scholarly journals Response Growth With Sound Level in Auditory-Nerve Fibers After Noise-Induced Hearing Loss

2004 ◽  
Vol 91 (2) ◽  
pp. 784-795 ◽  
Author(s):  
Michael G. Heinz ◽  
Eric D. Young
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Auditory Nerve ◽  
Outer Hair Cell ◽  
Dynamic Range ◽  
Nerve Fibers ◽  
Sound Level ◽  
Broadband Noise ◽  
Noise Induced Hearing Loss ◽  
Rate Level

People with sensorineural hearing loss are often constrained by a reduced acoustic dynamic range associated with loudness recruitment; however, the neural correlates of loudness and recruitment are still not well understood. The growth of auditory-nerve (AN) activity with sound level was compared in normal-hearing cats and in cats with a noise-induced hearing loss to test the hypothesis that AN-fiber rate-level functions are steeper in impaired ears. Stimuli included best-frequency and fixed-frequency tones, broadband noise, and a brief speech token. Three types of impaired responses were observed. 1) Fibers with rate-level functions that were similar across all stimuli typically had broad tuning, consistent with outer-hair-cell (OHC) damage. 2) Fibers with a wide dynamic range and shallow slope above threshold often retained sharp tuning, consistent with primarily inner-hair-cell (IHC) damage. 3) Fibers with very steep rate-level functions for all stimuli had thresholds above approximately 80 dB SPL and very broad tuning, consistent with severe IHC and OHC damage. Impaired rate-level slopes were on average shallower than normal for tones, and were steeper in only limited conditions. There was less variation in rate-level slopes across stimuli in impaired fibers, presumably attributable to the lack of suppression-induced reductions in slopes for complex stimuli relative to BF-tone slopes. Sloping saturation was observed less often in impaired fibers. These results illustrate that AN fibers do not provide a simple representation of the basilar-membrane I/O function and suggest that both OHC and IHC damage can affect AN response growth.

scholarly journals Noise-Induced Hearing Loss in Gerbil: Round Window Assays of Synapse Loss

2021 ◽  
Vol 15 ◽  
Author(s):  
Penelope W. C. Jeffers ◽  
Jérôme Bourien ◽  
Artem Diuba ◽  
Jean-Luc Puel ◽  
Sharon G. Kujawa
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Auditory Nerve ◽  
Outer Hair Cell ◽  
Round Window ◽  
Nerve Fibers ◽  
Distortion Product Otoacoustic Emission ◽  
Neural Noise ◽  
Distortion Product ◽  
Synapse Loss

Previous work in animals with recovered hearing thresholds but permanent inner hair cell synapse loss after noise have suggested initial vulnerability of low spontaneous rate (SR) auditory nerve fibers (ANF). As these fibers have properties of response that facilitate robust sound coding in continuous noise backgrounds, their targeted loss would have important implications for function. To address the issue of relative ANF vulnerabilities after noise, we assessed cochlear physiologic and histologic consequences of temporary threshold shift-producing sound over-exposure in the gerbil, a species with well-characterized distributions of auditory neurons by SR category. The noise exposure targeted a cochlear region with distributed innervation (low-, medium- and high-SR neurons). It produced moderate elevations in outer hair cell-based distortion-product otoacoustic emission and whole nerve compound action potential thresholds in this region, with accompanying reductions in suprathreshold response amplitudes, quantified at 24 h. These parameters of response recovered well with post-exposure time. Chronic synapse loss was maximum in the frequency region initially targeted by the noise. Cochlear round window recorded mass potentials (spontaneous neural noise and sound-driven peri-stimulus time responses, PSTR) reflected parameters of the loss not detected by the conventional assays. Spontaneous activity was acutely reduced. Steady-state (PSTR plateau) activity was correlated with synapse loss in frequency regions with high concentrations of low-SR neurons, whereas the PSTR onset peak and spontaneous round window noise, both dominated by high-SR fiber activity, were relatively unaltered across frequency in chronic ears. Together, results suggest that acute targets of noise were of mixed SR subtypes, but chronic targets were predominantly low-SR neurons. PSTRs captured key properties of the auditory nerve response and vulnerability to injury that should yield important diagnostic information in hearing loss etiologies producing cochlear synaptic and neural loss.

Water-soluble Coenzyme Q10 formulation (Q-ter) promotes outer hair cell survival in a guinea pig model of noise induced hearing loss (NIHL)

2009 ◽  
Vol 1257 ◽  
pp. 108-116 ◽  
Author(s):  
Anna Rita Fetoni ◽  
Roberto Piacentini ◽  
Antonella Fiorita ◽  
Gaetano Paludetti ◽  
Diana Troiani
Keyword(s):  
Hearing Loss ◽  
Guinea Pig ◽  
Hair Cell ◽  
Cell Survival ◽  
Coenzyme Q10 ◽  
Outer Hair Cell ◽  
Water Soluble ◽  
Pig Model ◽  
Noise Induced Hearing Loss ◽  
Guinea Pig Model

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.

Level dependence of cochlear nucleus onset unit responses and facilitation by second tones or broadband noise

1995 ◽  
Vol 73 (1) ◽  
pp. 141-159 ◽  
Author(s):  
I. M. Winter ◽  
A. R. Palmer
Keyword(s):  
Cochlear Nucleus ◽  
Discharge Rate ◽  
Nerve Fibers ◽  
Sound Level ◽  
Spike Timing ◽  
Broadband Noise ◽  
Sound System ◽  
Rate Level ◽  
Sound Levels ◽  
Level Function

1. The responses of onset units in the cochlear nucleus of the anesthetized guinea pig have been measured to single tones, two-tone complexes, and broadband noise (BBN; 20-kHz bandwidth). The onset units were subdivided into three groups, onset-I (OnI), onset-L (OnL), and onset-C (OnC), on the basis of a decision tree using their peristimulus time histogram (PSTH) shape and discharge rate in response to suprathreshold best-frequency (BF) tone bursts. 2. PSTHs were constructed from responses either to single tones at a unit's BF or to BBN as a function of level. When sufficient sustained activity could be elicited from the unit, arbitrarily defined as > 100 spikes/s, a coefficient of variation (CV) was calculated; the majority were characterized by a CV that was similar to transient chopper units (0.35 < CV < 0.5). First spike latency decreased monotonically with increasing sound level. For the majority of onset units, the first spike timing was very precise. 3. BF rate-level functions recorded from OnL and OnC units did not show any signs of discharge rate saturation at the highest sound levels we have used (100-115 dB SPL). No systematic relationship was observed between the threshold at BF and the shape of the rate-level function. BBN rate-level functions were typically characterized by higher discharge rates than in response to BF tones. However, for OnI units and a minority of other onset units, there was little difference in the shape of their rate-level functions in response to BF tones or BBN. 4. The threshold of most onset units to BBN was similar to the threshold to a BF tone that had similar overall root-mean-square (RMS) energy. The BBN threshold was, on average, 5.5 dB greater than the BF threshold. This result contrasts with that found in auditory-nerve fibers recorded in the same species, with the use of an identical sound system, where the threshold to BBN was, on average, 19.4 dB higher. The mean threshold difference between BBN and BF tones for a population of chopper units recorded in the same series of experiments was 17.7 dB. The relative thresholds to BBN and BF tones indicated that the bandwidths near the onset units' BF threshold were broader than could be estimated with the use of single tones. Ten units were characterized by bimodal response areas.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Association of cochlear outer hair cell - type II spiral ganglion afferents with protection from noise-induced hearing loss

2021 ◽  
Author(s):  
Jennie M.E. Cederholm ◽  
Kristina E. Parley ◽  
Chamini J. Perera ◽  
Georg von Jonquieres ◽  
Jeremy L. Pinyon ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Spiral Ganglion ◽  
Broadband Noise ◽  
Auditory Brainstem Responses ◽  
Type I ◽  
Type Ii ◽  
Noise Induced Hearing Loss ◽  
Distortion Product ◽  
Contralateral Suppression

The medial olivocochlear (MOC) efferent feedback circuit projecting to the cochlear outer hair cells (OHCs) confers protection from noise-induced hearing loss and is generally thought to be driven by inner hair cell (IHC) - type I spiral ganglion afferent (SGN) input. Knockout of the Prph gene (PrphKO) encoding the peripherin type III intermediate filament disrupted the OHC - type II SGN innervation and virtually eliminated MOC – mediated contralateral suppression from noise delivered to the opposite ear, measured as a reduction in cubic distortion product otoacoustic emissions. Electrical stimulation of the MOC pathway elicited contralateral suppression indistinguishable between wildtype (WT) and PrphKO mice, indicating that the loss of contralateral suppression was not due to disruption of the efferent arm of the circuit; IHC – type I SGN input was also normal, based on auditory brainstem responses. High-intensity, broadband noise (108 dB SPL, 1 hour) produced permanent hearing loss in PrphKO mice, but not in WT littermates. These findings associate OHC-type II input with MOC efferent - based otoprotection at loud sound levels.

Properties of auditory nerve responses in absence of outer hair cells

1978 ◽  
Vol 41 (2) ◽  
pp. 365-383 ◽  
Author(s):  
P. Dallos ◽  
D. Harris
Keyword(s):  
Hair Cell ◽  
Hair Cells ◽  
Auditory Nerve ◽  
Outer Hair Cell ◽  
Nerve Fibers ◽  
Outer Hair Cells ◽  
Border Region ◽  
Histological Evaluation ◽  
High Threshold ◽  
Time Pattern

1. Recordings were made from chinchilla auditory nerve fibers after portions of the cochlear outer hair cell (OHC) population were destroyed with the antibiotic kanamycin. In most cases the inner hair cell (IHC) population was completely preserved as determined by phase-contrast microscopy. We presume that the remaining IHCs are functionally normal, and thus that recordings obtained from fibers originating from the lesioned cochlear segment reflect IHC behavior. 2. Behavioral thresholds were measured for all animals both before and after the production of the cochlear lesion. The audiograms and the histological evaluation of the ears were the basis for assessing whether a particular fiber originated in a normal, pathological (shifted threshold; IHC only), or border region. These criteria also identified the animals that sustained IHC damage together with the destruction of part of the OHC population. Only the data obtained from those fibers which probably originated from the OHC-free segment of the cochlea are considered in detail. 3. Fibers whose characteristic frequency (CF) identified them as belonging to the normal (audiometrically and histologically) region, were found to be normal in all respects. 4. Fibers from the border region (where the audiogram has a steep slope between normal and hearing-loss regions probably corresponding to the segment where OHC loss progresses from less than 10% to more than 90%) had very complex response patterns. Their frequency threshold curves (FTC) showed great variability. In general, the closer the fiber was to the fully developed lesion, the more abnormal its FTC became. 5. Those units that were concluded to have originated from the OHC-free part of the cochlea could be divided into three categories on the basis of the shape of their FTCs. A small fraction had very broad tuning (9%). The majority (53%) had approximately normal tail segment, normal bandwidth of the tip segment, and highly elevated threshold at CF. A group of fibers (38%) could not be assigned a CF. Probably the FTC of most of these latter fibers are similar to those of the previous group, but the sharply tuned short tip segment was either missed or was not reachable on account of its extremely high threshold level. 6. Such indexes of fiber response as latency, spontaneous rate, and time pattern (PST histograms) were not affected by the loss of OHCs. 7. On the basis of the data and of the assumptions made it was suggested that outer hair cells provide a frequency-dependent sensitizing influence to the inner hair cells. The frequency dependence could best be expressed as a flat-topped band pass characteristic.

Psychophysical Tuning Curves in Subjects with Tinnitus Suggest Outer Hair Cell Lesions

1995 ◽  
Vol 113 (3) ◽  
pp. 223-233 ◽  
Author(s):  
Curtin R. Mitchell ◽  
Thomas A. Creedon
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Hair Cells ◽  
Outer Hair Cell ◽  
Tuning Curve ◽  
Control Design ◽  
Nerve Fibers ◽  
Outer Hair Cells ◽  
Tuning Curves ◽  
Hearing Thresholds

A study by Penner (J Speech Hear Res 1980;23:779–86) found evidence for Impaired lateral suppression in subjects with tinnitus and sensorineural hearing loss. If lateral suppression is related to tuning curve sharpness and lateral suppression is impaired, the shape of the tuning curve should be affected. The purpose of this study was to determine whether subjects with tinnitus have psychophysical tuning curves that are different from those of subjects without tinnitus. Psychophysical tuning curves and hearing thresholds were obtained from 18 subjects, 7 with tinnitus and 11 without tinnitus. Only subjects with normal audiograms (through 8 kHz) were selected for this study. In subjects with tinnitus psychophysical tuning curves were obtained in the region pitch-matched to their tinnitus. In nontinnitus subjects psychophysical tuning curves were determined at the same frequencies as for the tinnitus subjects in a yoked-control design. The slopes of the tails and tips and the Q10 and other measures were calculated for each tuning curve. The psychophysical tuning curves in subjects with tinnitus were significantly different (0.01 level) from those of control subjects and often had hypersensitive tails and some elevated tips. These shapes of tuning curves are consistent with cochlear lesions involving the loss of outer hair cells without damage to the Inner hair cells or nerve fibers.

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