Dynamics of Noise-Induced Cellular Injury and Repair in the Mouse Cochlea

Wang, Yong; Hirose, Keiko; Liberman, M. Charles

doi:10.1007/s101620020028

Cited by 486 publications

(518 citation statements)

References 19 publications

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“…The present report concerns loss of type IV fibrocytes in mice following noise exposure as a model for at least part of unexplained cell loss in the spiral ligament of humans. This work extends a previous study that showed type IV fibrocytes to have a surprisingly low threshold for noise-induced destruction (Wang et al 2002). In the present report, cytochemical traits that are useful for distinguishing type IV fibrocytes from nearby cells and for revealing physiological traits of these cells are presented.…”

Section: Introductionsupporting

confidence: 88%

“…Loss or damage to spiral ligament cells following acoustic trauma in animals has been reported (Johnsson and Hawkins 1976;Liberman and Kiang 1978;Wang et al 2002;Hirose and Liberman 2003;Ohlemiller and Gagnon 2007). The present report concerns loss of type IV fibrocytes in mice following noise exposure as a model for at least part of unexplained cell loss in the spiral ligament of humans.…”

Section: Introductionmentioning

confidence: 90%

“…The report that all fibrocytes within the spiral ligament of rats are connected by gap junctions (Kikuchi et al 1995), together with a variety of evidence from numerous laboratories, led to the realization that fibrocytes play key roles in K + ion uptake from perilymph and recycling of those ions back to endolymph. The reported gap junctional connectivity of all fibrocytes, together with imprecise information regarding cytochemical specializations of various cell types, has led to a common assumption that all fibrocytes within the ligament participate in K + ion recycling (e.g., Wang et al 2002;Qu et al 2007). Herein, evidence is presented that indicates that fibrocyte types III and IV probably have little to do with K + recycling.…”

Section: Introductionmentioning

confidence: 99%

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Immunocytochemical Traits of Type IV Fibrocytes and Their Possible Relations to Cochlear Function and Pathology

Adams

2009

JARO

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One of the more consistent and least understood changes in the aging human cochlea is the progressive loss of fibrocytes within the spiral ligament. This report presents an animal model for type IV fibrocyte loss, along with immunocytochemical evidence that noise-induced loss of these cells may account for previously unexplained hearing losses. The remarkably low threshold for noise-induced loss of type IV fibrocytes, approximately 24 dB less than the threshold for adjacent hair cell destruction, may account for the prevalence of missing fibrocytes in humans. In mice, changes in the spectrum of traumatizing noise had little effect upon the site of loss of the fibrocytes, suggesting that the primary site of damage that induced the loss was the basal-most cochlear turn, a site expected to be damaged by all three noise bands. Type IV fibrocytes were found to immunostain for connective tissue growth factor (CTGF) and for transforming growth factor beta receptor 3, a receptor that is known to activate CTGF expression. Type IV fibrocytes lack immunostaining for adenosine triphosphatase and connexins that are key players in potassium ion uptake and transmission, which suggests that they play little, if any, role in potassium recycling from perilymphatic space to the endolymphatic space. Consequently, their loss probably does not directly reduce this process. Immunostaining for a receptor for CTGF, low-density-lipoprotein-related protein 1, indicated that CTGF acts as an autocrine and a paracrine agent within the cochlea. The lack of CTGF paracrine effects following noise-induced loss of type IV fibrocytes may account for previously unexplained hearing losses.

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Section: Introductionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 99%

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Immunocytochemical Traits of Type IV Fibrocytes and Their Possible Relations to Cochlear Function and Pathology

Adams

2009

JARO

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“…This is a point in time where noise-induced damage to afferent terminals at inner hair cells is usually at a maximum (Lin et al 2011). It is therefore unlikely that mechanisms usually associated with common noise-induced temporary threshold shifts (Robertson 1982(Robertson , 1983Wang et al 2002) are responsible for the tinnitus-like sensations observed during the BP.…”

Section: Lf Sound-induced Transient Sound Perceptionsmentioning

confidence: 99%

Multiple Indices of the ‘Bounce’ Phenomenon Obtained from the Same Human Ears

Drexl

Überfuhr

Weddell

et al. 2013

JARO

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Loud low-frequency sounds can induce temporary oscillatory changes in cochlear sensitivity, which have been termed the 'bounce' phenomenon. The origin of these sensitivity changes has been attributed to slow fluctuations in cochlear homeostasis, causing changes in the operating points of the outer hair cell mechanoelectrical and electro-mechanical transducers. Here, we acquired three objective and subjective measures resulting in a comprehensive dataset of the bounce phenomenon in each of 22 normal-hearing human subjects. We analysed the level and phase of cubic and quadratic distortion product otoacoustic emissions and the auditory thresholds before and after presentation of a low-frequency stimulus (30 Hz sine wave, 120 dB SPL, 90 s) as a function of time. In addition, the perceived loudness of temporary, tinnitus-like sensations occurring in all subjects after cessation of the low-frequency stimulus was tracked over time. The majority of the subjects (70 %) showed a significant, biphasic change of quadratic, but not cubic, distortion product otoacoustic emissions of about 3-4 dB. Eighty-six percent of the tested subjects showed significant alterations of hearing thresholds after low-frequency stimulation. Four different types of threshold changes were observed, namely monophasic desensitisations (the majority of cases), monophasic sensitisations, biphasic alterations with initial sensitisation and biphasic alterations with initial desensitisation. The similar duration of the three bounce phenomenon measures indicates a common origin. The current findings are consistent with the hypothesis that slow oscillations of homeostatic control mechanisms and associated operating point shifts within the cochlea are the source of the bounce phenomenon.

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“…Nevertheless, damage within the inner ear is most likely to contribute. Noise trauma can have a range of chronic effects, such as stereocilia damage, loss of OHCs and IHCs, complete loss of the organ of Corti, and many more, with differences in spatial distribution, time course, and dependence on noise level (and presumably exposure duration) (e.g., Saunders et al 1985;Liberman 1987Liberman , 1990Wang et al 2002). …”

Section: Location Of Damages Captured By Altered Baseline and Gainmentioning

confidence: 99%

Towards a Unifying Basis of Auditory Thresholds: The Effects of Hearing Loss on Temporal Integration Reconsidered

Neubauer

Heil

2004

JARO

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For signal detection and identification, the auditory system needs to integrate sound over time. It is frequently assumed that the quantity ultimately integrated is sound intensity and that the integrator is located centrally. However, we have recently shown that absolute thresholds are much better specified as the temporal integral of the pressure envelope than of intensity, and we proposed that the integrator resides in the auditory pathway's first synapse. We also suggested a physiologically plausible mechanism for its operation, which was ultimately derived from the specific rate of temporal integration, i.e., the decrease of threshold sound pressure levels with increasing duration. In listeners with sensorineural hearing losses, that rate seems reduced, but it is not fully understood why. Here we propose that in such listeners there may be an elevation in the baseline above which sound pressure is effective in driving the system, in addition to a reduction in sensitivity. We test this simple model using thresholds of cats to stimuli of differently shaped temporal envelopes and durations obtained before and after hearing loss. We show that thresholds, specified as the temporal integral of the effective pressure envelope, i.e., the envelope of the pressure exceeding the elevated baseline, behave almost exactly as the lower thresholds, specified as the temporal integral of the total pressure envelope before hearing loss. Thus, the mechanism of temporal integration is likely unchanged after hearing loss, but the effective portion of the stimulus is. Our model constitutes a successful alternative to the model currently favored to account for altered temporal integration in listeners with sensorineural hearing losses, viz., reduced peripheral compression. Our model does not seem to be at variance with physiological observations and it also qualitatively accounts for a number of phenomena observed in such listeners with suprathreshold stimuli.

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Dynamics of Noise-Induced Cellular Injury and Repair in the Mouse Cochlea

Cited by 486 publications

References 19 publications

Immunocytochemical Traits of Type IV Fibrocytes and Their Possible Relations to Cochlear Function and Pathology

Immunocytochemical Traits of Type IV Fibrocytes and Their Possible Relations to Cochlear Function and Pathology

Multiple Indices of the ‘Bounce’ Phenomenon Obtained from the Same Human Ears

Towards a Unifying Basis of Auditory Thresholds: The Effects of Hearing Loss on Temporal Integration Reconsidered

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