Fine structure of the intracochlear potential field. I. The silent current

Zidanic, M.; Brownell, William E.

doi:10.1016/s0006-3495(90)82644-8

Cited by 123 publications

(102 citation statements)

References 34 publications

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“…On the basis of their location and gap junctional connections with other cell types, these specialized fibrocytes comprise the initial segments of syncytial cellular networks believed to have evolved for resorbing K ϩ leaked or effluxed from endolymph through hair cell activity and releasing it near epithelial cells for recycling back to endolymph (Schulte and Steel 1994;Spicer and Schulte 1996). The demonstration of high levels of NKCC1 in these cells lends further support to a model whereby the continuous recirculation of K ϩ between endolymph and perilymph, at least partly through intracellular pathways, generates a standing current on which the microphonic current from acoustic stimulation is superimposed (Zidanic and Brownell 1994).…”

Section: Discussionmentioning

confidence: 89%

Immunohistochemical Localization of the Na-K-Cl Co-transporter (NKCC1) in the Gerbil Inner Ear

Crouch

Sakaguchi

Lytle

et al. 1997

J Histochem Cytochem.

165

133

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SUMMARYWe mapped the cellular and subcellular distribution of the Na-K-Cl co-transporter (NKCC) in the adult gerbil inner ear by immunostaining with a monoclonal antibody (MAb T4) generated against human colon NKCC. Heavy immunolabeling was seen in the basolateral plasma membrane of marginal cells in the stria vascularis and dark cells in the vestibular system. Subpopulations of fibrocytes in the cochlear spiral ligament and limbus and underlying the vestibular neurosensory epithelium also stained with moderate to strong intensity, apparently along their entire plasmalemma. Because MAb T4 recognizes both the basolateral secretory (NKCC1) and the apical absorptive (NKCC2) isoforms of the co-transporter, we employed reverse transcription and the polymerase chain reaction (RT-PCR) to explore isoform diversity in inner ear tissues. Using NKCC1 and NKCC2 isoform-specific PCR primers based on mouse and human sequences, only transcripts for NKCC1 were detected in the gerbil inner ear. The presence of abundant NKCC1 in the basolateral plasmalemma of strial marginal and vestibular dark cells confirms conclusions drawn from pharmacological and physiological data. The co-expression of NKCC1 and Na,K-ATPase in highly specialized subpopulations of cochlear and vestibular fibrocytes provides further evidence for their role in recycling K ϩ leaked or effluxed through hair cells into perilymph back to endolymph, as postulated in current models of inner ear ion homeostasis.

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Section: Discussionmentioning

confidence: 89%

Immunohistochemical Localization of the Na-K-Cl Co-transporter (NKCC1) in the Gerbil Inner Ear

Crouch

Sakaguchi

Lytle

et al. 1997

J Histochem Cytochem.

165

133

View full text Add to dashboard Cite

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“…This measurement is experimental evidence for the existence of a continuous circulation current within the cochlea (13). Because the graded potential was modulated by acoustic stimuli (12), MET channels serve as the pathway for the circulation current across the hair cell layer. In the lateral wall, the pathway for the circulation current has been proposed to consist of the apical K + channels and basolateral K + uptake transporters in the syncytial and marginal cell layers that are crucial for the EP (4-7, 26, 27).…”

mentioning

confidence: 76%

“…In which case, such an idling current could both maintain electrochemical homeostasis within the cochlea and permit hair cells to respond rapidly to mechanical stimuli (3,7,12,13). An analogous dark current exists in retinal photoreceptors (14).…”

mentioning

confidence: 99%

Computational model of a circulation current that controls electrochemical properties in the mammalian cochlea

Nin

Hibino

Murakami

et al. 2012

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

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Sound-evoked mechanical stimuli permit endolymphatic K + to enter sensory hair cells. This transduction is sensitized by an endocochlear potential (EP) of +80 mV in endolymph. After depolarizing the cells, K + leaves hair cells in perilymph, and it is then circulated back to endolymph across the lateral cochlear wall. In theory, this process entails a continuous and unidirectional current carried by apical K + channels and basolateral K + uptake transporters in both the marginal cell and syncytial layers of the lateral wall. The transporters regulate intracellular and extracellular [K + ], allowing the channels to form K + diffusion potentials across each of the two layers. These diffusion potentials govern the EP. What remains uncertain is whether these transport mechanisms accumulating across diverse cell layers make up a continuous circulation current in the lateral wall and how this current might affect the characteristics of the endolymph. To address this question, we developed an electrophysiological model that incorporates channels and transporters of the lateral wall and channels of hair cells that derive a circulation current. The simulation replicated normal experimental EP values and reproduced experimentally measured changes in the EP and intra-and extracellular [K + ] in the lateral wall when different transporters and channels were blocked. The model predicts that, under these different conditions, the circulation current's contribution to the EP arises from different sources. Finally, our model also accurately simulated EP loss in a mouse model of a chloride channelopathy associated with deafness.hearing | homeostasis | inner ear | ion transport | modeling

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“…Cochlear microphonic (CM) potentials are extracellular potentials derived from the transducer currents of the OHCs (1,(26)(27)(28), and their symmetrical nature is known to result from the presence of the TM biasing the operating point of the hair bundle (21,29). Although the TM is detached from the spiral limbus in the Otoa EGFP/EGFP mice, the CM potentials recorded from the round window of Otoa EGFP/EGFP mice are similar to those recorded from WT mice (Fig.…”

Section: Cochlear Microphonic Potentials Are Symmetrical In Otoa Egfpmentioning

confidence: 91%

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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Fine structure of the intracochlear potential field. I. The silent current

Cited by 123 publications

References 34 publications

Immunohistochemical Localization of the Na-K-Cl Co-transporter (NKCC1) in the Gerbil Inner Ear

Immunohistochemical Localization of the Na-K-Cl Co-transporter (NKCC1) in the Gerbil Inner Ear

Computational model of a circulation current that controls electrochemical properties in the mammalian cochlea

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

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