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1
Robles, Luis, and Mario A. Ruggero. "Mechanics of the Mammalian Cochlea." Physiological Reviews 81, no. 3 (July 1, 2001): 1305–52. http://dx.doi.org/10.1152/physrev.2001.81.3.1305.
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In mammals, environmental sounds stimulate the auditory receptor, the cochlea, via vibrations of the stapes, the innermost of the middle ear ossicles. These vibrations produce displacement waves that travel on the elongated and spirally wound basilar membrane (BM). As they travel, waves grow in amplitude, reaching a maximum and then dying out. The location of maximum BM motion is a function of stimulus frequency, with high-frequency waves being localized to the “base” of the cochlea (near the stapes) and low-frequency waves approaching the “apex” of the cochlea. Thus each cochlear site has a characteristic frequency (CF), to which it responds maximally. BM vibrations produce motion of hair cell stereocilia, which gates stereociliar transduction channels leading to the generation of hair cell receptor potentials and the excitation of afferent auditory nerve fibers. At the base of the cochlea, BM motion exhibits a CF-specific and level-dependent compressive nonlinearity such that responses to low-level, near-CF stimuli are sensitive and sharply frequency-tuned and responses to intense stimuli are insensitive and poorly tuned. The high sensitivity and sharp-frequency tuning, as well as compression and other nonlinearities (two-tone suppression and intermodulation distortion), are highly labile, indicating the presence in normal cochleae of a positive feedback from the organ of Corti, the “cochlear amplifier.” This mechanism involves forces generated by the outer hair cells and controlled, directly or indirectly, by their transduction currents. At the apex of the cochlea, nonlinearities appear to be less prominent than at the base, perhaps implying that the cochlear amplifier plays a lesser role in determining apical mechanical responses to sound. Whether at the base or the apex, the properties of BM vibration adequately account for most frequency-specific properties of the responses to sound of auditory nerve fibers.
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Szczepek, Agnieszka J., Tatyana Dudnik, Betül Karayay, Valentina Sergeeva, Heidi Olze, and Alina Smorodchenko. "Mast Cells in the Auditory Periphery of Rodents." Brain Sciences 10, no. 10 (October 1, 2020): 697. http://dx.doi.org/10.3390/brainsci10100697.
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Mast cells (MCs) are densely granulated cells of myeloid origin and are a part of immune and neuroimmune systems. MCs have been detected in the endolymphatic sac of the inner ear and are suggested to regulate allergic hydrops. However, their existence in the cochlea has never been documented. In this work, we show that MCs are present in the cochleae of C57BL/6 mice and Wistar rats, where they localize in the modiolus, spiral ligament, and stria vascularis. The identity of MCs was confirmed in cochlear cryosections and flat preparations using avidin and antibodies against c-Kit/CD117, chymase, tryptase, and FcεRIα. The number of MCs decreased significantly during postnatal development, resulting in only a few MCs present in the flat preparation of the cochlea of a rat. In addition, exposure to 40 µM cisplatin for 24 h led to a significant reduction in cochlear MCs. The presence of MCs in the cochlea may shed new light on postnatal maturation of the auditory periphery and possible involvement in the ototoxicity of cisplatin. Presented data extend the current knowledge about the physiology and pathology of the auditory periphery. Future functional studies should expand and translate this new basic knowledge to clinics.
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Köles, László, Judit Szepesy, Eszter Berekméri, and Tibor Zelles. "Purinergic Signaling and Cochlear Injury-Targeting the Immune System?" International Journal of Molecular Sciences 20, no. 12 (June 18, 2019): 2979. http://dx.doi.org/10.3390/ijms20122979.
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Hearing impairment is the most common sensory deficit, affecting more than 400 million people worldwide. Sensorineural hearing losses currently lack any specific or efficient pharmacotherapy largely due to the insufficient knowledge of the pathomechanism. Purinergic signaling plays a substantial role in cochlear (patho)physiology. P2 (ionotropic P2X and the metabotropic P2Y) as well as adenosine receptors expressed on cochlear sensory and non-sensory cells are involved mostly in protective mechanisms of the cochlea. They are implicated in the sensitivity adjustment of the receptor cells by a K+ shunt and can attenuate the cochlear amplification by modifying cochlear micromechanics. Cochlear blood flow is also regulated by purines. Here, we propose to comprehend this field with the purine-immune interactions in the cochlea. The role of harmful immune mechanisms in sensorineural hearing losses has been emerging in the horizon of cochlear pathologies. In addition to decreasing hearing sensitivity and increasing cochlear blood supply, influencing the immune system can be the additional avenue for pharmacological targeting of purinergic signaling in the cochlea. Elucidating this complexity of purinergic effects on cochlear functions is necessary and it can result in development of new therapeutic approaches in hearing disabilities, especially in the noise-induced ones.
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Delprat, Benjamin, Jérôme Ruel, Matthieu J. Guitton, Ghyslaine Hamard, Marc Lenoir, Rémy Pujol, Jean-Luc Puel, Philippe Brabet, and Christian P. Hamel. "Deafness and Cochlear Fibrocyte Alterations in Mice Deficient for the Inner Ear Protein Otospiralin." Molecular and Cellular Biology 25, no. 2 (January 15, 2005): 847–53. http://dx.doi.org/10.1128/mcb.25.2.847-853.2005.
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ABSTRACT In the cochlea, the mammalian auditory organ, fibrocytes of the mesenchymal nonsensory regions play important roles in cochlear physiology, including the maintenance of ionic and hydric components in the endolymph. Occurrence of human deafness in fibrocyte alterations underlines their critical roles in auditory function. We recently described a novel gene, Otos, which encodes otospiralin, a small protein of unknown function that is produced by the fibrocytes of the cochlea and vestibule. We now have generated mice with deletion of Otos and found that they show moderate deafness, with no frequency predominance. Histopathology revealed a degeneration of type II and IV fibrocytes, while hair cells and stria vascularis appeared normal. Together, these findings suggest that impairment of fibrocytes caused by the loss in otospiralin leads to abnormal cochlear physiology and auditory function. This moderate dysfunction may predispose to age-related hearing loss.
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Meenderink, Sebastiaan W. F., and Marcel van der Heijden. "Reverse Cochlear Propagation in the Intact Cochlea of the Gerbil: Evidence for Slow Traveling Waves." Journal of Neurophysiology 103, no. 3 (March 2010): 1448–55. http://dx.doi.org/10.1152/jn.00899.2009.
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The inner ear can produce sounds, but how these otoacoustic emissions back-propagate through the cochlea is currently debated. Two opposing views exist: fast pressure waves in the cochlear fluids and slow traveling waves involving the basilar membrane. Resolving this issue requires measuring the travel times of emissions from their cochlear origin to the ear canal. This is problematic because the exact intracochlear location of emission generation is unknown and because the cochlea is vulnerable to invasive measurements. We employed a multi-tone stimulus optimized to measure reverse travel times. By exploiting the dispersive nature of the cochlea and by combining acoustic measurements in the ear canal with recordings of the cochlear-microphonic potential, we were able to determine the group delay between intracochlear emission-generation and their recording in the ear canal. These delays remained significant after compensating for middle-ear delay. The results contradict the hypothesis that the reverse propagation of emissions is exclusively by direct pressure waves.
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Kikidis, Dimitrios, and Athanasios Bibas. "A Clinically Oriented Introduction and Review on Finite Element Models of the Human Cochlea." BioMed Research International 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/975070.
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Due to the inaccessibility of the inner ear, direct in vivo information on cochlear mechanics is difficult to obtain. Mathematical modelling is a promising way to provide insight into the physiology and pathology of the cochlea. Finite element method (FEM) is one of the most popular discrete mathematical modelling techniques, mainly used in engineering that has been increasingly used to model the cochlea and its elements. The aim of this overview is to provide a brief introduction to the use of FEM in modelling and predicting the behavior of the cochlea in normal and pathological conditions. It will focus on methodological issues, modelling assumptions, simulation of clinical scenarios, and pathologies.
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Emadi, Gulam, Claus-Peter Richter, and Peter Dallos. "Stiffness of the Gerbil Basilar Membrane: Radial and Longitudinal Variations." Journal of Neurophysiology 91, no. 1 (January 2004): 474–88. http://dx.doi.org/10.1152/jn.00446.2003.
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Experimental data on the mechanical properties of the tissues of the mammalian cochlea are essential for understanding the frequency- and location-dependent motion patterns that result in response to incoming sound waves. Within the cochlea, sound-induced vibrations are transduced into neural activity by the organ of Corti, the gross motion of which is dependent on the motion of the underlying basilar membrane. In this study we present data on stiffness of the gerbil basilar membrane measured at multiple positions within a cochlear cross section and at multiple locations along the length of the cochlea. A basic analysis of these data using relatively simple models of cochlear mechanics reveals our most important result: the experimentally measured longitudinal stiffness gradient at the middle of the pectinate zone of the basilar membrane (4.43 dB/mm) can account for changes of best frequency along the length of the cochlea. Furthermore, our results indicate qualitative changes of stiffness-deflection curves as a function of radial position; in particular, there are differences in the rate of stiffness growth with increasing tissue deflection. Longitudinal coupling within the basilar membrane/organ of Corti complex is determined to have a space constant of 21 μm in the middle turn of the cochlea. The bulk of our data was obtained in the hemicochlea preparation, and we include a comparison of this set of data to data obtained in vivo.
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Jeong, Sung-Wook, and Lee-Suk Kim. "A New Classification of Cochleovestibular Malformations and Implications for Predicting Speech Perception Ability after Cochlear Implantation." Audiology and Neurotology 20, no. 2 (2015): 90–101. http://dx.doi.org/10.1159/000365584.
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Objectives: The aims of this study were to introduce a new classification of cochleovestibular malformation (CVM) and to investigate how well this classification can predict speech perception ability after cochlear implantation in children with CVM. Methods: Fifty-nine children with CVM who had used a cochlear implant for more than 3 years were included. CVM was classified into 4 subtypes based on the morphology of the cochlea and the modiolus on temporal bone computed tomography (TBCT): normal cochlea and normal modiolus (type A, n = 16), malformed cochlea and partial modiolus (type B, n = 31), malformed cochlea and no modiolus (type C, n = 6), and no cochlea and no modiolus (type D, n = 6). Speech perception test scores were compared between the subtypes of CVM using analysis of covariance with post hoc Bonferroni test. Univariate and multivariate regression analyses were used to identify the significant predictors of the speech perception test scores. Results: The speech perception test scores after implantation were significantly better in children with CVM type A or type B than in children with CVM type C or type D. The test scores did not differ significantly between the implanted children with CVM type A or type B and those without CVM. In univariate regression analysis, the type of CVM was a significant predictor of the speech perception test scores in implanted children with CVM. Multivariate regression analysis revealed that the age at cochlear implantation, cochlear nerve size and preimplantation speech perception test scores were significant predictors of the postimplantation speech perception test scores. The chance of cochlear nerve deficiency increased progressively from CVM type A to type D. Conclusion: The new classification of CVM based on the morphology of the cochlea and the modiolus is simple and easy to use, and correlated well with postimplantation speech perception ability and cochlear nerve status. This simple classification of CVM using TBCT with cochlear nerve assessment by magnetic resonance imaging is helpful in the preoperative evaluation of children with CVM.
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Jones, Timothy A., Sherri M. Jones, and Kristina C. Paggett. "Emergence of Hearing in the Chicken Embryo." Journal of Neurophysiology 96, no. 1 (July 2006): 128–41. http://dx.doi.org/10.1152/jn.00599.2005.
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It is commonly held that hearing generally begins on incubation day 12 (E12) in the chicken embryo ( Gallus domesticus). However, little is known about the response properties of cochlear ganglion neurons for ages younger than E18. We studied ganglion neurons innervating the basilar papilla of embryos (E12–E18) and hatchlings (P13–P15). We asked first, when do primary afferent neurons begin to encode sounds? Second, when do afferents evidence frequency selectivity? Third, what range of characteristic frequencies (CFs) is represented in the late embryo? Finally, how does sound transfer from air to the cochlea affect responses in the embryo and hatchling? Responses to airborne sound were compared with responses to direct columella footplate stimulation of the cochlea. Cochlear ganglion neurons exhibited a profound insensitivity to sound from E12 to E16 (stages 39–42). Responses to sound and frequency selectivity emerged at about E15. Frequency selectivity matured rapidly from E16 to E18 (stages 42 and 44) to reflect a mature range of CFs (170–4,478 Hz) and response sensitivity to footplate stimulation. Limited high-frequency sound transfer from air to the cochlea restricted the response to airborne sound in the late embryo. Two periods of ontogeny are proposed. First is a prehearing period (roughly E12–E16) of endogenous cochlear signaling that provides neurotrophic support and guides normal developmental refinements in central binaural processing pathways followed by a period (roughly E16–E19) wherein the cochlea begins to detect and encode sound.
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Zheng, Jiefu, Chunfu Dai, Peter S. Steyger, Youngki Kim, Zoltan Vass, Tianying Ren, and Alfred L. Nuttall. "Vanilloid Receptors in Hearing: Altered Cochlear Sensitivity by Vanilloids and Expression of TRPV1 in the Organ of Corti." Journal of Neurophysiology 90, no. 1 (July 2003): 444–55. http://dx.doi.org/10.1152/jn.00919.2002.
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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.
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Sumner, Christian J., Toby T. Wells, Christopher Bergevin, Joseph Sollini, Heather A. Kreft, Alan R. Palmer, Andrew J. Oxenham, and Christopher A. Shera. "Mammalian behavior and physiology converge to confirm sharper cochlear tuning in humans." Proceedings of the National Academy of Sciences 115, no. 44 (October 15, 2018): 11322–26. http://dx.doi.org/10.1073/pnas.1810766115.
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Frequency analysis of sound by the cochlea is the most fundamental property of the auditory system. Despite its importance, the resolution of this frequency analysis in humans remains controversial. The controversy persists because the methods used to estimate tuning in humans are indirect and have not all been independently validated in other species. Some data suggest that human cochlear tuning is considerably sharper than that of laboratory animals, while others suggest little or no difference between species. We show here in a single species (ferret) that behavioral estimates of tuning bandwidths obtained using perceptual masking methods, and objective estimates obtained using otoacoustic emissions, both also employed in humans, agree closely with direct physiological measurements from single auditory-nerve fibers. Combined with human behavioral data, this outcome indicates that the frequency analysis performed by the human cochlea is of significantly higher resolution than found in common laboratory animals. This finding raises important questions about the evolutionary origins of human cochlear tuning, its role in the emergence of speech communication, and the mechanisms underlying our ability to separate and process natural sounds in complex acoustic environments.
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Ueberfuhr, Margarete A., and Markus Drexl. "Slow oscillatory changes of DPOAE magnitude and phase after exposure to intense low-frequency sounds." Journal of Neurophysiology 122, no. 1 (July 1, 2019): 118–31. http://dx.doi.org/10.1152/jn.00204.2019.
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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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Campbell, Luke, Christofer Bester, Claire Iseli, David Sly, Adrian Dragovic, Anthony W. Gummer, and Stephen O'Leary. "Electrophysiological Evidence of the Basilar-Membrane Travelling Wave and Frequency Place Coding of Sound in Cochlear Implant Recipients." Audiology and Neurotology 22, no. 3 (2017): 180–89. http://dx.doi.org/10.1159/000478692.
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Aim: To obtain direct evidence for the cochlear travelling wave in humans by performing electrocochleography from within the cochlea in subjects implanted with an auditory prosthesis. Background: Sound induces a travelling wave that propagates along the basilar membrane, exhibiting cochleotopic tuning with a frequency-dependent phase delay. To date, evoked potentials and psychophysical experiments have supported the presence of the travelling wave in humans, but direct measurements have not been made. Methods: Electrical potentials in response to rarefaction and condensation acoustic tone bursts were recorded from multiple sites along the human cochlea, directly from a cochlear implant electrode during, and immediately after, its insertion. These recordings were made from individuals with residual hearing. Results: Electrocochleography was recorded from 11 intracochlear electrodes in 7 ears from 6 subjects, with detectable responses on all electrodes in 5 ears. Cochleotopic tuning and frequency-dependent phase delay of the cochlear microphonic were demonstrated. The response latencies were slightly shorter than those anticipated which we attribute to the subjects' hearing loss. Conclusions: Direct evidence for the travelling wave was observed. Electrocochleography from cochlear implant electrodes provides site-specific information on hair cell and neural function of the cochlea with potential diagnostic value.
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Schart-Morén, Nadine, Sune Larsson, Helge Rask-Andersen, and Hao Li. "Anatomical Characteristics of Facial Nerve and Cochlea Interaction." Audiology and Neurotology 22, no. 1 (2017): 41–49. http://dx.doi.org/10.1159/000475876.
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Objective: The aim was to study the relationship between the labyrinthine portion (LP) of the facial canal and the cochlea in human inner ear molds and temporal bones using micro-CT and 3D rendering. A reduced cochlea-facial distance may spread electric currents from the cochlear implant to the LP and cause facial nerve stimulation. Influencing factors may be the topographic anatomy and otic capsule properties. Methods: An archival collection of human temporal bones underwent micro-CT and 3D reconstruction. In addition, cochlea-facial distance was assessed in silicone and polyester resin molds, and the association between the LP and upper basal turn of the cochlea was analyzed. Results: Local thinning of the otic capsule and local anatomy may explain the development of cochlea-facial dehiscence, which was found in 1.4%. A reduced cochlea-facial distance was noted in 1 bone with a superior semicircular canal dehiscence but not in bones with superior semicircular canal “blue line.” The otic capsule often impinged upon the LP and caused narrowing. Conclusion: Micro-CT with 3D rendering offers new possibilities to study the topographic anatomy of the human temporal bone. The varied shape of the cross-section of the LP could often be explained by an “intruding” cochlea.
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Kitzes, L. M., and M. N. Semple. "Single-unit responses in the inferior colliculus: effects of neonatal unilateral cochlear ablation." Journal of Neurophysiology 53, no. 6 (June 1, 1985): 1483–500. http://dx.doi.org/10.1152/jn.1985.53.6.1483.
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Monaural responses of single units isolated in the inferior colliculus of adult gerbils that have developed postnatally with one cochlea were compared with monaural responses recorded in animals that have developed with both cochleas. One cochlea of 2-day-old gerbils was ablated, and at approximately 6 mo of age, excitatory responses to stimulation of the nonoperated ear were recorded in the ipsilateral inferior colliculus. These responses were compared quantitatively with responses evoked by ipsilateral and contralateral monaural stimulation in normal gerbils. Responses to ipsilateral stimulation in adult gerbils subjected at 2 days of age to ablation of the contralateral cochlea are significantly different from ipsilateral responses in nonoperated gerbils. In several respects they are very similar to contralateral responses in nonoperated gerbils. (Differences between monaural contralateral and ipsilateral responses in control animals are documented in the companion paper, Ref. 24.) These conclusions are based on analyses of response threshold, peak discharge rate, response pattern, and minimum response latency. The mean dynamic range of ipsilateral rate/intensity functions obtained in neonatally ablated gerbils is significantly larger than the mean ipsilateral and contralateral dynamic ranges in control animals. Analyses of threshold tuning curves indicate that the frequency tuning of units in the inferior colliculus of neonatally ablated animals does not differ significantly from the tuning of units in control animals in response to either ipsilateral or contralateral stimulation. These data reveal that in normal gerbils responses of single units in the inferior colliculus to stimulation of the ipsilateral ear result in part from interactions during postnatal development between pathways that convey information from the contralateral ear. The results are discussed in terms of the known anatomic consequences of a neonatal cochlear ablation and the competition for available synaptic space in the development of the retinotectal system.
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Lu, Yong, Julie A. Harris, and Edwin W. Rubel. "Development of Spontaneous Miniature EPSCs in Mouse AVCN Neurons During a Critical Period of Afferent-Dependent Neuron Survival." Journal of Neurophysiology 97, no. 1 (January 2007): 635–46. http://dx.doi.org/10.1152/jn.00915.2006.
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During a critical period prior to hearing onset, cochlea ablation leads to massive neuronal death in the mouse anteroventral cochlear nucleus (AVCN), where cell survival is believed to depend on glutamatergic input. We investigated the development of spontaneous miniature excitatory postsynaptic currents (mEPSCs) in AVCN neurons using whole cell patch-clamp techniques during [postnatal day 7 (P7)] and after (P14, P21) this critical period. We also examined the effects of unilateral cochlea ablation on mEPSC development. The two main AVCN neuron types, bushy and stellate cells, were distinguished electrophysiologically. Bushy cell mEPSCs became more frequent and faster between P7 and P14/P21 but with little change in amplitude. Dendritic filtering of mEPSCs was not detected as indicated by the lack of correlation between 10 and 90% rise times and decay time constants. Seven days after cochlea ablation at P7 or P14, mEPSCs in surviving bushy cells were similar to controls, except that rise and decay times were positively correlated ( R = 0.31 and 0.14 for surgery at P7 and P14, respectively). Consistent with this evidence for a shift of synaptic activity from the somata to the dendrites, SV2 staining (a synaptic vesicle marker) forms a ring around somata of control but not experimental bushy cells. In contrast, mEPSCs of stellate cells showed few significant changes over these ages with or without cochlea ablation. Taken together, mEPSCs in mouse AVCN bushy cells show dramatic developmental changes across this critical period, and cochlea ablation may lead to the emergence of excitatory synaptic inputs impinging on bushy cell dendrites.
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Phillips, James O., Leo Ling, Amy Nowack, Brenda Rebollar, and Jay T. Rubinstein. "Interactions between Auditory and Vestibular Modalities during Stimulation with a Combined Vestibular and Cochlear Prosthesis." Audiology and Neurotology 25, Suppl. 1-2 (2020): 96–108. http://dx.doi.org/10.1159/000503846.
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Background: A combined vestibular and cochlear prosthesis may restore hearing and balance to patients who have lost both. To do so, the device should activate each sensory system independently. Objectives: In this study, we quantify auditory and vestibular interactions during interleaved stimulation with a combined 16-channel cochlear and 6-channel vestibular prosthesis in human subjects with both hearing and vestibular loss. Methods: Three human subjects were implanted with a combined vestibular and cochlear implant. All subjects had severe-to-profound deafness in the implanted ear. We provided combined stimulation of the cochlear and vestibular arrays and looked for interactions between these separate inputs. Our main outcome measures were electrically evoked slow-phase eye velocities during nystagmus elicited by brief trains of biphasic pulse stimulation of the vestibular end organs with and without concurrent stimulation of the cochlea, and Likert scale assessments of perceived loudness and pitch during stimulation of the cochlea, with and without concurrent stimulation of the vestibular ampullae. Results: All subjects had no auditory sensation resulting from semicircular canal stimulation alone, and no sensation of motion or slow-phase eye movement resulting from cochlear stimulation alone. However, interleaved cochlear stimulation did produce changes in the slow-phase eye velocities elicited by electrical stimulation. Similarly, interleaved semicircular canal stimulation did elicit changes in the perceived pitch and loudness resulting from stimulation at multiple sites in the cochlea. Conclusions: There are significant interactions between different sensory modalities during stimulation with a combined vestibular and cochlear prosthesis. Such interactions present potential challenges for stimulation strategies to simultaneously restore auditory and vestibular function with such an implant.
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El Afia, Fahd, Fabrice Giraudet, Laurent Gilain, Thierry Mom, and Paul Avan. "Resistance of Gerbil Auditory Function to Reversible Decrease in Cochlear Blood Flow." Audiology and Neurotology 22, no. 2 (2017): 89–95. http://dx.doi.org/10.1159/000478650.
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The objective was to design in gerbils a model of reversible decrease in cochlear blood flow (CBF) and analyze its influence on cochlear function. In Mongolian gerbils injected with ferromagnetic microbeads, a magnet placed near the porus acusticus allowed CBF to be manipulated. The cochlear microphonic potential (CM) from the basal cochlea was monitored by a round-window electrode. In 13 of the 20 successfully injected gerbils, stable CBF reduction was obtained for 11.5 min on average. The CM was affected only when CBF fell to less than 60% of its baseline, yet remained >40% of its initial level in about 2/3 of such cases. After CBF restoration, CM recovery was fast and usually complete. Reduced CM came with a 35- to 45-dB threshold elevation of neural responses determined by compound action potentials. This method allowing reversible changes of CBF confirms the robustness of cochlear function to decreased CBF. It can be used to study whether a hypovascularized cochlea is abnormally sensitive to stress.
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Kössl, M., E. Foeller, M. Drexl, M. Vater, E. Mora, F. Coro, and I. J. Russell. "Postnatal Development of Cochlear Function in the Mustached Bat, Pteronotus parnellii." Journal of Neurophysiology 90, no. 4 (October 2003): 2261–73. http://dx.doi.org/10.1152/jn.00100.2003.
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Postnatal development of the mustached bat's cochlea was studied by measuring cochlear microphonic and compound action potentials. In adults, a cochlear resonance is involved in enhanced tuning to the second harmonic constant frequency component (CF2) of their echolocation calls at ∼61 kHz This resonance is present immediately after birth in bats that do not yet echolocate. Its frequency is lower (46 kHz) and the corresponding threshold minimum of cochlear microphonic potentials is broader than in adults. Long-lasting ringing of the cochlear microphonic potential after tone stimulus offset that characterizes the adult auditory response close to CF2 is absent in newborns. In the course of the first 5 postnatal weeks, there is a concomitant upward shift of CF2 and the frequency of cochlear threshold minima. Up to the end of the third postnatal week, sensitivity of auditory threshold minima and the Q value of the cochlear resonance increase at a fast rate. Between 2 and 4 wk of age, two cochlear microphonic threshold minima are found consistently in the CF2 range that differ in their level-dependent dynamic growth behavior and are 1.5–5.7 kHz apart from each other. In older animals, there is a single minimum that approaches adult tuning in its sharpness. The data provide evidence to show that during maturation of the cochlea, the frequency and the sensitivity of the threshold minimum associated with CF2 increases and that these increases are associated with the fusion of two resonances that are partly dissociated in developing animals.
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Horvath, Lukas, Daniel Bodmer, Vesna Radojevic, and Arianne Monge Naldi. "Activin Signaling Disruption in the Cochlea Does Not Influence Hearing in Adult Mice." Audiology and Neurotology 20, no. 1 (November 26, 2014): 51–61. http://dx.doi.org/10.1159/000366152.
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Activin, a member of the TGF-F superfamily, was found to play an important role in the development, repair and apoptosis of different tissues and organs. Accordingly, activin signaling is involved in the development of the cochlea. Activin binds to its receptor ActRII, then dimerizes with ActRI and induces a signaling pathway resulting in gene expression. A study reported a case of fibrodysplasia ossificans progressiva with an unusual mutation in the ActRI gene leading to sensorineural hearing loss. This draws attention to the role of activin and its receptors in the developed cochlea. To date, only the expression of ActRII is known in the adult mammalian cochlea. In this study, we present for the first time the presence of activin A and ActRIB in the adult cochlea. Transgenic mice with postnatal dominant-negative ActRIB expression causing disruption of activin signaling in vivo were used for assessing cochlear morphology and hearing ability through the auditory brainstem response (ABR) threshold. Nonfunctioning ActRIB did not affect the ABR thresholds and did not alter the microscopic anatomy of the cochlea. We conclude, therefore, that activin signaling is not necessary for hearing in adult mice under physiological conditions but may be important during and after damaging events in the inner ear. i 2014 S. Karger AG, Basel
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Sun, Jianjun, Shoab Ahmad, Shanping Chen, Wenxue Tang, Yanping Zhang, Ping Chen, and Xi Lin. "Cochlear gap junctions coassembled from Cx26 and 30 show faster intercellular Ca2+ signaling than homomeric counterparts." American Journal of Physiology-Cell Physiology 288, no. 3 (March 2005): C613—C623. http://dx.doi.org/10.1152/ajpcell.00341.2004.
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The importance of connexins (Cxs) in cochlear functions has been demonstrated by the finding that mutations in Cx genes cause a large proportion of sensorineural hearing loss cases. However, it is still unclear how Cxs contribute to the cochlear function. Recent data ( 33 ) obtained from Cx30 knockout mice showing that a reduction of Cx diversity in assembling gap junctions is sufficient to cause deafness suggest that functional interactions of different subtypes of Cxs may be essential in normal hearing. In this work we show that the two major forms of Cxs (Cx26 and Cx30) in the cochlea have overlapping expression patterns beginning at early embryonic stages. Cx26 and Cx30 were colocalized in most gap junction plaques in the cochlea, and their coassembly was tested by coimmunoprecipitation. To compare functional differences of gap junctions with different molecular configurations, homo- and heteromeric gap junctions composed of Cx26 and/or Cx30 were reconstituted by transfections in human embryonic kidney-293 cells. The ratio imaging technique and fluorescent tracer diffusion assays were used to assess the function of reconstituted gap junctions. Our results revealed that gap junctions with different molecular configurations show differences in biochemical coupling, and that intercellular Ca2+ signaling across heteromeric gap junctions consisting of Cx26 and Cx30 was at least twice as fast as their homomerically assembled counterparts. Our data suggest that biochemical permeability and the dynamics of intercellular signaling through gap junction channels, in addition to gap junction-mediated intercellular ionic coupling, may be important factors to consider for studying functional roles of gap junctions in the cochlea.
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Wangemann, Philine, Hyoung-Mi Kim, Sara Billings, Kazuhiro Nakaya, Xiangming Li, Ruchira Singh, David S. Sharlin, Douglas Forrest, Daniel C. Marcus, and Peying Fong. "Developmental delays consistent with cochlear hypothyroidism contribute to failure to develop hearing in mice lacking Slc26a4/pendrin expression." American Journal of Physiology-Renal Physiology 297, no. 5 (November 2009): F1435—F1447. http://dx.doi.org/10.1152/ajprenal.00011.2009.
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Mutations of SLC26A4 cause an enlarged vestibular aqueduct, nonsyndromic deafness, and deafness as part of Pendred syndrome. SLC26A4 encodes pendrin, an anion exchanger located in the cochlea, thyroid, and kidney. The goal of the present study was to determine whether developmental delays, possibly mediated by systemic or local hypothyroidism, contribute to the failure to develop hearing in mice lacking Slc26a4 ( Slc26a4−/−). We evaluated thyroid function by voltage and pH measurements, by array-assisted gene expression analysis, and by determination of plasma thyroxine levels. Cochlear development was evaluated for signs of hypothyroidism by microscopy, in situ hybridization, and quantitative RT-PCR. No differences in plasma thyroxine levels were found in Slc26a4−/− and sex-matched Slc26a4+/− littermates between postnatal day 5 ( P5) and P90. In adult Slc26a4−/− mice, the transepithelial potential and the pH of thyroid follicles were reduced. No differences in the expression of genes that participate in thyroid hormone synthesis or ion transport were observed at P15, when plasma thyroxine levels peaked. Scala media of the cochlea was 10-fold enlarged, bulging into and thereby displacing fibrocytes, which express Dio2 to generate a cochlear thyroid hormone peak at P7. Cochlear development, including tunnel opening, arrival of efferent innervation at outer hair cells, endochondral and intramembraneous ossification, and developmental changes in the expression of Dio2, Dio3, and Tectb were delayed by 1–4 days. These data suggest that pendrin functions as a HCO3− transporter in the thyroid, that Slc26a4−/− mice are systemically euthyroid, and that delays in cochlear development, possibly due to local hypothyroidism, lead to the failure to develop hearing.
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Zheng, Jiefu, Niranjan Deo, Yuan Zou, Karl Grosh, and Alfred L. Nuttall. "Chlorpromazine Alters Cochlear Mechanics and Amplification: In Vivo Evidence for a Role of Stiffness Modulation in the Organ of Corti." Journal of Neurophysiology 97, no. 2 (February 2007): 994–1004. http://dx.doi.org/10.1152/jn.00774.2006.
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Although prestin-mediated outer hair cell (OHC) electromotility provides mechanical force for sound amplification in the mammalian cochlea, proper OHC stiffness is required to maintain normal electromotility and to transmit mechanical force to the basilar membrane (BM). To investigate the in vivo role of OHC stiffness in cochlear amplification, chlorpromazine (CPZ), an antipsychotic drug that alters OHC lateral wall biophysics, was infused into the cochleae in living guinea pigs. The effects of CPZ on cochlear amplification and OHC electromotility were observed by measuring the acoustically and electrically evoked BM motions. CPZ significantly reduced cochlear amplification as measured by a decline of the acoustically evoked BM motion near the best frequency (BF) accompanied by a loss of nonlinearity and broadened tuning. It also substantially reduced electrically evoked BM vibration near the BF and at frequencies above BF (≤80 kHz). The high-frequency notch (near 50 kHz) in the electrically evoked BM response shifted toward higher frequency in a CPZ concentration-dependent manner with a corresponding phase change. In contrast, salicylate resulted in a shift in this notch toward lower frequency. These results indicate that CPZ reduces OHC-mediated cochlear amplification probably via its effects on the mechanics of the OHC plasma membrane rather than via a direct effect on the OHC motor, prestin. Through modeling, we propose that with a combined OHC somatic and hair bundle forcing, the upward-shift of the ∼50-kHz notch in the electrically-evoked BM motion may indicate stiffness increase of the OHCs that is responsible for the reduced cochlear amplification.
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Kugler, Kathrin, Lutz Wiegrebe, Benedikt Grothe, Manfred Kössl, Robert Gürkov, Eike Krause, and Markus Drexl. "Low-frequency sound affects active micromechanics in the human inner ear." Royal Society Open Science 1, no. 2 (October 2014): 140166. http://dx.doi.org/10.1098/rsos.140166.
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Noise-induced hearing loss is one of the most common auditory pathologies, resulting from overstimulation of the human cochlea, an exquisitely sensitive micromechanical device. At very low frequencies (less than 250 Hz), however, the sensitivity of human hearing, and therefore the perceived loudness is poor. The perceived loudness is mediated by the inner hair cells of the cochlea which are driven very inadequately at low frequencies. To assess the impact of low-frequency (LF) sound, we exploited a by-product of the active amplification of sound outer hair cells (OHCs) perform, so-called spontaneous otoacoustic emissions. These are faint sounds produced by the inner ear that can be used to detect changes of cochlear physiology. We show that a short exposure to perceptually unobtrusive, LF sounds significantly affects OHCs: a 90 s, 80 dB(A) LF sound induced slow, concordant and positively correlated frequency and level oscillations of spontaneous otoacoustic emissions that lasted for about 2 min after LF sound offset. LF sounds, contrary to their unobtrusive perception, strongly stimulate the human cochlea and affect amplification processes in the most sensitive and important frequency range of human hearing.
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Cooper, N. P., and W. S. Rhode. "Mechanical Responses to Two-Tone Distortion Products in the Apical and Basal Turns of the Mammalian Cochlea." Journal of Neurophysiology 78, no. 1 (July 1, 1997): 261–70. http://dx.doi.org/10.1152/jn.1997.78.1.261.
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Cooper, N. P. and W. S. Rhode. Mechanical responses to two-tone distortion products in the apical and basal turns of the mammalian cochlea. J. Neurophysiol. 78: 261–270, 1997. Mechanical responses to one- and two-tone acoustic stimuli were recorded from the cochlear partition in the apical turn of the chinchilla cochlea, the basal turn of the guinea pig cochlea, and the hook region of the guinea pig cochlea. The most sensitive or “best” frequencies (BFs) for the sites studied were ∼500 Hz, 17 kHz, and 30 kHz, respectively. Responses to the cubic difference tone (CDT), 2 F 1 − F 2 (where F 1 and F 2 are the frequencies of the primary stimuli), were characterized at each site. Responses to the quadratic difference tone (QDT), F 2 − F 1, were also characterized in the apical turn preparations (QDT responses were too small to measure in the basal cochlea). The observed responses to BF QDTs and CDTs and to BF CDTs at each site appeared similar in many ways; the relative magnitudes of the responses were highest at low-to-moderate sound pressure levels (SPLs), for example, and the absolute magnitudes grew nonmonotonically with increases in the level of either primary ( L 1 or L 2) alone. The peak effective levels of the CDT and QDT responses were also similar, at around −20 dB re L 1 and/or L 2. In other respects, however, the responses to CDTs and QDTs and to BF CDTs at each site behaved quite differently. At low-to-moderate SPLs, for example, most CDT phase leads decreased with increases in either L 1 or L 2, whereas most QDT phase leads increased with increasing L 1 and varied little with L 2. Most CDT responses also varied monotonically with equal-level primaries (i.e., when L 1 = L 2), whereas most QDT responses varied nonmonotonically. Different responses also varied in different ways when F 1 and F 2 were varied. Apical turn QDT responses were observed over a very wide F 1/ F 2 range ( F 1 =1–12 kHz), but were usually largest for stimuli <2–4 kHz. Apical turn CDT levels decreased (at rates of ∼40–80 dB/octave) only when the frequency ratio F 2/ F 1 increased beyond ∼1.4–1.5. In the basal turn and hook regions, the CDT levels depended nonmonotonically on F 2/ F 1, with the eventual rates of decrease being ∼200 dB/octave. Optimal frequency ratios for the CDT increased from ( F 2 < 1.1 F 1) to ( F 2 ≈ 1.2 F 1) with increasing SPL in the basal turn, but were stable at around F 2/ F 1 ≈ 1.05 in the hook region. CDT phase leads tended to increase with increasing F 2/ F 1 in all three regions of the cochlea, particularly at low-to-moderate SPLs. These findings are discussed in relation to previous studies of cochlear mechanics, physiology, and psychophysics.
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Nie, Liping, Haitao Song, Mei-Fang Chen, Nipavan Chiamvimonvat, Kirk W. Beisel, Ebenezer N. Yamoah, and Ana E. Vázquez. "Cloning and Expression of a Small-Conductance Ca2+-Activated K+ Channel From the Mouse Cochlea: Coexpression with α9/α10 Acetylcholine Receptors." Journal of Neurophysiology 91, no. 4 (April 2004): 1536–44. http://dx.doi.org/10.1152/jn.00630.2003.
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Functional interactions between ligand-gated, voltage-, and Ca2+-activated ion channels are essential to the properties of excitable cells and thus to the working of the nervous system. The outer hair cells in the mammalian cochlea receive efferent inputs from the brain stem through cholinergic nerve fibers that form synapses at their base. The acetylcholine released from these efferent fibers activates fast inhibitory postsynaptic currents mediated, to some extent, by small-conductance Ca2+-activated K+ channels (SK) that had not been cloned. Here we report the cloning, characterization, and expression of a complete SK2 cDNA from the mouse cochlea. The cDNAs of the mouse cochlea α9 and α10 acetylcholine receptors were also obtained, sequenced, and coexpressed with the SK2 channels. Human cultured cell lines transfected with SK2 yielded Ca2+-sensitive K+ current that was blocked by dequalinium chloride and apamin, known blockers of SK channels. Xenopus oocytes injected with SK2 in vitro transcribed RNA, under conditions where only outward K+ currents could be recorded, expressed an outward current that was sensitive to EGTA, dequalinium chloride, and apamin. In HEK-293 cells cotransfected with cochlear SK2 plus α9/α10 receptors, acetylcholine induced an inward current followed by a robust outward current. The results indicate that SK2 and the α9/α10 acetylcholine receptors are sufficient to partly recapitulate the native hair cell efferent synaptic response.
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Skinner, Liam J., Véronique Enée, Maryline Beurg, Hak Hyun Jung, Allen F. Ryan, Aziz Hafidi, Jean-Marie Aran, and Didier Dulon. "Contribution of BK Ca2+-Activated K+ Channels to Auditory Neurotransmission in the Guinea Pig Cochlea." Journal of Neurophysiology 90, no. 1 (July 2003): 320–32. http://dx.doi.org/10.1152/jn.01155.2002.
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Large-conductance calcium-activated potassium (BK) channels are known to play a prominent role in the hair cell function of lower vertebrates where these channels determine electrical tuning and regulation of neurotransmitter release. Very little is known, by contrast, about the role of BK channels in the mammalian cochlea. In the current study, we perfused specific toxins in the guinea pig cochlea to characterize the role of BK channels in cochlear neurotransmission. Intracochlear perfusion of charybdotoxin (ChTX) or iberiotoxin (IbTX) reversibly reduced the compound action potential (CAP) of the auditory nerve within minutes. The cochlear microphonics (CM at f1 = 8 kHz and f2 = 9.68 kHz) and their distortion product (DPCM at 2f1–f2) were essentially not affected, suggesting that the BK specific toxins do not alter the active cochlear amplification at the outer hair cells (OHCs). We also tested the effects of these toxins on the whole cell voltage-dependent membrane current of isolated guinea pig inner hair cells (IHCs). ChTX and IbTX reversibly reduced a fast outward current (activating above –40 mV, peaking at 0 mV with a mean activation time constant τ ranging between 0.5 and 1 ms). A similar block of a fast outward current was also observed with the extracellular application of barium ions, which we believe permeate through Ca2+ channels and block BK channels. In situ hybridization of Slo antisense riboprobes and immunocytochemistry demonstrated a strong expression of BK channels in IHCs and spiral ganglion and to a lesser extent in OHCs. Overall, our results clearly revealed the importance of BK channels in mammalian cochlear neurotransmission and demonstrated that at the presynaptic level, fast BK channels are a significant component of the repolarizing current of IHCs.
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van der Beek, Feddo B., Jeroen J. Briaire, Kim S. van der Marel, Berit M. Verbist, and Johan H. M. Frijns. "Intracochlear Position of Cochlear Implants Determined Using CT Scanning versus Fitting Levels: Higher Threshold Levels at Basal Turn." Audiology and Neurotology 21, no. 1 (2016): 54–67. http://dx.doi.org/10.1159/000442513.
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Objectives: In this study, the effects of the intracochlear position of cochlear implants on the clinical fitting levels were analyzed. Design: A total of 130 adult subjects who used a CII/HiRes 90K cochlear implant with a HiFocus 1/1J electrode were included in the study. The insertion angle and the distance to the modiolus of each electrode contact were determined using high-resolution CT scanning. The threshold levels (T-levels) and maximum comfort levels (M-levels) at 1 year of follow-up were determined. The degree of speech perception of the subjects was evaluated during routine clinical follow-up. Results: The depths of insertion of all the electrode contacts were determined. The distance to the modiolus was significantly smaller at the basal and apical cochlear parts compared with that at the middle of the cochlea (p < 0.05). The T-levels increased toward the basal end of the cochlea (3.4 dB). Additionally, the M-levels, which were fitted in our clinic using a standard profile, also increased toward the basal end, although with a lower amplitude (1.3 dB). Accordingly, the dynamic range decreased toward the basal end (2.1 dB). No correlation was found between the distance to the modiolus and the T-level or the M-level. Furthermore, the correlation between the insertion depth and stimulation levels was not affected by the duration of deafness, age at implantation or the time since implantation. Additionally, the T-levels showed a significant correlation with the speech perception scores (p < 0.05). Conclusions: The stimulation levels of the cochlear implants were affected by the intracochlear position of the electrode contacts, which were determined using postoperative CT scanning. Interestingly, these levels depended on the insertion depth, whereas the distance to the modiolus did not affect the stimulation levels. The T-levels increased toward the basal end of the cochlea. The level profiles were independent of the overall stimulation levels and were not affected by the biographical data of the patients, such as the duration of deafness, age at implantation or time since implantation. Further research is required to elucidate how fitting using level profiles with an increase toward the basal end of the cochlea benefits speech perception. Future investigations may elucidate an explanation for the effects of the intracochlear electrode position on the stimulation levels and might facilitate future improvements in electrode design.
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Rajan, R. "Effect of electrical stimulation of the crossed olivocochlear bundle on temporary threshold shifts in auditory sensitivity. I. Dependence on electrical stimulation parameters." Journal of Neurophysiology 60, no. 2 (August 1, 1988): 549–68. http://dx.doi.org/10.1152/jn.1988.60.2.549.
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1. This study examines the effect on auditory desensitization of electrically stimulating the crossed olivocochlear bundle (COCB) at the floor of the fourth ventricle. Auditory desensitization was induced by a loud high-frequency pure tone exposure and measured as temporary threshold shifts (TTS) in the sensitivity of the compound action potential recorded from the cochlea. COCB stimulation simultaneous with the loud sound exposure reduced the TTS. This reduction was contingent on the COCB stimulus being presented as a continuous burst for the entire duration (1 min) of the exposure. 2. The reduction in TTS could be abolished by prior administration of strychnine. The action of strychnine on these TTS effects of continuous COCB stimulation paralleled its action on the classical COCB effects elicited by pulsed short COCB trains. If the action of strychnine on the classical COCB effects was allowed to reverse, then continuous COCB stimulation reduced TTS as effectively as before. 3. The most effective COCB stimulus was found to be one that was presented at a high rate of stimulation simultaneous with the exposure. The COCB effect on TTS was also found to be a tonic one; smaller but significant reductions in TTS could still be obtained with the exposure presented 5 min after COCB stimulation though not when the delay was 10 min. The tonic reductions in TTS appeared to occur without any persisting changes at the cochlea. Normal cochlear responses remeasured in the delay between the stimulus and exposure were not altered. 4. It was hypothesized that the persisting effect responsible for TTS reductions did not occur at the cochlea but at some central site facilitated by antidromic action potentials along the COCB fibers. Subsequent exposure to loud sounds would activate the central site primed by the prior COCB stimulus. This hypothesis was tested by stimulating the COCB alone as before, but then lesioning the fibers before presenting the exposure. Persistent cochlear effects of the COCB stimulus should have still resulted in a reduction in TTS. However, if the persistent effect was at a more central location, lesioning the fibers would allow afferent input to act at the facilitated central location but would not allow subsequent expression of COCB effects at the cochlea. In this case, no reductions in TTS could be expected--precisely the results that were obtained in these experiments. Thus the COCB system appeared to have a "memory" component facilitated by prior stimulation and activated by a subsequent exposure.
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Brown, M. Christian. "Single-unit labeling of medial olivocochlear neurons: the cochlear frequency map for efferent axons." Journal of Neurophysiology 111, no. 11 (June 1, 2014): 2177–86. http://dx.doi.org/10.1152/jn.00045.2014.
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Medial olivocochlear (MOC) neurons are efferent neurons that project axons from the brain to the cochlea. Their action on outer hair cells reduces the gain of the “cochlear amplifier,” which shifts the dynamic range of hearing and reduces the effects of noise masking. The MOC effects in one ear can be elicited by sound in that ipsilateral ear or by sound in the contralateral ear. To study how MOC neurons project onto the cochlea to mediate these effects, single-unit labeling in guinea pigs was used to study the mapping of MOC neurons for neurons responsive to ipsilateral sound vs. those responsive to contralateral sound. MOC neurons were sharply tuned to sound frequency with a well-defined characteristic frequency (CF). However, their labeled termination spans in the organ of Corti ranged from narrow to broad, innervating between 14 and 69 outer hair cells per axon in a “patchy” pattern. For units responsive to ipsilateral sound, the midpoint of innervation was mapped according to CF in a relationship generally similar to, but with more variability than, that of auditory-nerve fibers. Thus, based on CF mappings, most of the MOC terminations miss outer hair cells involved in the cochlear amplifier for their CF, which are located more basally. Compared with ipsilaterally responsive neurons, contralaterally responsive neurons had an apical offset in termination and a larger span of innervation (an average of 10.41% cochlear distance), suggesting that when contralateral sound activates the MOC reflex, the actions are different than those for ipsilateral sound.
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Lee, C., J. J. Guinan, M. A. Rutherford, W. A. Kaf, K. M. Kennedy, C. A. Buchman, A. N. Salt, and J. T. Lichtenhan. "Cochlear compound action potentials from high-level tone bursts originate from wide cochlear regions that are offset toward the most sensitive cochlear region." Journal of Neurophysiology 121, no. 3 (March 1, 2019): 1018–33. http://dx.doi.org/10.1152/jn.00677.2018.
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Little is known about the spatial origins of auditory nerve (AN) compound action potentials (CAPs) evoked by moderate to intense sounds. We studied the spatial origins of AN CAPs evoked by 2- to 16-kHz tone bursts at several sound levels by slowly injecting kainic acid solution into the cochlear apex of anesthetized guinea pigs. As the solution flowed from apex to base, it sequentially reduced CAP responses from low- to high-frequency cochlear regions. The times at which CAPs were reduced, combined with the cochlear location traversed by the solution at that time, showed the cochlear origin of the removed CAP component. For low-level tone bursts, the CAP origin along the cochlea was centered at the characteristic frequency (CF). As sound level increased, the CAP center shifted basally for low-frequency tone bursts but apically for high-frequency tone bursts. The apical shift was surprising because it is opposite the shift expected from AN tuning curve and basilar membrane motion asymmetries. For almost all high-level tone bursts, CAP spatial origins extended over 2 octaves along the cochlea. Surprisingly, CAPs evoked by high-level low-frequency (including 2 kHz) tone bursts showed little CAP contribution from CF regions ≤ 2 kHz. Our results can be mostly explained by spectral splatter from the tone-burst rise times, excitation in AN tuning-curve “tails,” and asynchronous AN responses to high-level energy ≤ 2 kHz. This is the first time CAP origins have been identified by a spatially specific technique. Our results show the need for revising the interpretation of the cochlear origins of high-level CAPs-ABR wave 1. NEW & NOTEWORTHY Cochlear compound action potentials (CAPs) and auditory brain stem responses (ABRs) are routinely used in laboratories and clinics. They are typically interpreted as arising from the cochlear region tuned to the stimulus frequency. However, as sound level is increased, the cochlear origins of CAPs from tone bursts of all frequencies become very wide and their centers shift toward the most sensitive cochlear region. The standard interpretation of CAPs and ABRs from moderate to intense stimuli needs revision.
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Couloigner, Vincent, Michel Fay, Sabri Djelidi, Nicolette Farman, Brigitte Escoubet, Isabelle Runembert, Olivier Sterkers, Gérard Friedlander, and Evelyne Ferrary. "Location and function of the epithelial Na channel in the cochlea." American Journal of Physiology-Renal Physiology 280, no. 2 (February 1, 2001): F214—F222. http://dx.doi.org/10.1152/ajprenal.2001.280.2.f214.
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In the cochlea, endolymph is a K-rich and Na-poor fluid. The purpose of the present study was to check the presence and to assess the role of epithelial Na channel (ENaC) in this organ. α-, β-, and γ-ENaC subunit mRNA, and proteins were detected in rat cochlea by RT-PCR and Western blot. α-ENaC subunit mRNA was localized by in situ hybridization in both epithelial (stria vascularis, spiral prominence, spiral limbus) and nonepithelial structures (spiral ligament, spiral ganglion). The α-ENaC-positive tissues were also positive for β-subunit mRNA (except spiral ganglion) or for γ-subunit mRNA (spiral limbus, spiral ligament, and spiral ganglion), but the signals of β- and γ-subunits were weaker than those observed for α-subunit. In vivo, the endocochlear potential was recorded in guinea pigs under normoxic and hypoxic conditions after endolymphatic perfusion of ENaC inhibitors (amiloride, benzamil) dissolved either in K-rich or Na-rich solutions. ENaC inhibitors altered the endocochlear potential when Na-rich but not when K-rich solutions were perfused. In conclusion, ENaC subunits are expressed in epithelial and nonepithelial cochlear structures. One of its functions is probably to maintain the low concentration of Na in endolymph.
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Kamakura, Takefumi, Daniel J. Lee, Barbara S. Herrmann, and Joseph B. Nadol Jr. "Histopathology of the Human Inner Ear in the Cogan Syndrome with Cochlear Implantation." Audiology and Neurotology 22, no. 2 (2017): 116–23. http://dx.doi.org/10.1159/000477534.
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The Cogan syndrome is a rare disorder characterized by nonsyphilitic interstitial keratitis and audiovestibular symptoms. Profound sensorineural hearing loss has been reported in approximately half of the patients with the Cogan syndrome resulting in candidacy for cochlear implantation in some patients. The current study is the first histopathologic report on the temporal bones of a patient with the Cogan syndrome who during life underwent bilateral cochlear implantation. Preoperative MRI revealed tissue with high density in the basal turns of both cochleae and both vestibular systems consistent with fibrous tissue due to labyrinthitis. Histopathology demonstrated fibrous tissue and new bone formation within the cochlea and vestibular apparatus, worse on the right. Severe degeneration of the vestibular end organs and new bone formation in the labyrinth were seen more on the right than on the left. Although severe bilateral degeneration of the spiral ganglion neurons was seen, especially on the right, the postoperative word discrimination score was between 50 and 60% bilaterally. Impedance measures were generally higher in the right ear, possibly related to more fibrous tissue and new bone found in the scala tympani on the right side.
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Zirpel, L., E. A. Lachica, and W. R. Lippe. "Deafferentation increases the intracellular calcium of cochlear nucleus neurons in the embryonic chick." Journal of Neurophysiology 74, no. 3 (September 1, 1995): 1355–57. http://dx.doi.org/10.1152/jn.1995.74.3.1355.
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1. Ratiometric fura-2 imaging was used to measure the intracellular calcium concentration ([Ca2+]i) of neurons in the embryonic avian cochlear nucleus, nucleus magnocellularis (NM), after an in ovo unilateral cochlea removal (deafferentation). 2. The mean [Ca2+]i of NM neurons receiving normal input was 113 nM. 3. Deafferentation increased the mean [Ca2+]i of NM neurons to 247, 311, 339, and 314 nM at 1, 3, 6, and 12 h after cochlear removal, respectively. These values did not differ significantly. 4. The percent frequency distribution of deafferented NM neuron [Ca2+]i shifts away from normative levels toward higher [Ca2+]i at 1 and 3 h after cochlear removal, but shifts back toward normative levels at 6 and 12 h after cochlear removal. 5. This increased [Ca2+]i following cochlear removal temporally coincides with well-characterized changes in NM neurons following activity deprivation. 6. These data suggest that deregulation of [Ca2+]i homeostasis plays a key role in NM neuron degeneration and death following activity deprivation.
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Zhang, Si Yi, Donald Robertson, Graeme Yates, and Alan Everett. "Role of L-Type Ca2+ Channels in Transmitter Release From Mammalian Inner Hair Cells I. Gross Sound-Evoked Potentials." Journal of Neurophysiology 82, no. 6 (December 1, 1999): 3307–15. http://dx.doi.org/10.1152/jn.1999.82.6.3307.
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Intracochlear perfusion and gross potential recording of sound-evoked neural and hair cell responses were used to study the site of action of the L-type Ca2+ channel blocker nimodipine in the guinea pig inner ear. In agreement with previous work nimodipine (1–10 μM) caused changes in both the compound auditory nerve action potential (CAP) and the DC component of the hair cell receptor potential (summating potential, or SP) in normal cochleae. For 20-kHz stimulation, the effect of nimodipine on the CAP threshold was markedly greater than the effect on the threshold of the negative SP. This latter result was consistent with a dominant action of nimodipine at the final output stage of cochlear transduction: either the release of transmitter from inner hair cells (IHCs) or the postsynaptic spike generation process. In animals in which the outer hair cells (OHCs) had been destroyed by prior administration of kanamycin, nimodipine still caused a large change in the 20-kHz CAP threshold, but even less change was observed in the negative SP threshold than in normal cochleae. When any neural contamination of the SP recording in kanamycin-treated animals was removed by prior intracochlear perfusion with TTX, nimodipine caused no significant change in SP threshold. Some features of the data also suggest a separate involvement of nimodipine-sensitive channels in OHC function. Perfusion of the cochlea with solutions containing Ni2+ (100 μM) caused no measurable change in either CAP or SP. These results are consistent with, but do not prove, the notion that L-type channels are directly involved in controlling transmitter release from the IHCs and that T-type Ca2+channels are not involved at any stage of cochlear transduction.
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Kim, Kyunghee X., and Robert Fettiplace. "Developmental changes in the cochlear hair cell mechanotransducer channel and their regulation by transmembrane channel–like proteins." Journal of General Physiology 141, no. 1 (December 31, 2012): 141–48. http://dx.doi.org/10.1085/jgp.201210913.
Full textAbstract:
Vibration of the stereociliary bundles activates calcium-permeable mechanotransducer (MT) channels to initiate sound detection in cochlear hair cells. Different regions of the cochlea respond preferentially to different acoustic frequencies, with variation in the unitary conductance of the MT channels contributing to this tonotopic organization. Although the molecular identity of the MT channel remains uncertain, two members of the transmembrane channel–like family, Tmc1 and Tmc2, are crucial to hair cell mechanotransduction. We measured MT channel current amplitude and Ca2+ permeability along the cochlea’s longitudinal (tonotopic) axis during postnatal development of wild-type mice and mice lacking Tmc1 (Tmc1−/−) or Tmc2 (Tmc2−/−). In wild-type mice older than postnatal day (P) 4, MT current amplitude increased ∼1.5-fold from cochlear apex to base in outer hair cells (OHCs) but showed little change in inner hair cells (IHCs), a pattern apparent in mutant mice during the first postnatal week. After P7, the OHC MT current in Tmc1−/− (dn) mice declined to zero, consistent with their deafness phenotype. In wild-type mice before P6, the relative Ca2+ permeability, PCa, of the OHC MT channel decreased from cochlear apex to base. This gradient in PCa was not apparent in IHCs and disappeared after P7 in OHCs. In Tmc1−/− mice, PCa in basal OHCs was larger than that in wild-type mice (to equal that of apical OHCs), whereas in Tmc2−/−, PCa in apical and basal OHCs and IHCs was decreased compared with that in wild-type mice. We postulate that differences in Ca2+ permeability reflect different subunit compositions of the MT channel determined by expression of Tmc1 and Tmc2, with the latter conferring higher PCa in IHCs and immature apical OHCs. Changes in PCa with maturation are consistent with a developmental decrease in abundance of Tmc2 in OHCs but not in IHCs.
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Ramkumar, V., R. Ravi, M. C. Wilson, T. W. Gettys, C. Whitworth, and L. P. Rybak. "Identification of A1 adenosine receptors in rat cochlea coupled to inhibition of adenylyl cyclase." American Journal of Physiology-Cell Physiology 267, no. 3 (September 1, 1994): C731—C737. http://dx.doi.org/10.1152/ajpcell.1994.267.3.c731.
Full textAbstract:
A1 adenosine receptors (A1ARs) are found in a number of tissues in the body where their physiological roles have been identified. In the cochlea, neither the existence of these receptors nor a physiological role of adenosine has been described previously. Membranes prepared from rat cochlea demonstrated high affinity and saturable binding to N6-2-(4-amino-3-[125I]iodophenyl)ethyladenosine ([125I]APNEA), an A1AR agonist, with maximum binding capacity and dissociation constant values being 40.5 +/- 0.5 fmol/mg protein and 1.28 +/- 0.03 nM, respectively. Adenosine analogues competed for [125I]APNEA binding sites with a rank order of potency characteristic of these sites being the A1AR. The [125I]APNEA binding was significantly reduced by pertussis toxin, indicating coupling of these receptors with the Gi and/or Go proteins in cochlear membranes. Photoaffinity labeling of the receptor protein with the A1AR agonist N6-2-(4-azido-3[125I]iodophenyl)ethyladenosine showed specific labeling of a 36-kDa receptor protein. Activation of the A1AR with R-phenylisopropyladenosine (R-PIA) led to inhibition of forskolin-stimulated adenylyl cyclase activity. Amplification of reverse-transcribed RNA derived from cochlear tissue by polymerase chain reaction (using primers for the bovine A1AR) yielded a 770-bp product that hybridized to an A1AR cDNA probe on Southern blots. These data indicate the presence of an inhibitory receptor in the peripheral auditory system, which may play an important role in modulating auditory functions.
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Venail, Frederic, Caroline Mathiolon, Sophie Menjot de Champfleur, Jean Pierre Piron, Marielle Sicard, Françoise Villemus, Marie Aude Vessigaud, Françoise Sterkers-Artieres, Michel Mondain, and Alain Uziel. "Effects of Electrode Array Length on Frequency-Place Mismatch and Speech Perception with Cochlear Implants." Audiology and Neurotology 20, no. 2 (2015): 102–11. http://dx.doi.org/10.1159/000369333.
Full textAbstract:
Frequency-place mismatch often occurs after cochlear implantation, yet its effect on speech perception outcome remains unclear. In this article, we propose a method, based on cochlea imaging, to determine the cochlear place-frequency map. We evaluated the effect of frequency-place mismatch on speech perception outcome in subjects implanted with 3 different lengths of electrode arrays. A deeper insertion was responsible for a larger frequency-place mismatch and a decreased and delayed speech perception improvement by comparison with a shallower insertion, for which a similar but slighter effect was noticed. Our results support the notion that selecting an electrode array length adapted to each individual's cochlear anatomy may reduce frequency-place mismatch and thus improve speech perception outcome.
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Pappa, Andrew K., Kendall A. Hutson, William C. Scott, J. David Wilson, Kevin E. Fox, Maheer M. Masood, Christopher K. Giardina, et al. "Hair cell and neural contributions to the cochlear summating potential." Journal of Neurophysiology 121, no. 6 (June 1, 2019): 2163–80. http://dx.doi.org/10.1152/jn.00006.2019.
Full textAbstract:
The cochlear summating potential (SP) to a tone is a baseline shift that persists for the duration of the burst. It is often considered the most enigmatic of cochlear potentials because its magnitude and polarity vary across frequency and level and its origins are uncertain. In this study, we used pharmacology to isolate sources of the SP originating from the gerbil cochlea. Animals either had the full complement of outer and inner hair cells (OHCs and IHCs) and an intact auditory nerve or had systemic treatment with furosemide and kanamycin (FK) to remove the outer hair cells. Responses to tone bursts were recorded from the round window before and after the neurotoxin kainic acid (KA) was applied. IHC responses were then isolated from the post-KA responses in FK animals, neural responses were isolated from the subtraction of post-KA from pre-KA responses in NH animals, and OHC responses were isolated by subtraction of post-KA responses in FK animals from post-KA responses in normal hearing (NH) animals. All three sources contributed to the SP; OHCs with a negative polarity and IHCs and the auditory nerve with positive polarity. Thus the recorded SP in NH animals is a sum of contributions from different sources, contributing to the variety of magnitudes and polarities seen across frequency and intensity. When this information was applied to observations of the SP recorded from the round window in human cochlear implant subjects, a strong neural contribution to the SP was confirmed in humans as well as gerbils. NEW & NOTEWORTHY Of the various potentials produced by the cochlea, the summating potential (SP) is typically described as the most enigmatic. Using combinations of ototoxins and neurotoxins, we show contributions to the SP from the auditory nerve and from inner and outer hair cells, which differ in polarity and vary in size across frequency and level. This complexity of sources helps to explain the enigmatic nature of the SP.
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Xiong, Hao, Yongkang Ou, Yaodong Xu, Qiuhong Huang, Jiaqi Pang, Lan Lai, and Yiqing Zheng. "Resveratrol Promotes Recovery of Hearing following Intense Noise Exposure by Enhancing Cochlear SIRT1 Activity." Audiology and Neurotology 22, no. 4-5 (2017): 303–10. http://dx.doi.org/10.1159/000485312.
Full textAbstract:
The sirtuin SIRT1 is a highly conserved nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase known to have protective effects against a wide range of neurological disorders. In the present study, we discovered that C57BL/6 mice fed a long-term diet supplemented with high-dose resveratrol exhibited increased cochlear SIRT1 activity and presented a better recovery of hearing and less loss of hair cells after intense noise exposure compared with those fed a standard chew. Moreover, resveratrol attenuated cochlear SIRT1 decrease and reduced oxidative stress in the cochlea after noise exposure. These results suggest a considerable therapeutic potential of resveratrol for the treatment of noise-induced hearing loss.
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Patuzzi, R., and D. Robertson. "Tuning in the mammalian cochlea." Physiological Reviews 68, no. 4 (October 1988): 1009–82. http://dx.doi.org/10.1152/physrev.1988.68.4.1009.
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Szalai, R., K. Tsaneva-Atanasova, M. E. Homer, A. R. Champneys, H. J. Kennedy, and N. P. Cooper. "Nonlinear models of development, amplification and compression in the mammalian cochlea." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 369, no. 1954 (November 13, 2011): 4183–204. http://dx.doi.org/10.1098/rsta.2011.0192.
Full textAbstract:
This paper reviews current understanding and presents new results on some of the nonlinear processes that underlie the function of the mammalian cochlea. These processes occur within mechano-sensory hair cells that form part of the organ of Corti. After a general overview of cochlear physiology, mathematical modelling results are presented in three parts. First, the dynamic interplay between ion channels within the sensory inner hair cells is used to explain some new electrophysiological recordings from early development. Next, the state of the art is reviewed in modelling the electro-motility present within the outer hair cells (OHCs), including the current debate concerning the role of cell body motility versus active hair bundle dynamics. A simplified model is introduced that combines both effects in order to explain observed amplification and compression in experiments. Finally, new modelling evidence is presented that structural longitudinal coupling between OHCs may be necessary in order to capture all features of the observed mechanical responses.
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Fessenden, James D., and Jochen Schacht. "Localization of Soluble Guanylate Cyclase Activity in the Guinea Pig Cochlea Suggests Involvement in Regulation of Blood Flow and Supporting Cell Physiology." Journal of Histochemistry & Cytochemistry 45, no. 10 (October 1997): 1401–8. http://dx.doi.org/10.1177/002215549704501008.
Full textAbstract:
Although the nitric oxide/cGMP pathway has many important roles in biology, studies of this system in the mammalian cochlea have focused on the first enzyme in the pathway, nitric oxide synthase (NOS). However, characterization of the NO receptor, soluble guanylate cyclase (sGC), is crucial to determine the cells targeted by NO and to develop rational hypotheses of the function of this pathway in auditory processing. In this study we characterized guinea pig cochlear sGC by determining its enzymatic activity and cellular localization. In cytosolic fractions of auditory nerve, lateral wall tissues, and co-chlear neuroepithelium, addition of NO donors resulted in three- to 15-fold increases in cGMP formation. NO-stimulated sGC activity was not detected in particulate fractions. We also localized cochlear sGC activity through immunocytochemical detection of NO-stimulated cGMP. sGC activity was detected in Hensen's and Deiters' cells of the organ of Corti, as well as in vascular pericytes surrounding small capillaries in the lateral wall tissues and sensory neuroepithelium. sGC activity was not observed in sensory cells. Using NADPH-diaphorase histochemistry, NOS was localized to pillar cells and nerve fibers underlying hair cells. These results indicate that the NO/cGMP pathway may influence diverse elements of the auditory system, including cochlear blood flow and supporting cell physiology.
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Liu, Qing, and Robin L. Davis. "Regional Specification of Threshold Sensitivity and Response Time in CBA/CaJ Mouse Spiral Ganglion Neurons." Journal of Neurophysiology 98, no. 4 (October 2007): 2215–22. http://dx.doi.org/10.1152/jn.00284.2007.
Full textAbstract:
Previous studies of spiral ganglion neuron electrophysiology have shown that specific parameters differ according to cochlear location, with apical neurons being distinctly different from basal neurons. To align these features more precisely along the tonotopic axis of the cochlea, we developed a novel spiral ganglion culture system in which positional information is retained. Patch-clamp recordings made from neurons of known gangliotopic location revealed two basic firing pattern distributions. Membrane characteristics related to spike timing, such as accommodation, latency and onset tau, were distinctly heterogeneous, yet when averaged, they were distributed in a graded manner along the length of the cochlea. Action potential threshold levels also displayed a wide range, the averages of which were distributed nonmonotonically such that neurons with the greatest sensitivity were localized to the mid-regions of the ganglion. These studies shed new light on the complexity and sophistication of the intrinsic firing features of spiral ganglion neurons. Because timing-related elements are organized in an overall tonotopic manner, it is hypothesized that they contribute to aspects of frequency-dependent acoustic processing. On the other hand, the different distribution of threshold levels, with the greatest sensitivity in the middle region of the tonotopic map, suggests that this neuronal parameter is regulated differently and thus may contribute a distinct realm of auditory sensory processing.
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Hu, Xintian, Burt N. Evans, and Peter Dallos. "Direct Visualization of Organ of Corti Kinematics in a Hemicochlea." Journal of Neurophysiology 82, no. 5 (November 1, 1999): 2798–807. http://dx.doi.org/10.1152/jn.1999.82.5.2798.
Full textAbstract:
The basilar membrane in the mammalian cochlea vibrates when the cochlea receives a sound stimulus. This mechanical vibration is transduced into hair cell receptor potentials and thereafter encoded by action potentials in the auditory nerve. Knowledge of the mechanical transformation that converts basilar membrane vibration into hair cell stimulation has been limited, until recently, to hypothetical geometric models. Experimental observations are largely lacking to prove or disprove the validity of these models. We have developed a hemicochlea preparation to visualize the kinematics of the cochlear micromechanism. Direct mechanical drive of 1–2 Hz sinusoidal command was applied to the basilar membrane. Vibration patterns of the basilar membrane, inner and outer hair cells, supporting cells, and tectorial membrane have been recorded concurrently by means of a video optical flow technique. Basilar membrane vibration was driven in a direction transversal to its plane. However, the direction of the resulting vibration was found to be essentially radial at the level of the reticular lamina and cuticular plates of inner and outer hair cells. The tectorial membrane vibration was mainly transversal. The transmission ratio between cilia displacement of inner and outer hair cells and basilar membrane vibration is in the range of 0.7–1.1. These observations support, in part, the classical geometric models at low frequencies. However, there appears to be less tectorial membrane motion than predicted, and it is largely in the transversal direction.
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Abel, Cornelius, Anna Wittekindt, and Manfred Kössl. "Contralateral Acoustic Stimulation Modulates Low-Frequency Biasing of DPOAE: Efferent Influence on Cochlear Amplifier Operating State?" Journal of Neurophysiology 101, no. 5 (May 2009): 2362–71. http://dx.doi.org/10.1152/jn.00026.2009.
Full textAbstract:
The mammalian efferent medial olivocochlear system modulates active amplification of low-level sounds in the cochlea. Changes of the cochlear amplifier can be monitored by distortion product otoacoustic emissions (DPOAEs). The quadratic distortion product f2–f1 is known to be sensitive to changes in the operating point of the amplifier transfer function. We investigated the effect of contralateral acoustic stimulation (CAS), known to elicit efferent activity, on DPOAEs in the gerbil. During CAS, a significant increase of the f2–f1 level occurred already at low contralateral noise levels (20 dB SPL), whereas 2f1–f2 was much less affected. The effect strength depended on the CAS level and as shown in experiments with pure tones on the frequency of the contralateral stimulus. In a second approach, we biased the position of the cochlear partition and thus the cochlear amplifier operating point periodically by a ipsilateral low-frequency tone, which resulted in a phase-related amplitude modulation of f2–f1. This modulation pattern was changed considerably during contralateral noise stimulation, in dependence on the noise level. The experimental results were in good agreement with a simple model of distortion product generation and suggest that the olivocochlear efferents might change the operating state of cochlear amplification.
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Bing, Dan, Sze Chim Lee, Dario Campanelli, Hao Xiong, Masahiro Matsumoto, Rama Panford-Walsh, Stephan Wolpert, et al. "Cochlear NMDA Receptors as a Therapeutic Target of Noise-Induced Tinnitus." Cellular Physiology and Biochemistry 35, no. 5 (2015): 1905–23. http://dx.doi.org/10.1159/000374000.
Full textAbstract:
Background: Accumulating evidence suggests that tinnitus may occur despite normal auditory sensitivity, probably linked to partial degeneration of the cochlear nerve and damage of the inner hair cell (IHC) synapse. Damage to the IHC synapses and deafferentation may occur even after moderate noise exposure. For both salicylate- and noise-induced tinnitus, aberrant N-methyl-d-aspartate (NMDA) receptor activation and related auditory nerve excitation have been suggested as origin of cochlear tinnitus. Accordingly, NMDA receptor inhibition has been proposed as a pharmacologic approach for treatment of synaptopathic tinnitus. Methods: Round-window application of the NMDA receptor antagonist AM-101 (Esketamine hydrochloride gel; Auris Medical AG, Basel, Switzerland) was tested in an animal model of tinnitus induced by acute traumatic noise. The study included the quantification of IHC ribbon synapses as a correlate for deafferentation as well as the measurement of the auditory brainstem response (ABR) to close-threshold sensation level stimuli as an indication of sound-induced auditory nerve activity. Results: We have shown that AM-101 reduced the trauma-induced loss of IHC ribbons and counteracted the decline of ABR wave I amplitude generated in the cochlea/auditory nerve. Conclusion: Local round-window application of AM-101 may be a promising therapeutic intervention for the treatment of synaptopathic tinnitus.
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Fettiplace, Robert, and Kyunghee X. Kim. "The Physiology of Mechanoelectrical Transduction Channels in Hearing." Physiological Reviews 94, no. 3 (July 2014): 951–86. http://dx.doi.org/10.1152/physrev.00038.2013.
Full textAbstract:
Much is known about the mechanotransducer (MT) channels mediating transduction in hair cells of the vertrbrate inner ear. With the use of isolated preparations, it is experimentally feasible to deliver precise mechanical stimuli to individual cells and record the ensuing transducer currents. This approach has shown that small (1–100 nm) deflections of the hair-cell stereociliary bundle are transmitted via interciliary tip links to open MT channels at the tops of the stereocilia. These channels are cation-permeable with a high selectivity for Ca2+; two channels are thought to be localized at the lower end of the tip link, each with a large single-channel conductance that increases from the low- to high-frequency end of the cochlea. Ca2+ influx through open channels regulates their resting open probability, which may contribute to setting the hair cell resting potential in vivo. Ca2+ also controls transducer fast adaptation and force generation by the hair bundle, the two coupled processes increasing in speed from cochlear apex to base. The molecular intricacy of the stereocilary bundle and the transduction apparatus is reflected by the large number of single-gene mutations that are linked to sensorineural deafness, especially those in Usher syndrome. Studies of such mutants have led to the discovery of many of the molecules of the transduction complex, including the tip link and its attachments to the stereociliary core. However, the MT channel protein is still not firmly identified, nor is it known whether the channel is activated by force delivered through accessory proteins or by deformation of the lipid bilayer.
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Ulfendahl, M., S. M. Khanna, A. Fridberger, A. Flock, B. Flock, and W. Jager. "Mechanical response characteristics of the hearing organ in the low-frequency regions of the cochlea." Journal of Neurophysiology 76, no. 6 (December 1, 1996): 3850–62. http://dx.doi.org/10.1152/jn.1996.76.6.3850.
Full textAbstract:
1. With the use of an in vitro preparation of the guinea pig temporal bone, in which the apical turns of the cochlea are exposed, the mechanical and electrical responses of the cochlea in the low-frequency regions were studied during sound stimulation. 2. The mechanical characteristics were investigated in the fourth and third turns of the cochlea with the use of laser heterodyne interferometry, which allows the vibratory responses of both sensory and supporting cells to be recorded. The electrical responses, which can be maintained for several hours, were recorded only in the most apical turn. 3. In the most apical turn, the frequency locations and shapes of the mechanical and electrical responses were very similar. 4. The shapes of the tuning curves and the spatial locations of the frequency maxima in the temporal bone preparation compared very favorably with published results from in vivo recordings of hair cell receptor potentials and sound-induced vibrations of the Reissner's membrane. 5. Compressive nonlinearities were present in both the mechanical and the electrical responses at moderate sound pressure levels. 6. The mechanical tuning changed along the length of the cochlea, the center frequencies in the fourth and third turns being approximately 280 and 570 Hz, respectively. 7. The mechanical responses of sensory and supporting cells were almost identical in shape but differed significantly in amplitude radially across the reticular lamina.
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Hancock, Kenneth E., and Herbert F. Voigt. "Intracellularly Labeled Fusiform Cells in Dorsal Cochlear Nucleus of the Gerbil. II. Comparison of Physiology and Anatomy." Journal of Neurophysiology 87, no. 5 (May 1, 2002): 2520–30. http://dx.doi.org/10.1152/jn.2002.87.5.2520.
Full textAbstract:
Fusiform cells represent the major class of dorsal cochlear nucleus (DCN) projection neuron. Although much is understood about their physiology and anatomy, there remain unexplored issues with important functional implications. These include interspecies differences in DCN physiology and the nature of the cell-to-cell variations in fusiform cell physiology. To address these issues, a quantitative examination was made of the physiology and anatomy of 17 fusiform cells from a companion study. The results suggest that the basal dendrites of gerbil fusiform cells may be electrotonically more compact than those of the cat. This relative decrease in the filtering of excitatory inputs might account for the lower incidence of type IV units in that species. These data also suggest that the gerbil DCN lacks the high-frequency specialization described in the cat, because the tonotopic arrangement of the gerbil fusiform cells quantitatively matches the place-frequency map for the gerbil cochlea. Certain physiological properties have anatomical correlates. First, the basal dendrites of low spontaneous rate cells are directed away from the soma only in the caudal direction, while the high spontaneous rate cells have basal dendrites extending rostrally and caudally. Second, input resistance was dominated by the surface area of the apical dendrite. Third, the discharge pattern was correlated with apical dendrite orientation. Finally, there was a spatial gradient of sensitivity to broadband noise organized at least partially within an isofrequency axis. Such trends indicate that neighboring fusiform cells are endowed with different signal processing capabilities.