and, consequently, greater susceptibility to stressors. This work provides the molecular bases to further understand hearing disorders linked to IGF-1 deficiency.

scholarly journals mTOR Signaling in the Inner Ear as Potential Target to Treat Hearing Loss

2021 ◽  
Vol 22 (12) ◽  
pp. 6368
Author(s):  
Maurizio Cortada ◽  
Soledad Levano ◽  
Daniel Bodmer
Keyword(s):  
Hearing Loss ◽  
Cell Survival ◽  
Inner Ear ◽  
Hearing Aids ◽  
Noise Exposure ◽  
Mammalian Target Of Rapamycin ◽  
Mtor Signaling ◽  
Curative Therapy ◽  
Age Related ◽  
Survival Pathways

Hearing loss affects many people worldwide and occurs often as a result of age, ototoxic drugs and/or excessive noise exposure. With a growing number of elderly people, the number of people suffering from hearing loss will also increase in the future. Despite the high number of affected people, for most patients there is no curative therapy for hearing loss and hearing aids or cochlea implants remain the only option. Important treatment approaches for hearing loss include the development of regenerative therapies or the inhibition of cell death/promotion of cell survival pathways. The mammalian target of rapamycin (mTOR) pathway is a central regulator of cell growth, is involved in cell survival, and has been shown to be implicated in many age-related diseases. In the inner ear, mTOR signaling has also started to gain attention recently. In this review, we will emphasize recent discoveries of mTOR signaling in the inner ear and discuss implications for possible treatments for hearing restoration.

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 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.

scholarly journals Enhancing the sensitivity of the envelope-following response for cochlear synaptopathy screening in humans: the role of stimulus envelope

2020 ◽  
Author(s):  
Viacheslav Vasilkov ◽  
Markus Garrett ◽  
Manfred Mauermann ◽  
Sarah Verhulst
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Sensorineural Hearing Loss ◽  
Auditory Nerve ◽  
Outer Hair Cell ◽  
Cell Damage ◽  
Modulation Depth ◽  
Auditory Evoked Potential ◽  
Sensorineural Hearing ◽  
Age Related

AbstractAuditory de-afferentation, a permanent reduction in the number of innerhair-cells and auditory-nerve synapses due to cochlear damage or synaptopathy, can reliably be quantified using temporal bone histology and immunostaining. However, there is an urgent need for non-invasive markers of synaptopathy to study its perceptual consequences in live humans and to develop effective therapeutic interventions. While animal studies have identified candidate auditory-evoked-potential (AEP) markers for synaptopathy, their interpretation in humans has suffered from translational issues related to neural generator differences, unknown hearing-damage histopathologies or lack of measurement sensitivity. To render AEP-based markers of synaptopathy more sensitive and differential to the synaptopathy aspect of sensorineural hearing loss, we followed a combined computational and experimental approach. Starting from the known characteristics of auditory-nerve physiology, we optimized the stimulus envelope to stimulate the available auditory-nerve population optimally and synchronously to generate strong envelope-following-responses (EFRs). We further used model simulations to explore which stimuli evoked a response that was sensitive to synaptopathy, while being maximally insensitive to possible co-existing outer-hair-cell pathologies. We compared the model-predicted trends to AEPs recorded in younger and older listeners (N=44, 24f) who had normal or impaired audiograms with suspected age-related synaptopathy in the older cohort. We conclude that optimal stimulation paradigms for EFR-based quantification of synaptopathy should have sharply rising envelope shapes, a minimal plateau duration of 1.7-2.1 ms for a 120-Hz modulation rate, and inter-peak intervals which contain near-zero amplitudes. From our recordings, the optimal EFR-evoking stimulus had a rectangular envelope shape with a 25% duty cycle and a 95% modulation depth. Older listeners with normal or impaired audiometric thresholds showed significantly reduced EFRs, which were consistent with how (age-induced) synaptopathy affected these responses in the model.Significance StatementCochlear synaptopathy was in 2009 identified as a new form of sensorineural hearing loss (SNHL) that also affects primates and humans. However, clinical practice does not routinely screen for synaptopathy, and hence its consequences for degraded sound and speech perception remain unclear. Cochlear synaptopathy may thus remain undiagnosed and untreated in the aging population who often report self-reported hearing difficulties. To enable an EEG-based differential diagnosis of synaptopathy in humans, it is crucial to develop a recording method that evokes a robust response and emphasizes inter-individual differences. These differences should reflect the synaptopathy aspect of SNHL, while being insensitive to other aspects of SNHL (e.g. outer-hair-cell damage). This study uniquely combines computational modeling with experiments in normal and hearing-impaired listeners to design an EFR stimulation and recording paradigm that can be used for the diagnosis of synaptopathy in humans.

scholarly journals Occupational Exposure to Noise and Age-related Hearing Loss in an Elderly Population of Southern Italy

2020 ◽  
Vol 13 (1) ◽  
pp. 69-74 ◽  
Author(s):  
Luigi De Maria ◽  
Antonio Caputi ◽  
Rodolfo Sardone ◽  
Enza Sabrina Silvana Cannone ◽  
Francesca Mansi ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Occupational Exposure ◽  
Elderly Population ◽  
Noise Exposure ◽  
Exposed Population ◽  
Age Related ◽  
Age Dependent ◽  
Occupationally Exposed ◽  
Age Related Hearing Loss

Background: Age-Related Hearing Loss (ARHL) is a gradual and irreversible age-dependent decline in auditory function. There is still no consensus on the long-term functional effects of noise exposure on ARHL. Objective: This study aimed to compare the prevalence of ARHL in an elderly population occupationally exposed to noise in a non-exposed population. Methods: The population was divided into two groups: a group of 482 subjects professionally exposed to noise for over 10 years and a group of 1129 non-exposed subjects. Among the exposed subjects, a subgroup of 298 who worked for over 10 years in the glassware industry was selected. All the participants underwent a thorough otorhinolaryngological examination. Results: The presence of ARHL was found in 81% of exposed subjects and in 4% of non-exposed subjects. In the sub-group of glassware workers, the prevalence was 88%. The statistical analysis showed a significant association between previous occupational exposure to noise and ARHL (OR = 1.09; 95% CI = 1.067-1.124; p = 0.0012) and between exposure to the glassware industry and ARHL (OR = 1.89; 95% CI = 1.78-1.96; p = 0.006). Conclusion: Consistent with recent studies, we found a significantly higher prevalence of ARHL among workers exposed to noise; however, further studies are needed to support these findings.

scholarly journals Redox activation of excitatory pathways in auditory neurons as mechanism of age-related hearing loss

Redox Biology ◽  
2020 ◽  
Vol 30 ◽  
pp. 101434 ◽  
Author(s):  
Francis Rousset ◽  
German Nacher-Soler ◽  
Marta Coelho ◽  
Sten Ilmjarv ◽  
Vivianne Beatrix Christina Kokje ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Auditory Neurons ◽  
Redox Activation ◽  
Age Related ◽  
Excitatory Pathways ◽  
Age Related Hearing Loss

Impulse noise exposure in early adulthood accelerates age-related hearing loss

2013 ◽  
Vol 271 (6) ◽  
pp. 1351-1354 ◽  
Author(s):  
Min Xiong ◽  
Chuanhong Yang ◽  
Huangwen Lai ◽  
Jian Wang
Keyword(s):  
Hearing Loss ◽  
Impulse Noise ◽  
Noise Exposure ◽  
Early Adulthood ◽  
Age Related ◽  
Age Related Hearing Loss

scholarly journals A comparison of three different methods of eliciting rapid activity-dependent synaptic plasticity at the Drosophila NMJ

PLoS ONE ◽  
2021 ◽  
Vol 16 (11) ◽  
pp. e0260553
Author(s):  
Carolina Maldonado-Díaz ◽  
Mariam Vazquez ◽  
Bruno Marie
Keyword(s):  
Synaptic Plasticity ◽  
Red Light ◽  
Membrane Resistance ◽  
Resting Potential ◽  
Electrophysiological Properties ◽  
Electrophysiological Studies ◽  
Rich Solution ◽  
And Function ◽  
Synaptic Structures ◽  
Activity Dependent

The Drosophila NMJ is a system of choice for investigating the mechanisms underlying the structural and functional modifications evoked during activity-dependent synaptic plasticity. Because fly genetics allows considerable versatility, many strategies can be employed to elicit this activity. Here, we compare three different stimulation methods for eliciting activity-dependent changes in structure and function at the Drosophila NMJ. We find that the method using patterned stimulations driven by a K+-rich solution creates robust structural modifications but reduces muscle viability, as assessed by resting potential and membrane resistance. We argue that, using this method, electrophysiological studies that consider the frequency of events, rather than their amplitude, are the only reliable studies. We contrast these results with the expression of CsChrimson channels and red-light stimulation at the NMJ, as well as with the expression of TRPA channels and temperature stimulation. With both these methods we observed reliable modifications of synaptic structures and consistent changes in electrophysiological properties. Indeed, we observed a rapid appearance of immature boutons that lack postsynaptic differentiation, and a potentiation of spontaneous neurotransmission frequency. Surprisingly, a patterned application of temperature changes alone is sufficient to provoke both structural and functional plasticity. In this context, temperature-dependent TRPA channel activation induces additional structural plasticity but no further increase in the frequency of spontaneous neurotransmission, suggesting an uncoupling of these mechanisms.

Sign in / Sign up

Export Citation Format

Share Document