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Hearing Research Jun 2017For decades, we have presumed the death of hair cells and spiral ganglion neurons are the main cause of hearing loss and difficulties understanding speech in noise, but... (Review)
Review
For decades, we have presumed the death of hair cells and spiral ganglion neurons are the main cause of hearing loss and difficulties understanding speech in noise, but new findings suggest synapse loss may be the key contributor. Specifically, recent preclinical studies suggest that the synapses between inner hair cells and spiral ganglion neurons with low spontaneous rates and high thresholds are the most vulnerable subcellular structures, with respect to insults during aging and noise exposure. This cochlear synaptopathy can be "hidden" because this synaptic loss can occur without permanent hearing threshold shifts. This new discovery of synaptic loss opens doors to new research directions. Here, we review a number of recent studies and make suggestions in two critical future research directions. First, based on solid evidence of cochlear synaptopathy in animal models, it is time to apply molecular approaches to identify the underlying molecular mechanisms; improved understanding is necessary for developing rational, effective therapies against this cochlear synaptopathy. Second, in human studies, the data supporting cochlear synaptopathy are indirect although rapid progress has been made. To fully identify changes in function that are directly related this hidden synaptic damage, we argue that a battery of tests including both electrophysiological and behavior tests should be combined for diagnosis of "hidden hearing loss" in clinical studies. This new approach may provide a direct link between cochlear synaptopathy and perceptual difficulties.
Topics: Animals; Auditory Perception; Hair Cells, Auditory, Inner; Hearing; Hearing Loss, Noise-Induced; Hearing Tests; Humans; Noise; Predictive Value of Tests; Psychoacoustics; Spiral Ganglion; Synapses; Synaptic Transmission
PubMed: 28007526
DOI: 10.1016/j.heares.2016.12.008 -
Hearing Research Jun 2019Acquired sensorineural hearing loss is one of the most prevalent chronic diseases, and aging and acoustic overexposure are common contributors. Decades of study in... (Review)
Review
Acquired sensorineural hearing loss is one of the most prevalent chronic diseases, and aging and acoustic overexposure are common contributors. Decades of study in animals and humans have clarified the cellular targets and perceptual consequences of these forms of hearing loss, and preclinical studies have led to the development of therapeutics designed to slow, prevent or reverse them. Here, we review the histopathological changes underlying age-related and noise-induced hearing loss and the functional consequences of these pathologies. Based on these relations, we consider the ambiguities that arise in diagnosing underlying pathology from minimally invasive tests of auditory function, and how those ambiguities present challenges in the design and interpretation of clinical trials.
Topics: Age Factors; Aging; Animals; Auditory Perception; Cochlea; Disease Models, Animal; Hearing; Hearing Loss, Noise-Induced; Humans; Noise; Presbycusis; Species Specificity; Translational Research, Biomedical
PubMed: 30903954
DOI: 10.1016/j.heares.2019.03.003 -
Nature Communications Jun 2023TRPA1 channels are expressed in nociceptive neurons, where they detect noxious stimuli, and in the mammalian cochlea, where their function is unknown. Here we show that...
TRPA1 channels are expressed in nociceptive neurons, where they detect noxious stimuli, and in the mammalian cochlea, where their function is unknown. Here we show that TRPA1 activation in the supporting non-sensory Hensen's cells of the mouse cochlea causes prolonged Ca responses, which propagate across the organ of Corti and cause long-lasting contractions of pillar and Deiters' cells. Caged Ca experiments demonstrated that, similar to Deiters' cells, pillar cells also possess Ca-dependent contractile machinery. TRPA1 channels are activated by endogenous products of oxidative stress and extracellular ATP. Since both these stimuli are present in vivo after acoustic trauma, TRPA1 activation after noise may affect cochlear sensitivity through supporting cell contractions. Consistently, TRPA1 deficiency results in larger but less prolonged noise-induced temporary shift of hearing thresholds, accompanied by permanent changes of latency of the auditory brainstem responses. We conclude that TRPA1 contributes to the regulation of cochlear sensitivity after acoustic trauma.
Topics: Animals; Mice; Cochlea; Epithelial Cells; Evoked Potentials, Auditory, Brain Stem; Hearing Loss, Noise-Induced; Labyrinth Supporting Cells; TRPA1 Cation Channel
PubMed: 37391431
DOI: 10.1038/s41467-023-39589-w -
Hearing Research Jun 2017
Review
Topics: Auditory Fatigue; Auditory Pathways; Hearing; Hearing Loss, Noise-Induced; Humans; Military Personnel; Noise, Occupational; Occupational Diseases; Occupational Exposure; Risk Assessment; Risk Factors; Time Factors
PubMed: 27780746
DOI: 10.1016/j.heares.2016.10.006 -
Hearing Research Mar 2024Chronic tinnitus is a debilitating condition with very few management options. Acoustic trauma that causes tinnitus has been shown to induce neuronal hyperactivity in...
Chronic tinnitus is a debilitating condition with very few management options. Acoustic trauma that causes tinnitus has been shown to induce neuronal hyperactivity in multiple brain areas in the auditory pathway, including the inferior colliculus. This neuronal hyperactivity could be attributed to an imbalance between excitatory and inhibitory neurotransmission. However, it is not clear how the levels of neurotransmitters, especially neurotransmitters in the extracellular space, change over time following acoustic trauma and the development of tinnitus. In the present study, a range of amino acids were measured in the inferior colliculus of rats during acoustic trauma as well as at 1 week and 5 months post-trauma using in vivo microdialysis and high-performance liquid chromatography. Amino acid levels in response to sound stimulation were also measured at 1 week and 5 months post-trauma. It was found that unilateral exposure to a 16 kHz pure tone at 115 dB SPL for 1 h caused immediate hearing loss in all the animals and chronic tinnitus in 58 % of the animals. Comparing to the sham condition, extracellular levels of GABA were significantly increased at both the acute and 1 week time points after acoustic trauma. However, there was no significant difference in any of the amino acid levels measured between sham, tinnitus positive and tinnitus negative animals at 5 months post-trauma. There was also no clear pattern in the relationship between neurochemical changes and sound frequency/acoustic trauma/tinnitus status, which might be due to the relatively poorer temporal resolution of the microdialysis compared to electrophysiological responses.
Topics: Rats; Animals; Hearing Loss, Noise-Induced; Tinnitus; Acoustic Stimulation; Amino Acids; Inferior Colliculi; Neurotransmitter Agents
PubMed: 38219615
DOI: 10.1016/j.heares.2024.108948 -
Neural Plasticity 2016Recent studies on animal models have shown that noise exposure that does not lead to permanent threshold shift (PTS) can cause considerable damage around the synapses... (Review)
Review
Recent studies on animal models have shown that noise exposure that does not lead to permanent threshold shift (PTS) can cause considerable damage around the synapses between inner hair cells (IHCs) and type-I afferent auditory nerve fibers (ANFs). Disruption of these synapses not only disables the innervated ANFs but also results in the slow degeneration of spiral ganglion neurons if the synapses are not reestablished. Such a loss of ANFs should result in signal coding deficits, which are exacerbated by the bias of the damage toward synapses connecting low-spontaneous-rate (SR) ANFs, which are known to be vital for signal coding in noisy background. As there is no PTS, these functional deficits cannot be detected using routine audiological evaluations and may be unknown to subjects who have them. Such functional deficits in hearing without changes in sensitivity are generally called "noise-induced hidden hearing loss (NIHHL)." Here, we provide a brief review to address several critical issues related to NIHHL: (1) the mechanism of noise induced synaptic damage, (2) reversibility of the synaptic damage, (3) the functional deficits as the nature of NIHHL in animal studies, (4) evidence of NIHHL in human subjects, and (5) peripheral and central contribution of NIHHL.
Topics: Acoustic Stimulation; Animals; Cochlea; Hearing Loss, Noise-Induced; Humans; Noise; Synapses
PubMed: 27738526
DOI: 10.1155/2016/6143164 -
Noise & Health 2019Choir singing is a very popular activity with 4.5% of the European population regularly participating. London South Bank University was approached in January 2019 by St...
Choir singing is a very popular activity with 4.5% of the European population regularly participating. London South Bank University was approached in January 2019 by St Paul's Cathedral to undertake noise dosimetry for the Music Department. Rehearsals and performances were identified and measured using acoustic instrumentation to determine if the choristers, adult choir, choir master or organist were compliant with the Control of Noise at Work Regulations 2005. These data were then matched to the daily and weekly work schedules of the musicians and the sound exposure estimated. The adult choir, organist and choir master were found to be under the set daily limits, 85 dBA (L). The most exposed chorister was above this limit. However, when adjusted for their shorter working year and using the weekly noise exposure limit of 87 dBA (L), the estimated exposure was compliant with the regulations. Recommendations were presented to the Music Department focusing on management techniques to reduce the weekly exposure of the choristers without effecting the spirit, tradition or musicality of the performance. It was also strongly suggested to reduce the number of performances for the boys by introducing a second choir.
Topics: Adolescent; Adult; Auditory Threshold; Child; Environmental Monitoring; Female; Hearing Loss, Noise-Induced; Humans; London; Male; Music; Noise, Occupational; Occupational Exposure; Singing
PubMed: 32098930
DOI: 10.4103/nah.NAH_40_19 -
International Journal of Molecular... Oct 2019Noise exposure affects the organ of Corti and the lateral wall of the cochlea, including the stria vascularis and spiral ligament. Although the inner ear vasculature and...
Noise exposure affects the organ of Corti and the lateral wall of the cochlea, including the stria vascularis and spiral ligament. Although the inner ear vasculature and spiral ligament fibrocytes in the lateral wall consist of a significant proportion of cells in the cochlea, relatively little is known regarding their functional significance. In this study, 6-week-old male C57BL/6 mice were exposed to noise trauma to induce transient hearing threshold shift (TTS) or permanent hearing threshold shift (PTS). Compared to mice with TTS, mice with PTS exhibited lower cochlear blood flow and lower vessel diameter in the stria vascularis, accompanied by reduced expression levels of genes involved in vasodilation and increased expression levels of genes related to vasoconstriction. Ultrastructural analyses by transmission electron microscopy revealed that the stria vascularis and spiral ligament fibrocytes were more damaged by PTS than by TTS. Moreover, mice with PTS expressed significantly higher levels of proinflammatory cytokines in the cochlea (e.g., IL-1β, IL-6, and TNF-α). Overall, our findings suggest that cochlear microcirculation and lateral wall pathologies are differentially modulated by the severity of acoustic trauma and are associated with changes in vasoactive factors and inflammatory responses in the cochlea.
Topics: Animals; Blood Flow Velocity; Cochlea; Cytokines; Disease Models, Animal; Hearing Loss, Noise-Induced; Male; Mice; Wounds and Injuries
PubMed: 31731459
DOI: 10.3390/ijms20215316 -
Journal of Neurophysiology Feb 2022Noise-induced hearing deficits are important health problems in the industrialized world. As the underlying physiological dysfunctions are not well understood, research... (Comparative Study)
Comparative Study
Noise-induced hearing deficits are important health problems in the industrialized world. As the underlying physiological dysfunctions are not well understood, research in suitable animal models is urgently needed. Three rodent species (Mongolian gerbil, rat, and mouse) were studied to compare the temporal dynamics of noise-induced hearing loss after identical procedures of noise exposure. Auditory brainstem responses (ABRs) were measured before, during, and up to 8 wk after noise exposure for threshold determination and ABR waveform analysis. Trauma induction with stepwise increasing sound pressure level was interrupted by five interspersed ABR measurements. Comparing short- and long-term dynamics underlying the following noise-induced hearing loss revealed diverging time courses between the three species. Hearing loss occurred early on during noise exposure in all three rodent species at or above trauma frequency. Initial noise level (105 dB SPL) was most effective in rats whereas the delayed level increase to 115 dB SPL affected mice much stronger. Induced temporary threshold shifts in rats and mice were larger in animals with lower pretrauma ABR thresholds. The increase in activity (gain) along the auditory pathway was derived by comparing the amplitudes of short- and long-latency ABR waveform components. Directly after trauma, significant effects were found for rats (decreasing gain) and mice (increasing gain) whereas gerbils revealed high individual variability in gain changes. Taken together, our comparative study revealed pronounced species-specific differences in the development of noise-induced hearing loss and the related processing along the auditory pathway. We compared deficits after noise trauma in different rodents that are typically used in hearing research (Mongolian gerbil, rat, and mouse). We observed noise-induced threshold changes and alterations in the activity of processing auditory information along the ascending auditory pathway. Our results reveal pronounced differences in the characteristics of trauma-induced damage in these different rodent groups.
Topics: Animals; Auditory Pathways; Auditory Threshold; Behavior, Animal; Disease Models, Animal; Evoked Potentials, Auditory, Brain Stem; Gerbillinae; Hearing Loss, Noise-Induced; Mice; Noise; Rats; Species Specificity
PubMed: 35020518
DOI: 10.1152/jn.00081.2021 -
Otolaryngologia Polska = the Polish... Aug 2017Hearing impairment caused by noise, traditionally called - depending on the duration of exposure - acute or chronic acoustic trauma, includes, in addition to...
Hearing impairment caused by noise, traditionally called - depending on the duration of exposure - acute or chronic acoustic trauma, includes, in addition to presbyacusis, the most common adult population of hearing impaired. In Poland - according to the report of the Central Statistical Office (GUS, 2011), the number of workers employed in NDN exceeded the noise level (85 dB) is about 200 thousand, the highest in the mining, metal and metal products production, textiles and wood production. According to the Regulation of the Council of Ministers of on June 30, 2009, on the list of occupational diseases (Journal of Laws No. 132, item 1115), it is defined as "bilateral permanent hearing loss of the cochlear or sensory-nerve type, expressed as an increase in hearing threshold of at least 45 dB in the ear better heard, calculated as an arithmetic mean for frequencies 1,2 and 3 kHz. Hearing impairments also occur in the military and police during field training and in combat where the source of acoustic injuries are firearms and pulse-inducing explosions (as in some industries) with high C peak levels (Lc peak) Time to rise to a maximum of <1 ms. The prevalence of loud music listening, particularly by personal stereo players, is also affecting children and adolescents with audiometric hearing loss, according to the World Health Organization (WHO) estimates of around 15-20%. The preventive action strategy is defined by the European Union legislation and the national implementing legislation that reduces or eliminates the risk and reduces (if not eliminated), taking into account available technical and organizational solutions to minimize the risk of hearing damage. If you can not reduce the noise levels with technical and organizational methods, you need individual hearing protectors. Ear protectors may be equipped with electronic systems with active noise reduction (which can improve low and medium frequency performance), adjustable attenuation (improves speech intelligibility and perception of warning signals), and wireless communication for verbal communication.
Topics: Disability Evaluation; Ear Protective Devices; Female; Hearing Loss, Noise-Induced; Humans; Male; Military Personnel; Noise, Occupational; Occupational Diseases; Poland; Police; Primary Prevention
PubMed: 29116045
DOI: 10.5604/01.3001.0010.2241