The location of the cochlear amplifier: Spatial representation of a single tone on the guinea pig basilar membrane

Russell, Ian J.; Nilsen, K. E.

doi:10.1073/pnas.94.6.2660

Cited by 152 publications

(104 citation statements)

References 27 publications

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“…Slight changes in the motion of the reticular lamina caused by changes in loading of the cochlear partition by the modified TM of the Otoa EGFP/EGFP mouse might cause this increase in DPOAE thresholds. The reticular lamina is, however, coupled compliantly to the BM via the OHC-Deiters' cell complex (41)(42)(43)(44), so any change in the load on the cochlear partition would be expected to affect amplification of BM motion and be reflected in the vibrations of the BM. It is therefore more likely that this mild loss in the sensitivity of the DPOAEs in Otoa EGFP/EGFP mice results from the detachment of the TM from the spiral limbus altering the transmission pathway between the source of the DPOAEs and the point of measurement at the eardrum.…”

Section: Discussionmentioning

confidence: 99%

A mouse model for human deafness DFNB22 reveals that hearing impairment is due to a loss of inner hair cell stimulation

Lukashkin

Legan

Weddell

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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The gene causative for the human nonsyndromic recessive form of deafness DFNB22 encodes otoancorin, a 120-kDa inner ear-specific protein that is expressed on the surface of the spiral limbus in the cochlea. Gene targeting in ES cells was used to create an EGFP knock-in, otoancorin KO (Otoa EGFP/EGFP ) mouse. In the Otoa EGFP/EGFP mouse, the tectorial membrane (TM), a ribbon-like strip of ECM that is normally anchored by one edge to the spiral limbus and lies over the organ of Corti, retains its general form, and remains in close proximity to the organ of Corti, but is detached from the limbal surface. Measurements of cochlear microphonic potentials, distortion product otoacoustic emissions, and basilar membrane motion indicate that the TM remains functionally attached to the electromotile, sensorimotor outer hair cells of the organ of Corti, and that the amplification and frequency tuning of the basilar membrane responses to sounds are almost normal. The compound action potential masker tuning curves, a measure of the tuning of the sensory inner hair cells, are also sharply tuned, but the thresholds of the compound action potentials, a measure of inner hair cell sensitivity, are significantly elevated. These results indicate that the hearing loss in patients with Otoa mutations is caused by a defect in inner hair cell stimulation, and reveal the limbal attachment of the TM plays a critical role in this process.T he sensory epithelium of the cochlea, the organ of Corti ( Fig. 1), contains two types of hair cell, the purely sensory inner hair cells (IHCs) and the electromotile, sensorimotor outer hair cells (OHCs). These cells are critically positioned between two strips of ECM, the basilar membrane (BM) and the tectorial membrane (TM). Signal processing in the cochlea is initiated when sound-induced changes in fluid pressure displace the BM in the transverse direction, causing radial shearing displacements between the surface of the organ of Corti (the reticular lamina) and the overlying TM (1). The radial shear is detected by the hair bundles of the IHCs and the OHCs (2), with the stereocilia of the OHC hair bundles forming an elastic link between the organ of Corti and the overlying TM (3). Deflection of the stereocilia gates the hair cell's mechanoelectrical transducer (MET) channels, thereby initiating a MET current (4) that promotes active mechanical force production by the OHCs, which, in turn, influences mechanical interactions between the TM and the BM (5, 6). This nonlinear frequency-dependent enhancement process, which boosts the sensitivity of cochlear responses to lowlevel sounds and compresses them at high levels, is known as the cochlear amplifier (7).Whereas the hair bundles of the OHCs are imbedded into the TM and therefore directly excited by relative displacement of the undersurface of the TM and the reticular lamina, those of the IHCs are not in direct contact with the TM, and the way in which they are driven by motion of the BM remains unclear. Intracellular recordings of the receptor potent...

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Section: Discussionmentioning

confidence: 99%

A mouse model for human deafness DFNB22 reveals that hearing impairment is due to a loss of inner hair cell stimulation

Lukashkin

Legan

Weddell

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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“…However, reducing mismatch by increasing transistor area will decrease the number of BM segments per octave, which will broaden frequency tuning. Alternatively, as mismatch perturbs BM properties at the finest spatial scale, it could be counteracted by increasing the wavelength, something the three-to-five-OHC tilt observed in the Organ of Corti [21], [22] would achieve. The caveat is that lengthening the wavelength will also broaden tuning.…”

Section: Discussionmentioning

confidence: 99%

A Silicon Cochlea With Active Coupling

Wen

Boahen

2009

IEEE Trans. Biomed. Circuits Syst.

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I. SILICON COCHLEAE SILICON (Si) cochleae emulate cochlear processing of sound stimuli in very-large scale integrated (VLSI) systems, attempting to match the biological cochlea's sound sensitivity, frequency selectivity, and dynamic range. The effort to build artificial cochleae in Si has been largely motivated by their potential applications in hearing aids, cochlear implants, and other portable devices that demand real-time, low-power signal processing for speech recognition; these requirements favor subthreshold analog VLSI designs [1]. Furthermore, analog VLSI is amenable to cochlea-like distributed processing due to its compact computational elements, large numbers of which can be integrated in a small area of Si. However, digital outputs are easier to interface with higher level processing, whether performed by other neuromorphic chips or implemented in computer software. Thus, a mixed-mode approach, where the cochlea's analog outputs are converted to digital pulses-a function performed by the auditory nerve (AN)-is most attractive.

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“…Olson's studies confining it to a 15-µm layer, the work of Russell and Nilsen (1997) localizes it to a narrow segment involving only a handful of active hair cells. The latter authors used a laser diode interferometer with a 10 µm spot to measure the basilar membrane responses of guinea pigs to a 15 kHz tone and found that amplification of the tone was confined to a remarkably narrow segment: some 1.25 mm "vibrat[ing] in unison" (p. 2662) for levels between 35 and 55 dB SPL.…”

Section: Discussionmentioning

confidence: 99%

Helmholtz's Piano Strings: Reverberation of Ripples on the Tectorial Membrane

Bell¹

2001

SSRN Journal

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Abstract:In 1857 Helmholtz proposed that the ear contained an array of sympathetic resonators, like piano strings, which served to give the ear its fine frequency discrimination. Since the discovery that most healthy human ears emit faint, pure tones (spontaneous otoacoustic emissions), it has been possible to view these narrowband signals as the continuous ringing of the resonant elements. But what are the elements? It is noteworthy that motile outer hair cells lie in a precise crystal-like array with their sensitive stereocilia in contact with the tectorial membrane, a gelatinous structure with an observed surface tension. This paper therefore speculates that ripples (surface tension waves) on the lower surface of the tectorial membrane propagate to and fro between neighbouring cells. This mechanism defines a surface acoustic wave (SAW) resonator, and relies on the outer hair cells directly sensing intracochlear fluid pressure through their cell bodies; in this way the theory revisits the resonance theory of hearing. The SAW resonator acts as a regenerative receiver of acoustic energy, a topology which was invoked in 1948 by Gold, who later drew the analogy to an 'underwater piano' to describe the cochlea's problem of how it could vibrate with high Q while immersed in fluid. The proposal also gives a physical description of the cochlear amplifier postulated by Davis in 1983. An active array of resonating cavities driven by outer hair cells can explain spontaneous emissions, the shape of the basilar membrane tuning curve, and evoked emissions, among others, and could relate strongly to music.At levels above which the cochlear amplifier saturates, ripples on the tectorial membrane can still be identified, this time due to vibration of the tectorial membrane against the sharp vestibular lip. This second putative mechanism provides time delays between initiation of the ripple by acoustic pressure variations and its detection by the inner hair cells, and so represents an alternative way of interpreting the traveling wave.Thus, by invoking two ways of generating ripples on the tectorial membrane, a comprehensive account of cochlear mechanics can be constructed, unifying a resonance theory (at low levels) with a traveling wave picture (at high levels).

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The location of the cochlear amplifier: Spatial representation of a single tone on the guinea pig basilar membrane

Cited by 152 publications

References 27 publications

A mouse model for human deafness DFNB22 reveals that hearing impairment is due to a loss of inner hair cell stimulation

A mouse model for human deafness DFNB22 reveals that hearing impairment is due to a loss of inner hair cell stimulation

A Silicon Cochlea With Active Coupling

Helmholtz's Piano Strings: Reverberation of Ripples on the Tectorial Membrane

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