Single-neuron labeling and chronic cochlear pathology. III. Stereocilia damage and alterations of threshold tuning curves

Liberman, M. Charles; Dodds, Leslie W.

doi:10.1016/0378-5955(84)90025-x

Cited by 539 publications

(304 citation statements)

References 17 publications

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“…Even at the limits of resolution of the light microscope, the hair cells and supporting cells of the organ of Corti looked completely normal in most cochlear regions of all exposure groups: representative highpower differential interference contrast (DIC) images are shown in Figure 7. Based on previous studies at both the light and electron microscopic levels (Liberman and Dodds, 1984), it is likely that initial noise-induced threshold shift in our mice was attributable to stereocilia damage, especially on outer hair cells, which is not well resolved in the type of histological material used in this study.…”

Section: Ahl/nihl Interactions Produce Primary Neural Degenerationmentioning

confidence: 98%

Acceleration of Age-Related Hearing Loss by Early Noise Exposure: Evidence of a Misspent Youth

Kujawa¹,

Liberman²

2006

J. Neurosci.

594

411

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Age-related and noise-induced hearing losses in humans are multifactorial, with contributions from, and potential interactions among, numerous variables that can shape final outcome. A recent retrospective clinical study suggests an age-noise interaction that exacerbates age-related hearing loss in previously noise-damaged ears (Gates et al., 2000). Here, we address the issue in an animal model by comparing noise-induced and age-related hearing loss (NIHL; AHL) in groups of CBA/CaJ mice exposed identically (8 -16 kHz noise band at 100 dB sound pressure level for 2 h) but at different ages (4 -124 weeks) and held with unexposed cohorts for different postexposure times (2-96 weeks). When evaluated 2 weeks after exposure, maximum threshold shifts in young-exposed animals (4 -8 weeks) were 40 -50 dB; older-exposed animals (Ն16 weeks) showed essentially no shift at the same postexposure time. However, when held for long postexposure times, animals with previous exposure demonstrated AHL and histopathology fundamentally unlike unexposed, aging animals or old-exposed animals held for 2 weeks only. Specifically, they showed substantial, ongoing deterioration of cochlear neural responses, without additional change in preneural responses, and corresponding histologic evidence of primary neural degeneration throughout the cochlea. This was true particularly for young-exposed animals; however, delayed neuropathy was observed in all noise-exposed animals held 96 weeks after exposure, even those that showed no NIHL 2 weeks after exposure. Data suggest that pathologic but sublethal changes initiated by early noise exposure render the inner ears significantly more vulnerable to aging.

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Section: Ahl/nihl Interactions Produce Primary Neural Degenerationmentioning

confidence: 98%

Acceleration of Age-Related Hearing Loss by Early Noise Exposure: Evidence of a Misspent Youth

Kujawa¹,

Liberman²

2006

J. Neurosci.

594

411

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“…This hypersensitivity is attributed to increased shear motion of the TM, due to slackened coupling to the organ of Corti in the absence of functional OHC; this is believed to confer on the basal cochlea an increased sensitivity to low-frequency vibrations (7). Comparison of abnormal neuronal TCs and normal reference TCs at similar CFs show that lowfrequency responses emerge in such situations at levels 10-15 dB lower than normal (7)(8)(9). In the less severe condition in which OHCs are damaged yet still present, the dips of neuronal TCs are found near the normal CF, and low-frequency tails with increased sensitivity are usually observed, the tail minimum being at about the same level as the dip.…”

Section: Discussionmentioning

confidence: 99%

“…In the hypersensitivity of the tail cases, TCs of individual auditory neurons innervating IHCs at cochlear places where OHCs stereocilia or these cells themselves are absent, have no sensitive dip at CF and display abnormally great sensitivity in response to low frequencies (7). This hypersensitivity is attributed to increased shear motion of the TM, due to slackened coupling to the organ of Corti in the absence of functional OHC; this is believed to confer on the basal cochlea an increased sensitivity to low-frequency vibrations (7).…”

Section: Discussionmentioning

confidence: 99%

An unusually powerful mode of low-frequency sound interference due to defective hair bundles of the auditory outer hair cells

Kamiya

Michel

Giraudet

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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A detrimental perceptive consequence of damaged auditory sensory hair cells consists in a pronounced masking effect exerted by low-frequency sounds, thought to occur when auditory threshold elevation substantially exceeds 40 dB. Here, we identified the submembrane scaffold protein Nherf1 as a hair-bundle component of the differentiating outer hair cells (OHCs). Nherf1 −/− mice displayed OHC hair-bundle shape anomalies in the mid and basal cochlea, normally tuned to mid-and high-frequency tones, and mild (22-35 dB) hearing-threshold elevations restricted to midhigh sound frequencies. This mild decrease in hearing sensitivity was, however, discordant with almost nonresponding OHCs at the cochlear base as assessed by distortion-product otoacoustic emissions and cochlear microphonic potentials. Moreover, unlike wild-type mice, responses of Nherf1 −/− mice to high-frequency (20-40 kHz) test tones were not masked by tones of neighboring frequencies. Instead, efficient maskers were characterized by their frequencies up to two octaves below the probe-tone frequency, unusually low intensities up to 25 dB below probe-tone level, and growth-ofmasker slope (2.2 dB/dB) reflecting their compressive amplification. Together, these properties do not fit the current acknowledged features of a hypersensitivity of the basal cochlea to lower frequencies, but rather suggest a previously unidentified mechanism. Low-frequency maskers, we propose, may interact within the unaffected cochlear apical region with midhigh frequency sounds propagated there via a mode possibly using the persistent contact of misshaped OHC hair bundles with the tectorial membrane. Our findings thus reveal a source of misleading interpretations of hearing thresholds and of hypervulnerability to low-frequency sound interference.off-frequency detection | Usher syndrome | hearing impairment | Nherf2 | tail hypersensitivity M ammalian hearing displays remarkable sensitivity, fine temporal acuity, and exquisite frequency selectivity, which contribute to auditory scene analysis and speech intelligibility. The first steps of sound processing, i.e., sound wave detection and neuronal encoding in the cochlea, are performed by two populations of hair cells, the inner hair cells (IHCs) and the outer hair cells (OHCs). These cells are sandwiched between the underlying basilar membrane (BM) and the overlying tectorial membrane (TM) (SI Appendix, Fig. S1A). IHCs are the genuine sensory cells that transduce the sound stimuli into electrical signals in the primary auditory neurons. OHCs are mechanical effectors that amplify the sound-evoked movements of the cochlear partition, sharpen its frequency selectivity, and produce waveform distortions (1, 2). A pure-tone stimulus entering the cochlea elicits a traveling wave that propagates along the BM from the cochlear base toward its apex, increasing in amplitude until it peaks at a characteristic place, where the mechanical properties of the cochlea are best tuned to the stimulus frequency. Beyond this characteristic place, the ampl...

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“…When sensorineural hearing loss begins to exceed approximately 60 dB, substantial inner hair cell loss is present (Liberman and Dodds, 1984). However, even severely hearing-impaired patients can perceive voicing cues, since they are generally signaled by low-frequency intensity differences.…”

Section: Limits Of Hearing Aid Benefitmentioning

confidence: 99%

Combined acoustic and electric hearing: Preserving residual acoustic hearing

2008

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The topic of this review is the strategy of preserving residual acoustic hearing in the implanted ear to provide combined electrical stimulation and acoustic hearing as a rehabilitative strategy for sensorineural hearing loss. This chapter will concentrate on research done with the Iowa/Nucleus 10mm Hybrid device, but we will also attempt to summarize strategies and results from other groups around the world who use slightly different approaches. A number of studies have shown that preserving residual acoustic hearing in the implanted ear is a realistic goal for many patients with severe high-frequency hearing loss. The addition of the electric stimulation to their existing acoustic hearing can provide increased speech recognition for these patients. In addition, the preserved acoustic hearing can offer considerable advantages, as compared to a traditional cochlear implant, for tasks such as speech recognition in backgrounds or appreciation of music and other situations where the poor frequency resolution of electric stimulation has been a disadvantage.

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Single-neuron labeling and chronic cochlear pathology. III. Stereocilia damage and alterations of threshold tuning curves

Cited by 539 publications

References 17 publications

Acceleration of Age-Related Hearing Loss by Early Noise Exposure: Evidence of a Misspent Youth

Acceleration of Age-Related Hearing Loss by Early Noise Exposure: Evidence of a Misspent Youth

An unusually powerful mode of low-frequency sound interference due to defective hair bundles of the auditory outer hair cells

Combined acoustic and electric hearing: Preserving residual acoustic hearing

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