scholarly journals A flexible anatomical set of mechanical models for the organ of Corti

2021 ◽  
Vol 8 (9) ◽  
pp. 210016
Author(s):  
Jorge Berger ◽  
Jacob Rubinstein

We build a flexible platform to study the mechanical operation of the organ of Corti (OoC) in the transduction of basilar membrane (BM) vibrations to oscillations of an inner hair cell bundle (IHB). The anatomical components that we consider are the outer hair cells (OHCs), the outer hair cell bundles, Deiters cells, Hensen cells, the IHB and various sections of the reticular lamina. In each of the components we apply Newton’s equations of motion. The components are coupled to each other and are further coupled to the endolymph fluid motion in the subtectorial gap. This allows us to obtain the forces acting on the IHB, and thus study its motion as a function of the parameters of the different components. Some of the components include a nonlinear mechanical response. We find that slight bending of the apical ends of the OHCs can have a significant impact on the passage of motion from the BM to the IHB, including critical oscillator behaviour. In particular, our model implies that the components of the OoC could cooperate to enhance frequency selectivity, amplitude compression and signal to noise ratio in the passage from the BM to the IHB. Since the model is modular, it is easy to modify the assumptions and parameters for each component.

2019 ◽  
Author(s):  
Jorge Berger ◽  
Jacob Rubinstein

We build a flexible platform for the study of the mechanical performance of the organ of Corti (OoC) in the transduction of basilar membrane (BM) vibrations to motion of an inner hair cell bundle (IHB). In this platform, each anatomic component of the OoC is described by an equation of motion that can be followed in time. We propose an initial set of models that attempt to capture the nonlinearities of somatic and bundle motility, but can nevertheless be easily handled. The anatomic components that we consider are the outer hair cells (OHCs), the outer hair cell bundles, Deiters cells, Hensen cells, the IHB and various sections of the reticular lamina. We study endolymph fluid motion in the subtectorial gap and then the mutual interactions among the components of the OoC, including the pressure exerted by endolymph. Minute bending of the apical ends of the OHCs can have a significant impact on the passage of motion from the BM to the IHB, including possible critical oscillator behaviour, even without the assistance of tectorial motion, shearing, or bundle motility. Thus, the components of the OoC could cooperate to enhance frequency selectivity, amplitude compression and signal to noise ratio in the passage from the BM to the IHB. Our models also provide a mechanism that could contribute to appropriate amplification of the wave travelling along the cochlea.


2015 ◽  
Vol 112 (47) ◽  
pp. 14723-14727 ◽  
Author(s):  
Chang Liu ◽  
Elisabeth Glowatzki ◽  
Paul Albert Fuchs

In the mammalian cochlea, acoustic information is carried to the brain by the predominant (95%) large-diameter, myelinated type I afferents, each of which is postsynaptic to a single inner hair cell. The remaining thin, unmyelinated type II afferents extend hundreds of microns along the cochlear duct to contact many outer hair cells. Despite this extensive arbor, type II afferents are weakly activated by outer hair cell transmitter release and are insensitive to sound. Intriguingly, type II afferents remain intact in damaged regions of the cochlea. Here, we show that type II afferents are activated when outer hair cells are damaged. This response depends on both ionotropic (P2X) and metabotropic (P2Y) purinergic receptors, binding ATP released from nearby supporting cells in response to hair cell damage. Selective activation of P2Y receptors increased type II afferent excitability by the closure of KCNQ-type potassium channels, a potential mechanism for the painful hypersensitivity (that we term “noxacusis” to distinguish from hyperacusis without pain) that can accompany hearing loss. Exposure to the KCNQ channel activator retigabine suppressed the type II fiber’s response to hair cell damage. Type II afferents may be the cochlea’s nociceptors, prompting avoidance of further damage to the irreparable inner ear.


1990 ◽  
Vol 99 (3) ◽  
pp. 215-220 ◽  
Author(s):  
Joseph B. Nadol ◽  
Barbara J. Burgess

The synaptic morphology of inner and outer hair cells of the organ of Corti of the chimpanzee was evaluated by serial section electron microscopy. The morphology of nerve terminals and synapses at both sites was very similar to that of human and other mammalian species. Two types of nerve terminals, nonvesiculated and vesiculated, with distinct synaptic morphology were found. In addition, between some nonvesiculated endings and outer hair cells, a reciprocal synaptic relationship was seen. In such terminals there was morphologic evidence for transmission from hair cell to neuron and from neuron to hair cell between a single neuron and an outer hair cell.


1981 ◽  
Vol 90 (1) ◽  
pp. 12-17 ◽  
Author(s):  
Joseph B. Nadol

Reciprocal synapses have been found between nerve terminals and the outer hair cells in the human organ of Corti. A single nerve ending of the nonvesiculated type may possess two types of synaptic specialization of opposite polarity. The first is typical of the “afferent” synapse with a presynaptic body in the hair cell and pre- and postsynaptic membrane thickening. The second consists of a small collection of presynaptic vesicles in the neural cytoplasm near the plasma membrane facing the hair cell and a subsynaptic cisterna within the hair cell cytoplasm. The second type of specialization is similar to the synapses seen in “efferent” endings. This suggests that both an afferent (hair cell to neuron) and efferent (neuron to hair cell) synaptic relationship may exist between an outer hair cell and a single nerve terminal.


Author(s):  
Paul Albert Fuchs

Cochlear afferents differ in form and function. The great majority are type I, large diameter, myelinated neurons that contact a single inner hair cell to transmit acoustic information. Each inner hair cell is presynaptic to a pool of 10–30 type I afferents, among which spontaneous activity and acoustic threshold vary widely. Variation in the number, voltage-gating, and density of L-type calcium channels at each presynaptic active zone (ribbon) may dictate this functional diversity. Despite contacting large numbers of outer hair cells, the scarce, unmyelinated type II afferents are acoustically insensitive, and only weakly depolarized by outer hair cell transmitter release. However, type II afferents respond strongly to adenosine triphosphate released by cochlear tissue damage, providing a biological basis for painful hearing (noxacusis).


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Wenxuan He ◽  
Tianying Ren

AbstractAlthough auditory harmonic distortion has been demonstrated psychophysically in humans and electrophysiologically in experimental animals, the cellular origin of the mechanical harmonic distortion remains unclear. To demonstrate the outer hair cell-generated harmonics within the organ of Corti, we measured sub-nanometer vibrations of the reticular lamina from the apical ends of the outer hair cells in living gerbil cochleae using a custom-built heterodyne low-coherence interferometer. The harmonics in the reticular lamina vibration are significantly larger and have broader spectra and shorter latencies than those in the basilar membrane vibration. The latency of the second harmonic is significantly greater than that of the fundamental at low stimulus frequencies. These data indicate that the mechanical harmonics are generated by the outer hair cells over a broad cochlear region and propagate from the generation sites to their own best-frequency locations.


2021 ◽  
Vol 5 (2) ◽  
pp. e202101068
Author(s):  
Kuu Ikäheimo ◽  
Anni Herranen ◽  
Vilma Iivanainen ◽  
Tuuli Lankinen ◽  
Antti A Aarnisalo ◽  
...  

Failure in the structural maintenance of the hair cell stereocilia bundle and ribbon synapse causes hearing loss. Here, we have studied how ER stress elicits hair cell pathology, using mouse models with inactivation of Manf (mesencephalic astrocyte-derived neurotrophic factor), encoding an ER-homeostasis-promoting protein. From hearing onset, Manf deficiency caused disarray of the outer hair cell stereocilia bundle and reduced cochlear sound amplification capability throughout the tonotopic axis. In high-frequency outer hair cells, the pathology ended in molecular changes in the stereocilia taper region and in strong stereocilia fusion. In high-frequency inner hair cells, Manf deficiency degraded ribbon synapses. The altered phenotype strongly depended on the mouse genetic background. Altogether, the failure in the ER homeostasis maintenance induced early-onset stereociliopathy and synaptopathy and accelerated the effect of genetic causes driving age-related hearing loss. Correspondingly, MANF mutation in a human patient induced severe sensorineural hearing loss from a young age onward. Thus, we present MANF as a novel protein and ER stress as a mechanism that regulate auditory hair cell maintenance in both mice and humans.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Mohammad Shokrian ◽  
Catherine Knox ◽  
Douglas H. Kelley ◽  
Jong-Hoon Nam

Abstract The cochlea is filled with two lymphatic fluids. Homeostasis of the cochlear fluids is essential for healthy hearing. The sensory epithelium called the organ of Corti separates the two fluids. Corti fluid space, extracellular fluid space within the organ of Corti, looks like a slender micro-tube. Substantial potassium ions are constantly released into the Corti fluid by sensory receptor cells. Excess potassium ions in the Corti fluid are resorbed by supporting cells to maintain fluid homeostasis. Through computational simulations, we investigated fluid mixing within the Corti fluid space. Two assumptions were made: first, there exists a longitudinal gradient of potassium ion concentration; second, outer hair cell motility causes organ of Corti deformations that alter the cross-sectional area of the Corti fluid space. We hypothesized that mechanical agitations can accelerate longitudinal mixing of Corti fluid. Corti fluid motion was determined by solving the Navier–Stokes equations incorporating nonlinear advection term. Advection–diffusion equation determined the mixing dynamics. Simulating traveling boundary waves, we found that advection and diffusion caused comparable mixing when the wave amplitude and speed were 25 nm and 7 m/s, respectively. Higher-amplitude and faster waves caused stronger advection. When physiological traveling waves corresponding to 70 dB sound pressure level at 9 kHz were simulated, advection speed was as large as 1 mm/s in the region basal to the peak responding location. Such physiological agitation accelerated longitudinal mixing by more than an order of magnitude, compared to pure diffusion. Our results suggest that fluid motion due to outer hair cell motility can help maintain longitudinal homeostasis of the Corti fluid.


eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Wenxuan He ◽  
David Kemp ◽  
Tianying Ren

Auditory sensory outer hair cells are thought to amplify sound-induced basilar membrane vibration through a feedback mechanism to enhance hearing sensitivity. For optimal amplification, the outer hair cell-generated force must act on the basilar membrane at an appropriate time at every cycle. However, the temporal relationship between the outer hair cell-driven reticular lamina vibration and the basilar membrane vibration remains unclear. By measuring sub-nanometer vibrations directly from outer hair cells using a custom-built heterodyne low-coherence interferometer, we demonstrate in living gerbil cochleae that the reticular lamina vibration occurs after, not before, the basilar membrane vibration. Both tone- and click-induced responses indicate that the reticular lamina and basilar membrane vibrate in opposite directions at the cochlear base and they oscillate in phase near the best-frequency location. Our results suggest that outer hair cells enhance hearing sensitivity through a global hydromechanical mechanism, rather than through a local mechanical feedback as commonly supposed.


2015 ◽  
Vol 113 (10) ◽  
pp. 3531-3542 ◽  
Author(s):  
Yohan Song ◽  
Anping Xia ◽  
Hee Yoon Lee ◽  
Rosalie Wang ◽  
Anthony J. Ricci ◽  
...  

Prestin is a membrane protein necessary for outer hair cell (OHC) electromotility and normal hearing. Its regulatory mechanisms are unknown. Several mouse models of hearing loss demonstrate increased prestin, inspiring us to investigate how hearing loss might feedback onto OHCs. To test whether centrally mediated feedback regulates prestin, we developed a novel model of inner hair cell loss. Injection of diphtheria toxin (DT) into adult CBA mice produced significant loss of inner hair cells without affecting OHCs. Thus, DT-injected mice were deaf because they had no afferent auditory input despite OHCs continuing to receive normal auditory mechanical stimulation and having normal function. Patch-clamp experiments demonstrated no change in OHC prestin, indicating that loss of information transfer centrally did not alter prestin expression. To test whether local mechanical feedback regulates prestin, we used TectaC1509G mice, where the tectorial membrane is malformed and only some OHCs are stimulated. OHCs connected to the tectorial membrane had normal prestin levels, whereas OHCs not connected to the tectorial membrane had elevated prestin levels, supporting an activity-dependent model. To test whether the endocochlear potential was necessary for prestin regulation, we studied TectaC1509G mice at different developmental ages. OHCs not connected to the tectorial membrane had lower than normal prestin levels before the onset of the endocochlear potential and higher than normal prestin levels after the onset of the endocochlear potential. Taken together, these data indicate that OHC prestin levels are regulated through local feedback that requires mechanoelectrical transduction currents. This adaptation may serve to compensate for variations in the local mechanical environment.


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