Differentiation of inner ear fibrocytes according to their ion transport related activity

Spicer, Samuel S.; Schulte, Bradley A.

doi:10.1016/0378-5955(91)90153-z

Cited by 230 publications

(187 citation statements)

References 30 publications

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“…It has been proposed that K + efflux from scala media at the organ of Corti cycles back to the stria vascularis by diffusion through extracellular and/or intracellular routes to the spiral ligament and then moves through the fibrocytes to the stria (Spicer and Schulte 1991;Weber et al 2001). Since the type II and IV fibrocytes occupy the space in the lateral wall between the stria vascularis and the organ of Corti (Spicer and Schulte 1991), the loss of these fibrocytes in the spiral ligament could reduce the flux of K + supplying the stria vascularis and thereby the secretory flux into scala media. The pattern of fibrocyte loss in old CD-1 mice corresponded with that of the hair cell degeneration found in present and previous studies, i.e., the hair cell loss started from the basal turn and advanced to the apical turn with aging (Le Calvez et al 1998a;Shone et al 1991).…”

Section: Discussionmentioning

confidence: 99%

“…6D) at the lower part of the spiral ligament compared with young CD-1 mice (n = 4). The location of the different types of fibrocytes is illustrated in Figure 7, based on the classification made by Spicer and Schulte (1991) and Schulte and Schmiedt (1992). The young group of CD-1 mice had a clear but less severe cell loss in the type IV fibrocytes of the basal turn (Fig.…”

Section: Cd-1 Mouse Strainmentioning

confidence: 99%

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Age-Related Changes in Cochlear Endolymphatic Potassium and Potential in CD-1 and CBA/CaJ Mice

Marcus

2003

JARO - Journal of the Association for Research in Otolaryngolog

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The CD-1 mouse strain is known to have early onset of hearing loss that is progressive with aging. We sought to determine whether a disturbance of K + homeostasis and pathological changes in the cochlear lateral wall were involved in the age-related hearing loss (AHL) of CD-1 as compared to the CBA/CaJ strain which has minimal AHL. In the present study, the endocochlear potential (EP) and endolymphatic K + concentration ([K + ] e ) were measured in both strains of mice with double-barrel microelectrodes at ''young'' (1-2 mo) and ''old'' (5-9 mo) ages. CBA/ CaJ mice displayed no changes with aging in EP and [K + ] e of the basal turn. In the apical turn, there was a small positive shift of the EP (10 mV) with aging under both normoxic and acute anoxic conditions ()EP), without any change of [K + ] e . Further, there were no obvious pathological changes in the lateral wall of CBA/CaJ mice. By contrast, old CD-1 mice displayed a significantly reduced [K + ] e by 30% in both basal and apical turns with no significant changes in normoxic EP. The )EP in the apical turn was significantly reduced in magnitude by 6 mV. A severe loss of cells with aging was observed in the region of type IV fibrocytes of the apical and basal turns and of type II fibrocytes in the basal turn. A complete degeneration of organ of Corti was also observed at the basal turn of old CD-1 mice, as well as a basalward decline of spiral ganglion neuron density. The pathological changes in spiral ligament of CD-1 mice were similar to those of an inbred mouse strain C57BL/6J that expresses an AHL gene (ahl) and might be a primary etiology of AHL of CD-1 mice. These findings have ramifications for our understanding of AHL and for interpretation of genetic mutations in a CD-1 background.

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Section: Discussionmentioning

confidence: 99%

Section: Cd-1 Mouse Strainmentioning

confidence: 99%

Age-Related Changes in Cochlear Endolymphatic Potassium and Potential in CD-1 and CBA/CaJ Mice

Marcus

2003

JARO - Journal of the Association for Research in Otolaryngolog

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“…There was no sign of regeneration of these cells in the 8-week animals. Loss of type I and II ®-brocytes [normally concentrated in the spiral prominence region of the ligament (Spicer and Schulte 1991)] was also seen at higher exposure levels (³112 dB). Degeneration of type III ®brocytes, which line the ligament next to the temporal bone, was never detectable.…”

Section: Overview Of Noise-induced Histopathology In the Mouse Cochleamentioning

confidence: 98%

“…Thus, the damage to both type II and type IV ®brocytes in the spiral ligament may occur secondarily to excessive K +¯u x through transduction channels or excessive production of glutamate or its analogs by IHCs. The idea that damage to the transduction apparatus, i.e., stereocilia, could locally reduce excessive K +¯u x during an acoustic overexposure is intriguing in light of the observation that both type II and type IV ®brocytes express a number of ion transporters including the Na + /K + -ATPase and the Na + /K + /Cl ) cotransporter and that both cell types have been implicated in the recycling of K + back to the stria vascularis (Spicer and Schulte 1991). It is possible that sound-induced K + overload leads to degeneration of these cell types.…”

Section: Mechanisms Of Noise Damagementioning

confidence: 99%

Dynamics of Noise-Induced Cellular Injury and Repair in the Mouse Cochlea

Wang

Hirose

Liberman

2002

JARO

486

450

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To assess the dynamics of noise-induced tissue injury and repair, groups of CBA/CaJ mice were exposed to an octave-band noise for 2 hours at levels of 94, 100, 106, 112, or 116 dB SPL and evaluated at survival times of 0, 12, 24 hours or 1, 2, or 8 weeks. Functional change, assessed via auditory brainstem response (ABR), ranged from a reversible threshold shift (at 94 dB) to a profound permanent loss (at 116 dB). Light microscopic histopathology was assessed in serial thick plastic sections and involved quantitative evaluation of most major cell types within the cochlear duct, including hair cells (and their stereocilia), supporting cells, ganglion cells, spiral ligament ®-brocytes, spiral limbus ®brocytes, and the stria vascularis. Morphometry allowed patterns of damage to be systematically assessed as functions of (1) cochlear location, (2) exposure level, and (3) postexposure survival. Insights into mechanisms of acute and chronic noise-induced cellular damage are discussed.

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“…Morphological and cytochemical traits have led to the recognition of four types of fibrocytes (Spicer and Schulte 1991). The different fibrocyte types are found preferentially in different sites within the spiral ligament, but it is often necessary to employ electron microscopy or immunostaining to positively identify individual cell types.…”

Section: Introductionmentioning

confidence: 99%

Immunocytochemical Traits of Type IV Fibrocytes and Their Possible Relations to Cochlear Function and Pathology

Adams

2009

JARO

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One of the more consistent and least understood changes in the aging human cochlea is the progressive loss of fibrocytes within the spiral ligament. This report presents an animal model for type IV fibrocyte loss, along with immunocytochemical evidence that noise-induced loss of these cells may account for previously unexplained hearing losses. The remarkably low threshold for noise-induced loss of type IV fibrocytes, approximately 24 dB less than the threshold for adjacent hair cell destruction, may account for the prevalence of missing fibrocytes in humans. In mice, changes in the spectrum of traumatizing noise had little effect upon the site of loss of the fibrocytes, suggesting that the primary site of damage that induced the loss was the basal-most cochlear turn, a site expected to be damaged by all three noise bands. Type IV fibrocytes were found to immunostain for connective tissue growth factor (CTGF) and for transforming growth factor beta receptor 3, a receptor that is known to activate CTGF expression. Type IV fibrocytes lack immunostaining for adenosine triphosphatase and connexins that are key players in potassium ion uptake and transmission, which suggests that they play little, if any, role in potassium recycling from perilymphatic space to the endolymphatic space. Consequently, their loss probably does not directly reduce this process. Immunostaining for a receptor for CTGF, low-density-lipoprotein-related protein 1, indicated that CTGF acts as an autocrine and a paracrine agent within the cochlea. The lack of CTGF paracrine effects following noise-induced loss of type IV fibrocytes may account for previously unexplained hearing losses.

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Differentiation of inner ear fibrocytes according to their ion transport related activity

Cited by 230 publications

References 30 publications

Age-Related Changes in Cochlear Endolymphatic Potassium and Potential in CD-1 and CBA/CaJ Mice

Age-Related Changes in Cochlear Endolymphatic Potassium and Potential in CD-1 and CBA/CaJ Mice

Dynamics of Noise-Induced Cellular Injury and Repair in the Mouse Cochlea

Immunocytochemical Traits of Type IV Fibrocytes and Their Possible Relations to Cochlear Function and Pathology

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