The origin of the low-frequency microphonic in the first cochlear turn of guinea-pig

Patuzzi, Robert; Yates, Graeme K.; Johnstone, Brian M.

doi:10.1016/0378-5955(89)90089-0

Cited by 128 publications

(80 citation statements)

References 31 publications

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“…In order to assess the ability of the TM to stimulate the OHCs in vivo, we measured the cochlear microphonic (CM), a field potential thought to emanate predominantly from the receptor potential within OHCs of the basal turn (Patuzzi et al, 1989). We used a stimulus frequency of 6 kHz in order to minimize the impact of the cochlear amplifier on the response, and varied the stimulus intensity to assess forward transduction.…”

Section: Assessment Of Cochlear Function In Vivomentioning

confidence: 99%

“…The CM is a field potential that reflects the summation of hair cell transduction currents, primarily from OHCs, at the basal turn of the cochlea (Dallos, 1975;Cheatham and Dallos, 1982;Patuzzi et al, 1989;Cheatham and Dallos, 1997;Patuzzi and Moleirinho, 1998). After rigidly securing the mouse in a head holder, the pinna was surgically resected.…”

Section: Cochlear Microphonic (Cm) Measurementsmentioning

confidence: 99%

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Deficient forward transduction and enhanced reverse transduction in the alpha tectorin C1509G human hearing loss mutation

Xia

Gao

Tao

et al. 2010

Disease Models &Amp; Mechanisms

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SUMMARYMost forms of hearing loss are associated with loss of cochlear outer hair cells (OHCs). OHCs require the tectorial membrane (TM) for stereociliary bundle stimulation (forward transduction) and active feedback (reverse transduction). Alpha tectorin is a protein constituent of the TM and the C1509G mutation in alpha tectorin in humans results in autosomal dominant hearing loss. We engineered and validated this mutation in mice and found that the TM was shortened in heterozygous Tecta C1509G/+ mice, reaching only the first row of OHCs. Thus, deficient forward transduction renders OHCs within the second and third rows non-functional, producing partial hearing loss. Surprisingly, both Tecta C1509G/+ and Tecta C1509G/C1509G mice were found to have increased reverse transduction as assessed by sound-and electrically-evoked otoacoustic emissions. We show that an increase in prestin, a protein necessary for electromotility, in all three rows of OHCs underlies this phenomenon. This mouse model demonstrates a human hearing loss mutation in which OHC function is altered through a non-cell-autonomous variation in prestin.

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Section: Assessment Of Cochlear Function In Vivomentioning

confidence: 99%

Section: Cochlear Microphonic (Cm) Measurementsmentioning

confidence: 99%

Deficient forward transduction and enhanced reverse transduction in the alpha tectorin C1509G human hearing loss mutation

Xia

Gao

Tao

et al. 2010

Disease Models &Amp; Mechanisms

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“…The stored potentials could then be digitally filtered with a low-pass setting at 2.5 kHz to measure the compound action potential (CAP) of the auditory nerve, and the summating potential (SP) reflecting the summed intracellular dc receptor potential, mainly generated by the inner hair cells (IHCs) (1). Filtering cochlear potentials with a band-pass filter centered on the frequency of tone burst stimulation allows extraction of the cochlear microphonic (CM) reflecting the summed intracellular ac receptor potential mainly generated by outer hair cells (OHCs) (17).…”

Section: Targeting Construction and Generation Of Otosmentioning

confidence: 99%

Deafness and Cochlear Fibrocyte Alterations in Mice Deficient for the Inner Ear Protein Otospiralin

Delprat

Ruel

Guitton

et al. 2005

Molecular and Cellular Biology

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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.Within the cochlea, the mammalian auditory organ, mesenchymal nonsensory regions (i.e., the spiral limbus proximal to the cochlear axis and the spiral ligament forming the lateral wall of the cochlea) contain fibrocytes that play important roles in cochlear physiology. In the spiral ligament, these fibrocytes form distinct groups according to their location, morphological appearance, and marker expression, which suggest their functional specialization (26). Thus, the circumferentially oriented type III fibrocytes lining the otic capsule and the spindleshaped type IV fibrocytes lateral to the basilar membrane package the cochlear content and buffer mechanical constraints generated by sound vibrations (8). The type I fibrocytes (behind the stria vascularis), tightly packed with collagen bundles, shape the curvature of the lateral wall. Type II fibrocytes (below the stria vascularis) and type V fibrocytes (above the stria vascularis) are rich in mitochondria and form many interdigitating processes, indicating high metabolic and exchange activities. Type I, II, and V fibrocytes and basal and intermediate cells of the stria vascularis are all interconnected with gap junctions (10). This gap-junctioned network is postulated to be involved in ion and water circulation, including potassium recycling (34). Potassium is indeed central to the cochlear physiology, since it is the charge-carrying ion for the sensory transduction. It is secreted by the marginal cells of the stria vascularis to maintain a very high concentration (150 mM) in the endolymph, the extracellular fluid bathing hair cell stereocilia. Recycling of potassium though the fibrocyte network is one of several processes that provide potassium to intermediate cells of the stria vascularis (28, 34). This permanent flux of potassium cycling in the cochlea generates the so-called "endocochlear potential " (ϩ85 mV), which gives the main driving force for potassium entry into the sensory hair cell.Progress in the functional characterization of the cochlear fibrocytes has been made with the discovery of proteins exp...

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“…Re-searchers have used the CM as an approximation of the local MET channel conductance and have fitted a first-order Boltzmann function to the relationship between the CM and the acoustic stimulus ͑Corey and Hudspeth, 1983;Crawford et al, 1989;Rajan, 1990, Patuzzi andMoleirinho, 1998;Sirjani et al, 2004͒, assuming that the CM is dominated by local hair cells ͑Dallos et al, 1972;Patuzzi et al, 1989͒ and that the MET channels are the dominant nonlinearity in the forward-transduction ͑Holton and Hudspeth, 1986;Kros, 1996͒. The three main parameters used to fit the Boltzmann function y = V off + ͩ−P sat + 2 · P sat 1 + exp͑2 · S · P sat ͑input + OP͒͒ ͪ are the OP, which is related to the asymmetry of transduction, the saturating voltage ͑P sat ͒, which is related to the potential between the open and closed states of the MET channels, and a sensitivity parameter ͑S͒, which represents the slope of the curve at the mid-point of the Boltzmann curve ͑Sirjani et al, 2004͒.…”

Section: Introductionmentioning

confidence: 99%

Estimating the operating point of the cochlear transducer using low-frequency biased distortion products

Brown

Hartsock

Gill

et al. 2009

The Journal of the Acoustical Society of America

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Distortion products in the cochlear microphonic ͑CM͒ and in the ear canal in the form of distortion product otoacoustic emissions ͑DPOAEs͒ are generated by nonlinear transduction in the cochlea and are related to the resting position of the organ of Corti ͑OC͒. A 4.8 Hz acoustic bias tone was used to displace the OC, while the relative amplitude and phase of distortion products evoked by a single tone ͓most often 500 Hz, 90 dB SPL ͑sound pressure level͔͒ or two simultaneously presented tones ͑most often 4 kHz and 4.8 kHz, 80 dB SPL͒ were monitored. Electrical responses recorded from the round window, scala tympani and scala media of the basal turn, and acoustic emissions in the ear canal were simultaneously measured and compared during the bias. Bias-induced changes in the distortion products were similar to those predicted from computer models of a saturating transducer with a first-order Boltzmann distribution. Our results suggest that biased DPOAEs can be used to non-invasively estimate the OC displacement, producing a measurement equivalent to the transducer operating point obtained via Boltzmann analysis of the basal turn CM. Low-frequency biased DPOAEs might provide a diagnostic tool to objectively diagnose abnormal displacements of the OC, as might occur with endolymphatic hydrops.

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The origin of the low-frequency microphonic in the first cochlear turn of guinea-pig

Cited by 128 publications

References 31 publications

Deficient forward transduction and enhanced reverse transduction in the alpha tectorin C1509G human hearing loss mutation

Deficient forward transduction and enhanced reverse transduction in the alpha tectorin C1509G human hearing loss mutation

Deafness and Cochlear Fibrocyte Alterations in Mice Deficient for the Inner Ear Protein Otospiralin

Estimating the operating point of the cochlear transducer using low-frequency biased distortion products

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