scholarly journals Intracochlear distortion products are broadly generated by outer hair cells but their contributions to otoacoustic emissions are spatially restricted

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Thomas Bowling ◽  
Haiqi Wen ◽  
Sebastiaan W. F. Meenderink ◽  
Wei Dong ◽  
Julien Meaud

AbstractDetection of low-level sounds by the mammalian cochlea requires electromechanical feedback from outer hair cells (OHCs). This feedback arises due to the electromotile response of OHCs, which is driven by the modulation of their receptor potential caused by the stimulation of mechano-sensitive ion channels. Nonlinearity in these channels distorts impinging sounds, creating distortion-products that are detectable in the ear canal as distortion-product otoacoustic emissions (DPOAEs). Ongoing efforts aim to develop DPOAEs, which reflects the ear’s health, into diagnostic tools for sensory hearing loss. These efforts are hampered by limited knowledge on the cochlear extent contributing to DPOAEs. Here, we report on intracochlear distortion products (IDPs) in OHC electrical responses and intracochlear fluid pressures. Experiments and simulations with a physiologically motivated cochlear model show that widely generated electrical IDPs lead to mechanical vibrations in a frequency-dependent manner. The local cochlear impedance restricts the region from which IDPs contribute to DPOAEs at low to moderate intensity, which suggests that DPOAEs may be used clinically to provide location-specific information about cochlear damage.

2020 ◽  
Author(s):  
C. Elliott Strimbu ◽  
Yi Wang ◽  
Elizabeth S. Olson

ABSTRACTThe mammalian hearing organ, the cochlea, contains an active amplifier to boost the vibrational response to low level sounds. Hallmarks of this active process are sharp location-dependent frequency tuning and compressive nonlinearity over a wide stimulus range. The amplifier relies on outer hair cell (OHC) generated forces driven in part by the endocochlear potential (EP), the ~ +80 mV potential maintained in scala media, generated by the stria vascularis. We transiently eliminated the EP in vivo by an intravenous injection of furosemide and measured the vibrations of different layers in the cochlea’s organ of Corti using optical coherence tomography. Distortion product otoacoustic emissions (DPOAE) were monitored at the same times. Following the injection, the vibrations of the basilar membrane lost the best frequency (BF) peak and showed broad tuning similar to a passive cochlea. The intra-organ of Corti vibrations measured in the region of the OHCs lost their BF peak and showed low-pass responses, but retained nonlinearity, indicating that OHC electromotility was still operational. Thus, while electromotility is presumably necessary for amplification, its presence is not sufficient for amplification. The BF peak recovered nearly fully within 2 hours, along with a non-monotonic DPOAE recovery that suggests that physical shifts in operating condition are a final step in the recovery process.SIGNIFICANCEThe endocochlear potential, the +80 mV potential difference across the fluid filled compartments of the cochlea, is essential for normal mechanoelectrical transduction, which leads to receptor potentials in the sensory hair cells when they vibrate in response to sound. Intracochlear vibrations are boosted tremendously by an active nonlinear feedback process that endows the cochlea with its healthy sensitivity and frequency resolution. When the endocochlear potential was reduced by an injection of furosemide, the basilar membrane vibrations resembled those of a passive cochlea, with broad tuning and linear scaling. The vibrations in the region of the outer hair cells also lost the tuned peak, but retained nonlinearity at frequencies below the peak, and these sub-BF responses recovered fairly rapidly. Vibration responses at the peak recovered nearly fully over 2 hours. The staged vibration recovery and a similarly staged DPOAE recovery suggests that physical shifts in operating condition are a final step in the process of cochlear recovery.


Author(s):  
Aras Karimiani ◽  
Nematollah Rouhbakhsh ◽  
Farzaneh Zamiri Abdollahi ◽  
Shohreh Jalaie

Background and Aim: It is not clear if the measurement of distortion product otoacoustic emissions (DPOAE) at frequencies above 8 kHz adds any value in determining the differences in the cochlear function between patients with and without tinnitus. This study aimed to compare DPOAE in the frequency range of 0.5−10 kHz in patients with normal hearing with and without tinnitus. Methods: This comparative cross-sectional study was conducted on 20 individuals with tinnitus and normal hearing as a study group (SG) and a control group (CG) of 20 normal-hearing individuals without tinnitus. The DPOAE was measured with F1/F2 = 1.22 and intensities of F1 = 65 dB SPL and F2 =55 dB SPL in the frequency range of 0.5−10 kHz, moreover in the frequency of tinnitus in SG and corresponding frequency in CG. Results: DPOAE level at 10 kHz did not differ significantly between SG and CG (p = 0.491). However, the mean of overall DPOAE level, DPOAE level at the frequency of tinnitus, and F2 values of 2.5, 5, and 6.298 kHz were significantly lower in SG than CG (p < 0.05). Conclusion: Measurement of DPOAE at 10 kHz did not seem to add any value in determining the differences in the cochlear function between patients with and without tinnitus. However, decreased DPOAE levels at 2.5, 5, and 6.298 kHz which were observed among patients who have tinnitus and normal hearing, indicates some outer hair cells damage that was not detectable by conventional audiometry. Keywords: Tinnitus; normal hearing; outer hair cell; distortion product otoacoustic emission


2013 ◽  
Vol 68 (11) ◽  
pp. 94-97
Author(s):  
I. N. D'yakonova ◽  
Yu. S. Ishanova ◽  
I. V. Rakhmanova

Aim: In our chronic experiment to  register changes of acoustic response of Distortion-Product Otoacoustic Emissions (DPOAE) of intact rabbits in postnatal ontogenesis for the purpose of getting normative data which can be used for studying impact of pathological factors on auditory function and maturation of activity of outer hair cell in ontogenesis. Materials and methods: Study of otoacoustic emissions used mature chinchilla rabbits with a 19 day life of up to 3 months. Results: in the course of ripening were obtained functional activity of outer hair cells of the cochlea. Conclusion: normative data obtained allow us to study using a rabbit model, the pathological effects of agents on the maturation of the outer hair cells of the cochlea in the experiment.


2003 ◽  
Vol 90 (1) ◽  
pp. 444-455 ◽  
Author(s):  
Jiefu Zheng ◽  
Chunfu Dai ◽  
Peter S. Steyger ◽  
Youngki Kim ◽  
Zoltan Vass ◽  
...  

Capsaicin, the vanilloid that selectively activates vanilloid receptors (VRs) on sensory neurons for noxious perception, has been reported to increase cochlear blood flow (CBF). VR-related receptors have also been found in the inner ear. This study aims to address the question as to whether VRs exist in the organ of Corti and play a role in cochlear physiology. Capsaicin or the more potent VR agonist, resiniferatoxin (RTX), was infused into the scala tympani of guinea pig cochlea, and their effects on cochlear sensitivity were investigated. Capsaicin (20 μM) elevated the threshold of auditory nerve compound action potential and reduced the magnitude of cochlear microphonic and electrically evoked otoacoustic emissions. These effects were reversible and could be blocked by a competitive antagonist, capsazepine. Application of 2 μM RTX resulted in cochlear sensitivity alterations similar to that by capsaicin, which could also be blocked by capsazepine. A desensitization phenomenon was observed in the case of prolonged perfusion with either capsaicin or RTX. Brief increase of CBF by capsaicin was confirmed, and the endocochlear potential was not decreased. Basilar membrane velocity (BM) growth functions near the best frequency and BM tuning were altered by capsaicin. Immunohistochemistry study revealed the presence of vanilloid receptor type 1 of the transient receptor potential channel family in the hair cells and supporting cells of the organ of Corti and the spiral ganglion cells of the cochlea. The results indicate that the main action of capsaicin is on outer hair cells and suggest that VRs in the cochlea play a role in cochlear homeostasis.


2020 ◽  
Vol 117 (20) ◽  
pp. 11109-11117
Author(s):  
Woongsu Han ◽  
Jeong-Oh Shin ◽  
Ji-Hyun Ma ◽  
Hyehyun Min ◽  
Jinsei Jung ◽  
...  

Outer hair cells (OHCs) play an essential role in hearing by acting as a nonlinear amplifier which helps the cochlea detect sounds with high sensitivity and accuracy. This nonlinear sound processing generates distortion products, which can be measured as distortion-product otoacoustic emissions (DPOAEs). The OHC stereocilia that respond to sound vibrations are connected by three kinds of extracellular links: tip links that connect the taller stereocilia to shorter ones and convey force to the mechanoelectrical transduction channels, tectorial membrane-attachment crowns (TM-ACs) that connect the tallest stereocilia to one another and to the overlying TM, and horizontal top connectors (HTCs) that link adjacent stereocilia. While the tip links have been extensively studied, the roles that the other two types of links play in hearing are much less clear, largely because of a lack of suitable animal models. Here, while analyzing genetic combinations of tubby mice, we encountered models missing both HTCs and TM-ACs or HTCs alone. We found that the tubby mutation causes loss of both HTCs and TM-ACs due to a mislocalization of stereocilin, which results in OHC dysfunction leading to severe hearing loss. Intriguingly, the addition of the modifier allele modifier of tubby hearing 1 in tubby mice selectively rescues the TM-ACs but not the HTCs. Hearing is significantly rescued in these mice with robust DPOAE production, indicating an essential role of the TM-ACs but not the HTCs in normal OHC function. In contrast, the HTCs are required for the resistance of hearing to damage caused by noise stress.


1994 ◽  
Vol 74 (1-2) ◽  
pp. 204-216 ◽  
Author(s):  
M. Subramaniam ◽  
R.J. Salvi ◽  
V.P. Spongr ◽  
D. Henderson ◽  
N.L. Powers

2019 ◽  
Vol 122 (1) ◽  
pp. 118-131
Author(s):  
Margarete A. Ueberfuhr ◽  
Markus Drexl

Sensitive sound detection within the mammalian cochlea is performed by hair cells surrounded by cochlear fluids. Maintenance of cochlear fluid homeostasis and tight regulation of intracellular conditions in hair cells are crucial for the auditory transduction process but can be impaired by intense sound stimulation. After a short, intense low-frequency sound, the cochlea shows the previously described “bounce phenomenon,” which manifests itself as slow oscillatory changes of hearing thresholds and otoacoustic emissions. In this study, distortion product otoacoustic emissions (DPOAEs) were recorded after Mongolian gerbils were exposed to intense low-frequency sounds (200 Hz, 100 dB SPL) with different exposure times up to 1 h. After all sound exposure durations, a certain percentage of recordings (up to 80% after 1.5-min-long exposure) showed oscillatory DPOAE changes, similar to the bounce phenomenon in humans. Changes were quite uniform with respect to size and time course, and they were independent from sound exposure duration. Changes showed states of hypo- and hyperactivity with either state preceding the other. The direction of changes was suggested to depend on the static position of the cochlear operating point. As assessed with DPOAEs, no indication for a permanent damage after several or long exposure times was detected. We propose that sensitivity changes occur due to alterations of the mechanoelectrical transduction process of outer hair cells. Those alterations could be induced by different challenged homeostatic processes with slow electromotility of outer hair cells being the most plausible source of the bounce phenomenon. NEW & NOTEWORTHY Low-frequency, high-intensity sound can cause slowly cycling activity changes in the mammalian cochlea. We examined the effect of low-frequency sound duration on the degree of these alterations. We found that cochlear changes showed a stereotypical biphasic pattern independent of sound exposure duration, but the probability that significant changes occurred decreased with increasing sound duration. Despite exposure durations of up to 1 h, no permanent or transient impairments of the cochlea were detected.


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