Role Of Outer Hair Cells Research Articles

Distortion Product Otoacoustic Emission and Tinnitus: Role of Outer Hair Cells in the Genesis of Tinnitus

Background: This study aims to detect outer hair cell (OHC) function in patients with tinnitus, by comparing the otoacoustic emissions (OAEs) in tinnitus patients with normal hearing and normal-hearing subjects without tinnitus, thereby revealing the role of OHC in the generation of tinnitus. Methods: After approval by the local research and ethics committee, this study was done in the department of otolaryngology and associated hospitals, from April 2022 to January 2023. Consent was obtained from all the participants in the present work after explaining the test procedure. The study group included 60 subjects with bilaterally normal hearing to participate. They were classified into two groups: Group 1, i.e., the control group, comprised 30 subjects who were unaffected by tinnitus, whereas Group 2, i.e., the study group, comprised 30 subjects who were suffering from tinnitus. Basic audiological tests and OAE test were done on the respondents of both the groups followed by a comparison of outcomes. Results: The authors of the present study found a statistically significant difference between the amplitude and signal-to-noise ratio (SNR) of distortion product OAE (DPOAE) in tinnitus patients and the control group without tinnitus, suggesting that OHCs have a role in the generation of tinnitus. Conclusion: It can be concluded that OHC activity was reduced in patients with tinnitus, as detected by reduced DPOAE amplitude and SNR, suggesting that the dysfunction of OHCs can be attributable to the generation of tinnitus.

Otoacoustic emissions and contralateral suppression in tinnitus sufferers with normal hearing

BackgroundThe general consensus on the role of hearing loss in generating tinnitus is not relevant in tinnitus patients with normal hearing thresholds. One source of tinnitus may be related to damage to outer hair cells (OHC) of the cochlea. If the OHC of the human cochlea are to be involved in the generation of tinnitus, testing of Otoacoustic emissions (OAE) could provide a reliable means of recording OHC dysfunction. We investigated the role of OHC and cochlear efferent system in tinnitus development in normal hearing ears through studying of Distortion Product Otoacoustic Emissions (DPOAE) and Transient Evoked Otoacoustic Emissions (TEOAE) amplitudes, contralateral suppression amplitudes and suppression value in 15 normal hearing tinnitus patients and 15 control subjects.ResultsMean f2 DPOAE amplitudes and contralateral suppression were significantly lower in tinnitus group compared to controls for all frequencies from 1001 to 6348 Hz. Suppression values of DPOAEs revealed lower but not significant difference between tinnitus and control groups for all frequencies except 1587 and 6348 Hz. TEOAE amplitudes and contralateral suppression were significantly lower in tinnitus groups for all frequencies from 1000 to 4000 Hz compared to the control group. Suppression value of TEOAEs revealed no significant difference between the two groups for all frequencies except 3000 and 4000 Hz were significantly lower in the tinnitus group compared to the control group.ConclusionsNormal hearing manifested by pure tone audiometry in non-vascular tinnitus sufferers does not exclude OHC and/or cochlear efferent pathology.

The Role of Electrophonics in Electroacoustic Stimulation of the Guinea Pig Cochlea

Interactions between cochlear responses to combined electrical and acoustic stimulation (EAS) depend on electrically evoked hair cell activity (i.e., electrophonics). Although relevant for EAS strategies in cochlear implant users with residual low-frequency hearing, cochlear responses to EAS are not well characterized. Previously, we have shown that acoustically evoked compound action potentials (CAPs) can be suppressed by electrical stimulation. In the present study, we characterized the role of electrophonics in CAP suppression in guinea pigs, under conditions representative of clinically applied EAS. Electrophonics depend on the frequency spectrum of the electric pulse train, which is mainly determined by pulse width and, to a lesser extent, by pulse rate. We measured suppression of tone-evoked CAPs by electric pulse trains, while varying the pulse width (80 - 400 μs, n = 5) and the pulse rate (500 - 4000 pps, n = 5). The role of outer hair cells (OHCs) in electrophonics was tested in animals with varying degrees of OHC loss (n = 24). Suppression of acoustically evoked CAPs varied with pulse width, indicating that electrophonics were involved. Short pulse widths resulted in minimal CAP suppression at low acoustic frequencies. Pulse rate did not significantly affect CAP suppression. OHC loss had no significant effect on electrophonic activity. Electrophonic activity was present in cochleae with extensive basal hair cell loss, indicating that electrophonics can occur in EAS users. Our results show that short pulse widths are optimal for use in EAS stimulation strategies, on the assumption that minimal suppression is best.

Effects of aspirin on psychophysical measures of frequency selectivity, two-tone suppression, and growth of masking.

Three psychophysical measures of nonlinearity were evaluated before and during a course of aspirin ingestion to investigate the role of outer hair cells (OHCs) in these measures, as aspirin is thought to alter the functioning of OHCs. Six normal-hearing individuals received a moderate dose (3.9 g/day) of aspirin for four days, producing essentially flat, temporary hearing losses that ranged from 5-20 dB. The losses were about 2 dB greater for a 300-ms signal than for a 15-ms signal, indicating reduced temporal integration with aspirin. On the final three days of aspirin use, three experiments were completed; each was designed to measure one aspect of nonlinear behavior: (1) the effects of level on frequency selectivity in simultaneous masking using notched-noise maskers, (2) two-tone suppression using forward maskers at the signal frequency (fs) and suppressor tones above fs, and (3) growth-of-masking functions in forward masking using a masking tone below fs. Signal frequencies of 750 and 3000 Hz were used to evaluate the effects of aspirin at relatively low- and high-frequency regions of the cochlea. In experiment 1, aspirin broadened the auditory filters and reduced the effect of level on frequency selectivity. In experiment 2, aspirin reduced or eliminated two-tone suppression. And, in experiment 3, aspirin reduced the slopes of the growth-of-masking functions. Thus, the aspirin was effective in reducing nonlinearity in all three experiments, suggesting that these measures reflect the same (or a similar) active, nonlinear mechanism, namely the compressive nonlinearity provided by the OHCs. In all experiments, aspirin tended to have larger detrimental effects on the nonlinear measures at 3000 Hz than at 750 Hz, which can be explained in terms of greater involvement of nonlinear processing at higher frequencies. Finally, these effects of aspirin were found to be similar to those observed in preliminary measurements in two subjects with mild, permanent hearing loss.

The hearing organ: active sound amplifier and highly sensitive measuring system

The present paper provides a brief review on topical issues of auditory physiology. Recent data on transduction mechanism and adaptation in hair cells as well as on the possible role of outer hair cells in amplifying basilar membrane motion are presented. Strategies of present physiological research in dealing with sensorineural deafness are discussed.

Cochlear function after selective inner hair cell degeneration induced by carboplatin

The ototoxicity of carboplatin, a second generation anti-cancer agent, was examined using the chinchilla as an animal model. In animals treated with a clinical therapeutic dose (400 mg/m 2), the dominant degenerative change is to inner hair cells (IHCs). This is in sharp contrast to most other ototoxic agents, which damage primarily the outer hair cells (OHCs). Functional changes to the cochlea have been evaluated in carboplatin treated subjects by recording cochlear action potentials (CAP) and cochlear microphonics (CM); cochlear lesions were evaluated using scanning electron microscopy. In carboplatin treated animals, CAP thresholds to tone-pip stimuli were elevated in proportion to IHC damage in corresponding cochlear regions. In contrast, CM amplitudes and ‘thresholds’ remained close to normal in most cases, reflecting the preservation of OHCs in the basal turn. These results indicate a high degree of independence between the inner and outer hair cell systems in the cochlear transduction mechanism. We suggest that this species-specific preparation with selective IHC loss will provide a valuable tool for studying, separately, the role of OHCs in both afferent and efferent cochlear function.

Outer hair cell receptor current and sensorineural hearing loss

It is argued in this paper that many nonlinear phenomena in audition and many types of sensorineural hearing loss can be explained by a disruption of the mechano-electrical transduction process at the apex of the outer hair cells. This is done using experimental data and a simple model of the active role of outer hair cells in cochlear mechanics based on our previous experiments with acoustic trauma. The causes of sensorineural loss addressed include acoustic trauma, aminoglycoside ototoxicity, intoxication with loop diuretics, hypoxia and Meniere's disease. The nonlinear phenomena discussed include loudness compression, two-tone suppression and modulation of cochlear sensitivity by very low-frequency tones. In every case considered the reduction in neural sensitivity was related to the reduction in outer hair cell receptor current in a quantitatively similar way. We conclude that the link is causal.

Outer hair cells do produce the preponderance of receptor potentials

Numerous experiments [e.g., Davis et al., Laryngoscope (1958); Dallos and Wang, Audiology (1974)] in which outer hair cell damage is accompanied by good preservation of inner hair cells, have indicated that, in such cochleas, the CM is suppressed by 30–40 dB. The conclusion drawn from such results was that outer hair cells generate a very large fraction of the recorded CM, and that in fact in a normal cochlea the CM is determined by the output of the outer hair cells. While these experiments are very suggestive, a direct confirmation of the dominant role of outer hair cells in CM production has been lacking. What is required for such confirmation is recording from cochlear regions that are denuded of inner hair cells. We are now reporting on such experiments. With very massive doses of kanamycin one can achieve a pattern of hair cell degeneration in the guinea pig's cochlea, whereby only outer hair cells remain in the fourth (apical) turn, and whatever inner hair cells are preserved are confined to more basal regions. Recordings of CM and SP from the scalar media of the fourth turn of such cochleas is compared to data from normal preparations. While many animals are seen to have severely depressed responses, several possess essentially normal receptor potentials. This finding tends to confirm the suggestion that outer hair cells are the primary source of the cochlear receptor potentials; both CM and SP. [Supported by grants from the NINCDS.]