Mechanoelectric Transduction of Adult Inner Hair Cells

Song, Jia; Dallos, Peter; He, David Z.Z.

doi:10.1523/jneurosci.5452-06.2007

Cited by 64 publications

(55 citation statements)

References 54 publications

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“…For example, a consequence of adaptation that all hair cells demonstrate is the severe attenuation of DC inputs to the mechanoelectric transducer (MET) (32,33). Such DC can originate from electromotile feedback via two mechanisms: motility in response to DC receptor potentials produced by rectification of MET, as well as DC components associated with length changes produced by rectification of electromechanical transduction (34).…”

Section: Discussionmentioning

confidence: 99%

Prestin-based outer hair cell electromotility in knockin mice does not appear to adjust the operating point of a cilia-based amplifier

Gao

Wang

et al. 2007

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

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The remarkable sensitivity and frequency selectivity of the mammalian cochlea is attributed to a unique amplification process that resides in outer hair cells (OHCs). Although the mammalian-specific somatic motility is considered a substrate of cochlear amplification, it has also been proposed that somatic motility in mammals simply acts as an operating-point adjustment for the ubiquitous stereocilia-based amplifier. To address this issue, we created a mouse model in which a mutation (C1) was introduced into the OHC motor protein prestin, based on previous results in transfected cells. In C1/C1 knockin mice, localization of C1-prestin, as well as the length and number of OHCs, were all normal. In OHCs isolated from C1/C1 mice, nonlinear capacitance and somatic motility were both shifted toward hyperpolarization, so that, compared with WT controls, the amplitude of cycle-bycycle (alternating, or AC) somatic motility remained the same, but the unidirectional (DC) component reversed polarity near the OHC's presumed in vivo resting membrane potential. No physiological defects in cochlear sensitivity or frequency selectivity were detected in C1/C1 or C1/؉ mice. Hence, our results do not support the idea that OHC somatic motility adjusts the operating point of a stereociliabased amplifier. However, they are consistent with the notion that the AC component of OHC somatic motility plays a dominant role in mammalian cochlear amplification.cochlear amplification ͉ mechanosensory ͉ prestin T he remarkable sensitivity, frequency range, and selectivity of the mammalian cochlea have been attributed to a unique amplification process that resides in outer hair cells (OHCs) (1, 2). Two different models have been proposed for cochlear amplification: the mammalian-specific somatic motility (3-5) and the ubiquitous stereociliary motility (6, 7). Somatic motility is known to possess the necessary high-frequency responsiveness (Ͼ79 kHz) (8), whereas the frequency response limitation of stereociliary motility is yet to be established. Somatic motility is believed to be driven by the motor molecule prestin (9). Lack of prestin in mice results in loss of OHC somatic motility, an Ϸ50 dB threshold shift in compound action potentials (CAP), brainstem evoked responses, and otoacoustic emissions, as well as the loss of frequency selectivity (10, 13-15, ʈ, and ** ). These studies provide evidence that prestin is required for OHC somatic motility and cochlear amplification.Recent studies raised the possibility that stereocilia-based amplification may be important in mammalian hearing (16)(17)(18)(19)(20). Because of low-pass filtering of somatic motility by the electrical impedance of the basolateral cell membrane, some believe that the dominant means of amplification must reside in stereociliary motility. In this view, the main function of prestin-based somatic motility is to somehow adjust the operating point of the stereocilia-based amplifier, i.e., that the DC (average or direct current) component of the somatic electromotile response prov...

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Section: Discussionmentioning

confidence: 99%

Prestin-based outer hair cell electromotility in knockin mice does not appear to adjust the operating point of a cilia-based amplifier

Gao

Wang

et al. 2007

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

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“…It was assumed that there is no adaptation in the voltage responses of the IHC, but recent studies suggest that there is indeed some adaptation at this level ͑Kros and Crawford, 1990; Zeddies and Siegel, 2004;Jia et al, 2007;Beurg et al, 2008͒. It would be important to explore the contribution of IHC adaptation to AN responses, especially at the onset and offset of tone bursts and in response to AM stimuli.…”

Section: F Limitationsmentioning

confidence: 99%

A phenomenological model of the synapse between the inner hair cell and auditory nerve: Long-term adaptation with power-law dynamics

Zilany

Bruce²,

Nelson³

et al. 2009

The Journal of the Acoustical Society of America

318

346

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There is growing evidence that the dynamics of biological systems that appear to be exponential over short time courses are in some cases better described over the long-term by power-law dynamics. A model of rate adaptation at the synapse between inner hair cells and auditory-nerve ͑AN͒ fibers that includes both exponential and power-law dynamics is presented here. Exponentially adapting components with rapid and short-term time constants, which are mainly responsible for shaping onset responses, are followed by two parallel paths with power-law adaptation that provide slowly and rapidly adapting responses. The slowly adapting power-law component significantly improves predictions of the recovery of the AN response after stimulus offset. The faster power-law adaptation is necessary to account for the "additivity" of rate in response to stimuli with amplitude increments. The proposed model is capable of accurately predicting several sets of AN data, including amplitude-modulation transfer functions, long-term adaptation, forward masking, and adaptation to increments and decrements in the amplitude of an ongoing stimulus.

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“…Dallos 1992). Experimental results are available that studied the micromechanics of the organ of Corti in excised cochlear preparations, including guinea pig temporal bone preparations, sections of the guinea pig, gerbil cochlea, and the gerbil hemicochlea (Chan and Hudspeth 2005;Edge et al 1998;Fridberger et al 2002a, b;Fridberger and de Monvel 2003;Hu et al 1995Hu et al , 1999Jacob et al 2011;Jia et al 2007;Karavitaki and Mountain 2007a, b;Karavitaki et al 1996;Mammano and Ashmore 1993;Morioka et al 1995;Nowotny and Gummer 2006;Reuter et al 1992;Dallos 2001, 2003;Richter et al 2002Richter et al , 2000von Tiedemann et al 2010). Results have been published using confocal microscopy or optical coherence tomography (OCT) to study micromechanics of the cochlea in vivo (Chen et al 2007(Chen et al , 2011Choudhury et al 2006;Gao et al 2011Gao et al , 2013Masaki et al 2009;Zha et al 2012).…”

Section: Introductionmentioning

confidence: 99%

Basilar Membrane and Tectorial Membrane Stiffness in the CBA/CaJ Mouse

Teudt

Richter

2014

JARO

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The mouse has become an important animal model in understanding cochlear function. Structures, such as the tectorial membrane or hair cells, have been changed by gene manipulation, and the resulting effect on cochlear function has been studied. To contrast those findings, physical properties of the basilar membrane (BM) and tectorial membrane (TM) in mice without gene mutation are of great importance. Using the hemicochlea of CBA/CaJ mice, we have demonstrated that tectorial membrane (TM) and basilar membrane (BM) revealed a stiffness gradient along the cochlea. While a simple spring mass resonator predicts the change in the characteristic frequency of the BM, the spring mass model does not predict the frequency change along the TM. Plateau stiffness values of the TM were 0.6±0.5, 0.2± 0.1, and 0.09±0.09 N/m for the basal, middle, and upper turns, respectively. The BM plateau stiffness values were 3.7±2.2, 1.2±1.2, and 0.5±0.5 N/m for the basal, middle, and upper turns, respectively. Estimations of the TM Young's modulus (in kPa) revealed 24.3±25.2 for the basal turns, 5.1±4.5 for the middle turns, and 1.9±1.6 for the apical turns. Young's modulus determined at the BM pectinate zone was 76.8±72, 23.9±30.6, and 9.4±6.2 kPa for the basal, middle, and apical turns, respectively. The reported stiffness values of the CBA/CaJ mouse TM and BM provide basic data for the physical properties of its organ of Corti.

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Mechanoelectric Transduction of Adult Inner Hair Cells

Cited by 64 publications

References 54 publications

Prestin-based outer hair cell electromotility in knockin mice does not appear to adjust the operating point of a cilia-based amplifier

Prestin-based outer hair cell electromotility in knockin mice does not appear to adjust the operating point of a cilia-based amplifier

A phenomenological model of the synapse between the inner hair cell and auditory nerve: Long-term adaptation with power-law dynamics

Basilar Membrane and Tectorial Membrane Stiffness in the CBA/CaJ Mouse

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