Relevant bibliographies by topics / Cochlea – Physiology

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Cochlea – Physiology'

Author: Grafiati
Published: 4 June 2021
Last updated: 19 February 2022

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Journal articles on the topic "Cochlea – Physiology"

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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Dissertations / Theses on the topic "Cochlea – Physiology"

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Jäger, Wanje. "Physiological aspects of cochlear excitation and neurotransmitter release /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3294-8/.

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Cheng, Jun. "Signal processing approaches on otoacoustic emissions /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4058-4.

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Ku, Emery Mayon. "Modelling the human cochlea." Thesis, University of Southampton, 2008. https://eprints.soton.ac.uk/64535/.

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One of the salient features of the human cochlea is the incredible dynamic range it possesses—the loudest bearable sound is 10,000,000 times greater than the softest detectable sound; this is in part due to an active process. More than twelve thousand hairlike cells known as outer hair cells are believed to expand and contract in time to amplify cochlear motions. However, the cochlea’s response is more than just the sum of its parts: the local properties of outer hair cells can have unexpected consequences for the global behaviour of the system. One such consequence is the existence of otoacoustic emissions (OAEs), sounds that (sometimes spontaneously!) propagate out of the cochlea to be detected in the ear canal. In this doctoral thesis, a classical, lumped-element model is used to study the cochlea and to simulate click-evoked and spontaneous OAEs. The original parameter values describing the microscopic structures of the cochlea are re-tuned to match several key features of the cochlear response in humans. The frequency domain model is also recast in a formulation known as state space; this permits the calculation of linear instabilities given random perturbations in the cochlea which are predicted to produce spontaneous OAEs. The averaged stability results of an ensemble of randomly perturbed models have been published in [(2008) ‘Statistics of instabilities in a state space model of the human cochlea,’ J. Acoust. Soc. Am. 124(2), 1068-1079]. These findings support one of the prevailing theories of SOAE generation. Nonlinear simulations of OAEs and the model’s response to various stimuli are performed in the time domain. Features observed in the model include the saturation of the forces generated by the OHCs, compression of amplitude growth with increasing stimulus level, harmonic and intermodulation distortion, limit cycle oscillations that travel along the cochlear membranes, and the mutual suppression of nearby linear instabilities.
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Jaggers, Robert Maxwell. "Is Polyvinylidene diflouride (PVDF) film biocompatible in the Murine Cochlea?" Wright State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=wright1440944212.

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Lennan, George William Thomas. "Mechanoelectrical transduction by hair cells of the neonatal mouse in tissue culture." Thesis, University of Sussex, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296617.

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McMahon, Catherine. "The mechanisms underlying normal spike activity of the primary afferent synapse in the cochlea and its dysfunction : an investigation of the possible mechanisms of peripheral tinnitus and auditory neuropathy." University of Western Australia. School of Biomedical and Chemical Sciences, 2004. http://theses.library.uwa.edu.au/adt-WU2003.0034.

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[Truncated abstract] One of the problems in researching tinnitus is that it has often been assumed that the physiological mechanisms underlying the tinnitus percept cannot be objectively measured. Nonetheless, it is generally accepted that the percept results from altered spontaneous neural activity at some site along the auditory pathway, although it is still debated whether it is produced by: synchronisation of activity of adjacent neurones; a change in the temporal pattern of activity of individual neurones; or an increase in the spontaneous firing rate per se. Similarly, it is possible that the recently coined “auditory neuropathy” is produced by under-firing of the primary afferent synapse, although several other mechanisms can also produce the symptoms described by this disorder (normal cochlear mechanical function but absent, or abnormal, synchronous neural firing arising from the cochlea and auditory brainstem, known as the auditory brainstem response, or ABR). Despite an absent ABR, some subjects can detect pure tones at near-normal levels, although their ability to integrate complex sounds, such as speech, is severely degraded in comparison with the pure-tone audiogram. The aim of the following study was to investigate the normal mechanisms underlying neural firing at the primary afferent synapse, and its regulation, to determine the possible mechanisms underlying over-firing (tinnitus) or under-firing (auditory neuropathy) of primary afferent neurones.
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O'Beirne, Greg A. "Mathematical modelling and electrophysiological monitoring of the regulation of cochlear amplification." University of Western Australia. School of Biomedical and Chemical Sciences, 2005. http://theses.library.uwa.edu.au/adt-WU2006.0115.

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[Truncated abstract] The cochlea presumably possesses a number of regulatory mechanisms to maintain cochlear sensitivity in the face of disturbances to its function. Evidence for such mechanisms can be found in the time-course of the recovery of CAP thresholds during experimental manipulations, and in observations of slow oscillations in cochlear micromechanics following exposure to low-frequency tones (the “bounce phenomenon”) and other perturbations. To increase our understanding of these oscillatory processes within the cochlea, and OHCs in particular, investigations into cochlear regulation were carried out using a combination of mathematical modelling of the ionic and mechanical interactions likely to exist within the OHCs, and electrophysiological experiments conducted in guinea pigs. The electrophysiological experiments consisted of electrocochleographic recordings and, in some cases, measurement of otoacoustic emissions, during a variety of experimental perturbations, including the application of force to the cochlear wall, exposure to very-low-frequency tones, injection of direct current into scala tympani, and intracochlear perfusions of artificial perilymph containing altered concentrations of potassium, sodium, and sucrose. To obtain a panoramic view of cochlear regulation under these conditions, software was written to enable the interleaved and near-simultaneous measurement of multiple indicators of cochlear function, including the compound action potential (CAP) threshold, amplitude and waveshape at multiple frequencies, the OHC transfer curves derived from low-frequency cochlear microphonic (CM) waveforms, distortion-product otoacoustic emissions (DPOAEs), the spectrum of the round-window neural noise (SNN), and the endocochlear potential (EP). ... The mathematical model we have developed provided a physiologically-plausible and internally-consistent explanation for the time-courses of the cochlear changes observed during a number of different perturbations. We show that much of the oscillatory behaviour within the cochlea is consistent with underlying oscillations in cytosolic calcium concentration. We conclude that a number of the discrepancies between the simulation results and the experimental data can be resolved if the cytosolic calcium functions as two distinct pools: one which controls basolateral permeability and one which controls slow motility. This two-calcium-pool model is discussed.
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Zagaeski, Mark. "Information processing in the mammalian auditory periphery." Thesis, Boston University, 1991. https://hdl.handle.net/2144/37176.

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Thesis (Ph.D.)--Boston University
PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
Inner hair cells (IHC) are the primary sensory cells of the mammalian cochlea. They transduce sound energy into a changing receptor potential which stimulates electrical activity in the Type I spiral ganglion cells of the auditory nerve. The auditory information thus encoded leads to the sensation of hearing. This thesis comprises my attempts to elucidate some of the biophysical mechanisms operating in the cochlea by analyzing intracellular recordings from guinea pigs, and to investigate the role these mechanisms play in auditory information processing via conceptual and computational models. Noise in the IHC receptor potential sets limits on the performance of a single cell. The magnitude of the intracellular noise averages 0.3 m V rms. A single IHC will be limited by this noise to: (i) a minimum detectable receptor potential of 0.3 mV (corresponding to about 0 dB SPL), (ii) a channel capacity of 5100 bits/sec, and (iii) a temporal resolution of 42 JLS. I compare these single cell limits to auditory performance as observed in published behavioral studies. The IHC receptor potential is shaped by at least two nonlinear processes: nonlinear transduction and a voltage dependent membrane conductance. I characterized the nonlinear conductance by analyzing recordings made during intracellular current injection. A simple model containing a two-state voltage-gated channel was sufficient to replicate the current-voltage characteristic found in these cells. I investigated the information transfer from inner hair cells to the auditory nerve by comparing the growth of the de receptor potential to the average firing rate in spiral ganglion cells. This comparison suggests that neural units with different thresholds encode different portions of the IHC dynamic range; at conditions well above threshold, low threshold units may be carrying predominantly temporal information while high threshold units may encode the absolute sound level. To help understand the complex behavior of the IHC receptor potential, I developed a computational model for its generation. The model contains gated ion channel descriptions of the nonlinear transducer and membrane conductance. Analysis of the model suggests a possible role for the voltage dependent conductance: efficiently trading sensitivity for temporal resolution as stimulus level increases.
2031-01-01
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Jing, Zhizi Verfasser], Nicola [Akademischer Betreuer] Strenzke, Tobias [Akademischer Betreuer] [Moser, Fred [Akademischer Betreuer] Wolf, and Martin [Akademischer Betreuer] Göpfert. "Sound Encoding in the Mouse Cochlea: Molecular Physiology and Optogenetic Stimulation / Zhizi Jing. Gutachter: Tobias Moser ; Fred Wolf ; Martin Göpfert. Betreuer: Nicola Strenzke." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2014. http://d-nb.info/1050288599/34.

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Markessis, Emily. "Development of an objective procedure allowing frequency selectivity measurements using the masking function of auditory steady state evoked potentials." Doctoral thesis, Universite Libre de Bruxelles, 2010. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209990.

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Introduction

Les surdités cochléaires induisent, outre une audibilité réduite, une série de distorsions de la représentation neurale des sons. Deux des mécanismes à la base de ces distorsions sont d’une part une atteinte de la sélectivité fréquentielle et d’autre part des zones neuro-épithéliales non fonctionnelles. Tant le premier que le second mécanisme apparaissent dans une proportion variable et non prédictible d’un sujet à un autre. Deux tests permettent le diagnostic de ces atteintes spécifiques: la Courbe d’Accord (Tuning Curve: TC) et le Threshold Equalising Noise (TEN) test. La TC, mesurée par une technique psychoacoustique chez un adulte collaborant (Psychophysical TC: PTC), consiste en la mesure du niveau de bruit (masqueur) nécessaire pour masquer un son pur (signal) de fréquence et d’intensité fixes. Le TEN test consiste en la mesure des seuils auditifs dans le silence et en présence d’un bruit égalisateur de seuil (TEN). Ces tests qui requièrent des capacités cognitives adultes normales, ne sont pas applicables aux populations pédiatriques prélinguales.

Ce travail de thèse avait pour but le développement d’un équivalent objectif et non invasif des TCs et du TEN test applicable aux populations pédiatriques. La méthode objective choisie fut les potentiels auditifs stationnaires ou ASSEPs (Auditory Steady State Evoked Potentials). Les ASSEPs sont une réponse électrophysiologique cérébrale évoquée par un stimulus acoustique de longue durée modulé en amplitude et/ou en fréquence.

Méthodes & Résultats

Etape 1

Les développements méthodologiques ont été réalisés sur l’espèce canine et humaine adulte. Les ASSEPs n’ayant jamais été préalablement enregistrés chez le chien, une première étape à consister à définir chez cette espèce les paramètres d’enregistrement optimaux (modulation en amplitude optimale) dont on sait qu’ils interagissent avec l’état veille-sommeil, avec la fréquence testée et probablement avec l’espèce animale investiguée.

A cette fin, les seuils auditifs obtenus chez 32 chiens à l’aide des ASSEPs ont été validés à cinq fréquences audiométriques par comparaison aux seuils obtenus avec les potentiels auditifs du tronc cérébral évoqués aux bouffées tonales.

Les seuils obtenus aux ASSEPs avec les paramètres optimaux d’enregistrement (légèrement différents des paramètres optimaux humains) étaient similaires à ceux obtenus aux bouffées tonales.

Ces résultats ont été publiés dans Clinical Neurophysiology (Markessis et al. 2006; 117: 1760-1771).

Etape 2

La possibilité de mesurer des TCs à l’aide des ASSEPs (ASSEP-TCs) a été évaluée sur 10 chiens. Les données canines ont été comparées à des données de la littérature, çàd aux TC enregistrées chez d’autres espèces et avec d’autres méthodes. Des ASSEP-TCs ont également été enregistrées chez 7 humains adultes et confrontées aux PTCs obtenues chez les mêmes sujets. Les PTCs sont typiquement energistrées avec un signal sinusoïdal alors que le stimulus utilisé pour évoquer un ASSEP est une sinusoïde modulée en amplitude. L’effet des sinusoïdes modulées en amplitude sur les paramètres qualitatifs et quantitatifs des TCs a donc été évalué en comparant les PTCs obtenues avec un son pur et avec un son pur modulé en amplitude chez 10 humains adultes.

Les résultats ont révélé que les ASSEP-TCs enregistrées chez le chien et l’humain présentaient des paramètres qualitatifs et quantitatifs similaires respectivement à ceux décrits dans la littérature et aux PTCs. Par ailleurs, auncun effet des stimuli modulés en amplitude sur les paramètres des PTCs n’a été démontré.

Ces données ont été publiées dans Ear & Hearing (Markessis et al. 2009, 30: 43-53).

Etape 3

Les ASSEP-TCs ont été validées chez 10 chiens en comparant les données aux TC enregistrées par électrocochléographie (Compound Action Potential TC: CAP-TC). Le masqueur utilisé pour les CAP-TCs est typiquement une sinusoïde alors que le masqueur utilisé pour les ASSEP-TCs est un bruit à bande étroite. Dès lors, une comparaison du type de masqueur (sinusoïde vs bruit à bande étroite) sur les paramètres des CAP-TCs et ASSEP-TCs a été réalisée chez 10 chiens.

Les ASSEP-TCs chez le chien se sont révélées qualitativement et quantitativement similaires aux CAP-TCs quel que soit le type de masqueur. Elles presentaient par ailleurs l’avantage d’être moins variables, plus précises et non invasives par rapport aux CAP-TCs.

Ces données ont été publiées dans International Journal of Audiology (Markessis et al. 2010, 49 ;455-62).

Etape 4

Afin d’étudier la validité de la procédure à mettre en évidence des changements de sélectivité fréquentielle dus à une atteinte cochléaire, des ASSEP-TCs ont été obtenues chez 10 chiens cochléo-lésés suite à un trauma acoustique. Les Produits de Distorsion Acoustiques, les potentiels évoqués auditifs du tronc cérébral évoqués par un clic et les ASSEPs à cinq fréquences audiométriques ont été enregisrés afin de délimiter l’étendue de la lésion.

Les ASSEP-TCs ont été fortement altérées, mais pas comme attendu ni suggéré par les mesures fonctionnelles indiquant que le trauma acoustique a créé une lésion différente de celle espérée.

Cette étude doit être poursuivie, des lésions moins importantes créées et une validation histopathologique réalisée.

Etape 5

Le TEN test a été mesuré à l’aide des ASSEPs (ASSEP-TEN) chez 12 adultes et cinq enfants normo-entendants. Les données adultes ont été confrontées aux données comportementales. L’effet des stimuli ASSEP (son pur modulé en amplitude) sur les TEN test a également été investigué en comparant les données comportementales obtenues avec une sinusoïde et avec une sinusoïde modulée en amplitude chez 24 adultes.

Les seuils masqués enregistrés aux ASSEPs étaient supérieurs à ceux mesurés par une épreuve comportementale. L’élévation des seuils masqués pose un problème potentiel de dynamique.

La procédure doit être testée chez des patients présentant une surdité cochléaire attendu que la différence entre les seuils auditifs mesurés aux ASSEPs et par une épreuve comportementale est moindre dans cette population. Dans la mesure où le problème de dynamique résiduelle persiste chez les patients malentendants, d’autres stimuli ou algorithmes d’enregistrement doivent être utilisés.

Etape 6

Le TEN est un stimulus large bande. Il peut dès lors se révéler intolérable chez des patients présentant une atteinte auditive restreinte à une region fréquentielle. L’effet du filtrage du TEN sur les seuils et la sonie du TEN a été étudié chez 24 sujets normo-entendants et 35 patients présentant une perte cochléaire dans les hautes fréquences.

Le filtrage passe-haut du TEN s’est avéré être une solution satisfaisante.

Ces données ont été publiées dans International Journal of Audiology (Markessis et al. 2006; 45: 91-98).

Etape 7

L’effet de l’intensité du TEN sur le diagnostic des zones neuro-épithéliales non fonctionnelles a été investigué chez 24 patients en mesurant les seuils masqués à quatre intensités de TEN différentes. La fiabilité du TEN test a également été évaluée.

Le TEN est une procédure fiable. L’intensité du TEN a affecté le diagnostic chez cinq patients. Ce résultat est interprété en termes de degré de l’atteinte du complexe neurosensoriel.

Ces données ont été publiées dans International Journal of Audiology (Markessis et al. 2009; 48: 55-62).

Conclusion

Un algorithme permettant la mesure de TC et du TEN test objective à l’aide des ASSEPs a été développé. L’implémentation clinique de l’algorithme appliqué à l’enregistrement des CA paraît envisageable. Une importante étape de la corrélation entre modifications anatomiques (à l’aide de l’histopathologie) et physiologiques (ASSEP-TC et CAP-TC) est maintenant celle qui s’impose. Les données préliminaires obtenues sur le TEN test électrophysiologique chez des sujets normo-entendants suggèrent que son implémentation clinique puisse se heurter à un problème de dynamique si ce dernier est confirmé en présence de surdités cochléaires. Plusieurs pistes potentielles de solutions ont été avancées.


Doctorat en Sciences biomédicales et pharmaceutiques
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Books on the topic "Cochlea – Physiology"

1

Williamstown, Mass ). Mechanics of Hearing Workshop (11th 2011. What fire is in mine ears: Progress in auditory biomechanics : proceedings of the 11th International Mechanics of Hearing Workshop, Williamstown, Massachusetts, 16-22 July 2011 / editors, Christopher A. Shera, Elizabeth S. Olson. Melville, N.Y: American Institute of Physics, 2011.

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service), SpringerLink (Online, ed. Cochlear Mechanics: Introduction to a Time Domain Analysis of the Nonlinear Cochlea. Boston, MA: Springer US, 2012.

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F, Grandori, Cianfrone G, and Kemp D. T, eds. Cochlear mechanisms and otoacoustic emissions: 2nd International Symposium on Cochlear Mechanics and Otoacoustic Emissions. Basel: Karger, 1990.

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College), NATO Advanced Research Workshop on Auditory Frequency Selectivity (1986 Wolfson. Auditory frequency selectivity. New York: Plenum Press, 1986.

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Harrison, Robert V. The biology ofhearing and deafness. Springfield, Ill., U.S.A: Thomas, 1988.

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The biology of hearing and deafness. Springfield, Ill., U.S.A: Thomas, 1988.

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Compression for clinicians. San Diego, Calif: Singular Pub. Group, 1998.

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Compression for clinicians. 2nd ed. Clifton Park, NY: Thomson Delmar, 2006.

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Mechanics, and Biophysics of Hearing (Conference) (1990 University of Wisconsin Madison WI). The Mechanics and biophysics of hearing: Proceedings of a conference held at the University of Wisconsin, Madison, WI, June 25-29, 1990. Berlin: Springer-Verlag, 1990.

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Salami, Angelo. Neuroplasticity in the auditory brainstem: From physiology to the drug therapy. New York: Nova Science Publishers, 2011.

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Book chapters on the topic "Cochlea – Physiology"

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Adunka, Oliver F. "Physiology of Cochlea." In Encyclopedia of Otolaryngology, Head and Neck Surgery, 2155–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-23499-6_805.

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Pusz, Max, and Philip Littlefield. "Physiology of Cochlear Nerve." In Encyclopedia of Otolaryngology, Head and Neck Surgery, 2159–63. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-23499-6_806.

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Abbas, Paul J., and Charles A. Miller. "Biophysics and Physiology." In Cochlear Implants: Auditory Prostheses and Electric Hearing, 149–212. New York, NY: Springer New York, 2004. http://dx.doi.org/10.1007/978-0-387-22585-2_5.

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Schmiedt, Richard A. "The Physiology of Cochlear Presbycusis." In The Aging Auditory System, 9–38. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0993-0_2.

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Irvine, Dexter R. F. "Cochlear Nucleus: Anatomy and Physiology." In The Auditory Brainstem, 40–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71057-5_4.

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Rhode, William S., and Steven Greenberg. "Physiology of the Cochlear Nuclei." In Springer Handbook of Auditory Research, 94–152. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2838-7_3.

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Manis, Paul B., John C. Scott, and George A. Spirou. "Physiology of the Dorsal Cochlear Nucleus Molecular Layer." In The Mammalian Cochlear Nuclei, 361–71. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2932-3_28.

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Vater, Marianne. "Cochlear Physiology and Anatomy in Bats." In Animal Sonar, 225–41. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-7493-0_20.

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Guinan, John J. "Physiology and Function of Cochlear Efferents." In Encyclopedia of Computational Neuroscience, 1–11. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7320-6_431-1.

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Kros, Corné J. "Physiology of Mammalian Cochlear Hair Cells." In Springer Handbook of Auditory Research, 318–85. New York, NY: Springer New York, 1996. http://dx.doi.org/10.1007/978-1-4612-0757-3_6.

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Conference papers on the topic "Cochlea – Physiology"

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Liu, Shuangqin, Douglas A. Gauthier, Ethan Mandelup, and Robert D. White. "Experimental Investigation of a Hydromechanical Scale Model of the Gerbil Cochlea." In ASME 2008 International Mechanical Engineering Congress and Exposition. ASMEDC, 2008. http://dx.doi.org/10.1115/imece2008-67778.

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In this research, an uncoiled scale gerbil cochlea is designed and fabricated. The cochlea model is an uncoiled, 16 times scale model of the real gerbil cochlea and has only one duct. Both the basilar membrane width and the duct size vary along the length of the device, in analogy to the physiology. The cochlea duct is filled with silicone oil and driven by a modal exciter (shaker) at different frequencies. The movement of the basilar membrane is measured using laser vibrometry at different locations along the basilar membrane. The ratio of the basilar membrane velocity to drive velocity is computed and plotted. The characteristic frequency of the model varies from 7000 Hz at 2 cm from the base of the cochlea to 350 Hz at the 15 cm from the base. Two different viscosities silicone oil, 20 cSt and 500 cSt are used for the basilar membrane movement measurements. A WKB method is applied to the calculation of the basilar membrane movement of the scale cochlea model, in which the fluid motion is fully three dimensional.
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Rios, Francisco, Raquel Fernandez-Ramos, Jorge Romero-Sanchez, and Jose Francisco Martin. "Corti's organ physiology-based cochlear model: a microelectronic prosthetic implant." In Microtechnologies for the New Millennium 2003, edited by Angel Rodriguez-Vazquez, Derek Abbott, and Ricardo Carmona. SPIE, 2003. http://dx.doi.org/10.1117/12.499032.

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Becker, Sebastian, and Herbert Hudde. "A physiology-based auditory model elucidating the function of the cochlear amplifier and related phenomena. Part II: Model parameters and simulations." In ICA 2013 Montreal. ASA, 2013. http://dx.doi.org/10.1121/1.4799318.

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Hudde, Herbert, and Sebastian Becker. "A physiology-based auditory model elucidating the function of the cochlear amplifier and related phenomena. Part I: Model structure and computational method." In ICA 2013 Montreal. ASA, 2013. http://dx.doi.org/10.1121/1.4798788.

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