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Results for “Labyrinth Supporting Cells”

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PubMed2002

Sensory organ development in the inner ear: molecular and cellular mechanisms.

The molecular mechanisms underlying the specification of sensory organs in the inner ear and the development of hair and supporting cells within these organs are described. The different organs are all derived from a common pro-sensory region, and may be specified by their proximity to the boundaries between compartments - broad domains within the otocyst defined by the asymmetric expression patterns of transcription factors. Activation of Notch may specify the pro-sensory region, and lateral inhibition mediated by Notch signalling influences whether cells of common lineage in a sensory patch differentiate as either hair cells or supporting cells. The transcription factors Math1 and Brn3.1 are required for hair cell differentiation, and supporting cells express negative regulators of neurogenesis, Hes1 and Hes5. Retinoic acid and thyroid hormone influence early aspects and timing of hair cell differentiation, respectively. Development of the hair cell's mechanosensory hair bundle involves interactions between the cytoskeleton, cell-surface adhesion molecules, receptors and associated extracellular matrix.

Animals↗

PubMed1982

Cochlear cytoarchitecture and ribostamycin ototoxicity.

Ribostamycin ototoxicity was tested in a group of 28 albino guinea-pigs of both sexes, body-weight about 250-450 g with auricular Prayer's reflex present. The mounting of the cochlea on a metal support and the scanning electron microscope observations are described, The cochleacytogram of the group treated daily with 200 mg/kg ten days consecutively is comparable to that of the non-treated group.

Animals↗

PubMed1996

Postnatal changes in the reticular lamina of the guinea pig organ of Corti.

The dimensions of the apical surfaces of hair cells were measured in guinea pigs, aged from 3 weeks before term to 25 weeks after birth. In the basal two-thirds of the cochlea, the apical surfaces of the outer hair cells and their supporting cells changed with age, shrinking in a direction radial across the cochlear duct. There was an associated widening of the angle of the 'V' of the rows of stereocilia. Further apically, between 12 and 16 mm from the base of the cochlea, the outer hair cells and their supporting cells underwent the opposite change, becoming wider in a radial direction with age. The changes were seen before birth and continued for more than 3 weeks after birth. The results suggest that the guinea pig cochlea continues certain developmental processes for a considerable time after birth.

Aging↗

PubMed1999

Glutamate-like immunoreactivity during hair cell recovery after gentamicin exposure in the chinchilla vestibular sensory periphery.

OBJECTIVE: Determine the expression of glutamate by immunohistochemistry in normal and recovering vestibular hair cells in the chinchilla crista ampullaris after gentamicin ototoxicity. STUDY DESIGN: In five groups of three animals each, ototoxicity was produced by placing gentamicin (50 microg)-impregnated Gelfoam pellets within the perilymphatic space of the superior semicircular canal. Animals were sacrificed at 1, 2, 4, 8, and 16 weeks after treatment. A group of normal (n=3) animals was also processed. METHODS: For the detection of glutamate the inner ears of these animals were dissected, and the horizontal cristae ampullaris embedded in plastic. Two-micron-thick tissue sections were obtained and incubated with monoclonal antibodies against glutamate. The immunoreaction was detected using the avidinbiotinylated-complex technique and diaminobenzidine was the chromogen. RESULTS: Normal sensory epithelia demonstrated type I and type II hair cells with moderate glutamate-like immunoreactivity. Supporting cells demonstrated no glutamate-like immunoreactivity. Afferent nerve fibers and calyxes surrounding type I hair cells demonstrated strong glutamate-like immunoreactivity. At 1 and 2 weeks after treatment the few type II hair cells surviving ototoxic treatment (15%-18%) contained moderate glutamate-like immunoreactivity, supporting cells showed no immunoreactivity, and nerve terminals and fibers displayed strong immunoreactivity. At 4 and 8 weeks after treatment, recovered hair cells (80%) had greater glutamate-like immunoreactivity when compared with normal hair cells, supporting cells displayed no glutamate-like immunoreactivity, and afferent fibers contained strong glutamate-like immunoreactivity. At 16 weeks, glutamate-like immunoreactivity in hair cells returned to normal level. CONCLUSION: Glutamate may be used as an indicator of hair cell differentiation and as an index of the molecular recovery of hair cells after ototoxicity.

Animals↗

PubMed2004

[Isolation of partial outer supporting cells from guinea pig cochlea].

OBJECTIVE: To investigate the method of isolating partial outer supporting cells (Deiters' cells, Hensen cells and Outer pillar cells) from guinea-pig cochlea and to try to establish the morphological criteria for these outer supporting cells viability. METHOD: The basal membrane was dissected from the pigmental guinea pig cochlea, and th incubated with enzyme (0.5 mg/ml), then mechanically trituated by micropipetee. RESULT: A large number of living Deiters' cells and Hensen cells could be obtained from the guinea pig cochlear which kept a good condition in the next eight hours. However, the isolated outer pillar cells, with a more vulnerable viability, had a low yield and degenerated in the followed five hours. CONCLUSION: The key to success in isolating outer supporting cells, mainly Deiters' cells and Hensen's cells, from the guinea pig cochlea is to familiarize with the anatomical characteristics of the cochlea and to get the intact organ of Corti, as well as to increase the concentration of enzyme. Moreever, the later four criteria for outer hair cells viability are also fit well for these isolated Deiters' cells, Hensen's cells and Outer pillar cells.

Animals↗

PubMed2003

Expression of glutamate transporter GLAST in the developing mouse cochlea.

The immunohistochemical localization of glutamate transporter GLAST in the developing mouse cochlea was studied at different ages between 0 and 30 days after birth (DAB). In the adult mouse cochlea, intense GLAST-like immunoreactivity was found in the supporting cells adjacent to the inner hair cells of the organ of Corti, the type II and suprastrial fibrocytes of the cochlear lateral wall, the fibrocytes of the spiral limbus and the satellite cells surrounding the spiral ganglion cells. At 0 DAB, weak GLAST-like immunoreactivity was found in the supporting cells around the immature inner hair cells. Immature fibrocytes in the cochlea were also positively immunostained. At 3 DAB, weak immunostaining of GLAST appeared in the immature satellite cells in the spiral ganglion. The GLAST-like immunoreactivity in the supporting cells around the inner hair cells, in the fiborocytes in the spiral ligament and the spiral limbus and in the satellite cells in the spiral ganglion increased progressively during the second postnatal week, and reached the adult level at 15 DAB. This time course correlates with the electrophysiological onset and maturation of the mouse auditory function, which is mediated by glutamatergic neurotransmission. These results suggest that the expression of GLAST may be needed for the efficient removal and metabolism of the released glutamate in the cochlea and may play important roles in the onset and maturation of the auditory system.

Amino Acid Transport System X-AG↗

PubMed2000

Directional rectification of gap junctional voltage gating between dieters cells in the inner ear of guinea pig.

Deiters cells (DCs) are the cochlear supporting cells in inner ear and contain multiple gap junction connexin genes, which when mutated can induce hearing loss. In the present study, the gap junctions between DCs were investigated by a double voltage clamp technique. Besides asymmetric responses to the polarities of transjunctional voltage (V(j)) and transmembrane potential (V(m)), the channels were also sensitive to which cell side was stimulated in a cell pair, i.e. voltage gating had directional dependence. The direction-dependent voltage gating could result in asymmetric current flow between the cells and influenced K(+) passage. Multiple connexins may constitute non-homotypic channels with directional dependence of voltage gating to mediate functional gap junction pathways in the cochlea. This may explain how a single connexin mutation can produce hearing loss.

Animals↗

PubMed1984

Microtubules in the cochlea of the hypothyroid developing rat.

In order to study the effects of hypothyroidism on the development of microtubules in the cochlea, rat pups were rendered hypothyroid by daily administration of propylthiouracil. Microtubules were studied by immunofluorescence and electron microscopy. The absence of immunostaining of pillar cells with antimicrotubule or antitubulin antibodies was correlated with a retarded morphological development of microtubules within these same structures. The above alterations induced an abnormal development of pillar cells, non-appearance of the tunnel of Corti, and stunted epithelial growth. In contrast, a distinct immunoreaction was observed under the outer hair cells. This was attributed to abnormal persistence of afferent dendrites containing microtubules. The results suggest that, while the effect of thyroid hormone on microtubules in afferent cochlear dendrites could not be demonstrated, thyroid hormone is necessary for the normal development of microtubules in epithelial structures.

Animals↗

PubMed2003

Cell type-specific reduction of beta tubulin isotypes synthesized in the developing gerbil organ of Corti.

There are seven isotypic forms of the microtubule protein beta tubulin in mammals, but not all isotypes are synthesized in every cell type. In the adult organ of Corti, each of the five major cell types synthesizes a different subset of isotypes. Inner hair cells synthesize only betaI and betaII tubulin, while outer hair cells make betaI and betaIV tubulin. Only betaII and betaIV tubulin are found in inner and outer pillar cells, while betaI, betaII, and betaIV tubulin are present in Deiters cells, and betaI, betaII and betaIII tubulin are found in organ of Corti dendrites. During post-natal organ of Corti development in the gerbil, microtubules are elaborated in an orderly temporal sequence beginning with hair cells, followed by pillar cells and Deiters cells. Using beta tubulin isotype-specific antibodies, we show that, in the gerbil cochlea, the same three isotypes are present in each cell type at birth, and that a cell type-specific reduction in the isotypes synthesized occurs in hair cells and pillar cells at an unusually late stage in development. No beta tubulin isotypes were detected in mature afferent dendrites, but we show that this is because few microtubules are present in mature dendrites. In addition, we show that primary cilia in inner hair cells, a feature of early development, persist much later than previously reported. The findings represent the first description of developmental cell type-specific reductions in tubulin isotypes in any system.

Aging↗

PubMed1994

Scar formation in the vestibular sensory epithelium after aminoglycoside toxicity.

Hair cell degeneration and the repair process due to differing types of trauma have been studied extensively in the organ of Corti. It has been determined that, during scar formation, after differing types of trauma to the auditory sensory system, the reticular lamina is maintained with adherens junctions and tight junctions. We investigated the repair process within the vestibular epithelium. Hair cell degeneration was induced by the unilateral application of streptomycin to the inner ears of guinea pigs. Whole mount preparations of all five vestibular organs were processed and examined by fluorescence, light and electron microscopy. Scar formation was seen as early as 4 days post-treatment with streptomycin and was noted to coincide with hair cell degeneration. Neighboring supporting cells swelled and filled the space beneath the degenerating hair cell. Between three and five supporting cells participate in the reparative process. The distribution of cytokeratin is also altered during scar formation. The area once occupied by the hair cell becomes filled with cytokeratin-rich processes of supporting cells. It appears that differing numbers of supporting cells are involved in the reparative process within the vestibular sensory epithelium as compared to the auditory system. The reticular lamina remains intact at all times. This may possibly prevent mixing of fluids between different compartments in the inner ear and dysfunction of the vestibular sensory organs.

Actins↗

PubMed1991

[Study of the mechanism of supporting cells repairing the organ of Corti in terms of cell kinetics--nuclear DNA synthesis of supporting cell of the organ of Corti in the cochlea damaged by nitromin administration].

3H-thymidine autoradiography in vivo was carried out on normal mature mice, whose organs of Corti were securely damaged by Nitrogen Mustard-N-oxide (nitromin). The cell kinetics of supporting cells of the organ of Corti were examined and relation between these changes and mechanisms of supporting cells to maintain the organ of Corti was discussed in this paper. A few grains in various kinds of supporting cells in S stage, which were not found in control mice without nitromin injection, were discovered. Those were detected in Hensen's cell, Deiters' cell, Claudius' cells, and inner phalangeal cell. Mitosis was seen in one Claudius' cell in addition. Therefore some supporting cells seem to be able to synthesize DNA and proliferate in the acutely damaged organ of Corti even in mature cochlea and those in G0 stage begin to go around cell cycle as occasion demands. Although labelled supporting cells decreased over time, the portion of supporting cell is likely to change in proportion as the extension of damage in the organ of Corti. If this new dynamic change of cell kinetics in the acutely damaged organ of Corti means the reaction to repair the organ of Corti, the supporting cells seem to have a reasonable role to maintain the organ of Corti including repairment of reticular lamina.

Animals↗

PubMed1996

Hair cell precursors are ultrastructurally indistinguishable from mature support cells in the ear of a postembryonic fish.

The ultrastructure of S-phase cells in the postembryonic fish ear was compared with that of mature support cells. S-phase cells were identified by injecting animals with [3H]thymidine and sacrificing 3 h later. Sensory epithelia (saccules, utricles, and canals) were processed for light-level autoradiography. Sections containing thymidine-labeled cells were re-embedded and re-examined using transmission electron microscopy. The results indicate that S-phase cells differ from mature support cells only in nuclear position and shape. Otherwise their cytoplasmic characteristics are indistinguishable. Both cell types, on the other hand, are readily distinguishable from hair cells. These data provide ultrastructural evidence for the ability of mature support cells to enter the cell cycle in postembryonic vertebrates.

Animals↗

PubMed2005

Adeno-associated virus-mediated gene transfer to hair cells and support cells of the murine cochlea.

More than 28 million Americans suffer from various forms of hearing loss. The lack of effective treatments for many forms of hearing disorders has prompted interest in the potential application of gene delivery techniques to treat both inherited and pathological hearing disorders. However, to develop a gene therapy strategy that will successfully treat hearing disorders, appropriate vectors that are capable of transducing cochlear hair cells and support cells must be identified. In the present study, we examined the efficiency with which AAV vectors (serotypes 1, 2, and 5) transduce hair cells and support cells in cochlear explants from P0 and E13 mice. We further examined the ability of the CBA and GFAP promoters to drive expression of a GFP marker gene in hair cells and support cells. Robust GFP expression was observed in hair cells and support cells following transduction of primary murine cochlear explants with AAV serotypes 1 and 2, but not serotype 5. The CBA promoter predominantly drove GFP expression in hair cells. In contrast, strong expression from the GFAP promoter was observed primarily in support cells. Thus, using AAV vectors and specific promoters, cell-type-specific expression of transgenes can be established within the cochlea.

Animals↗

PubMed2006

Distinct and gradient distributions of connexin26 and connexin30 in the cochlear sensory epithelium of guinea pigs.

Connexin26 (Cx26) and Cx30 are predominant isoforms of gap junction channels in the cochlea and play a critical role in hearing. In this study, the cellular distributions of Cx26 and Cx30 in the cochlear sensory epithelium of guinea pigs were examined by immunofluorescent staining and confocal microscopy in whole mounts of the cochlear sensory epithelium and dissociated cell preparations. The expression of Cx26 and Cx30 demonstrated a longitudinal gradient distribution in the epithelium and was reduced threefold from the cochlear apex to base. The reduction was more pronounced in the Deiters cells and pillar cells than in the Hensen cells. Cx26 was expressed in all types of supporting cells, but little Cx30 labeling was seen in the Hensen cells. Cx26 expression in the Hensen cells was concentrated mainly in the second and third rows, forming a distinct band along the sensory epithelium at its outer region. In the dissociated Deiters cells and pillar cells, Cx30 showed dense labeling at the cell bodies and processes in the reticular lamina. Cx26 labeling largely overlapped that of Cx30 in these regions. Cx26 and Cx30 were also coexpressed in the gap junctional plaques between Claudius cells. Neither Cx26 nor Cx30 labeling was seen in the hair cells and spiral ganglion neurons. These observations demonstrate that Cx26 and Cx30 have a longitudinal gradient distribution and distinct cellular expression in the auditory sensory epithelium. This further supports our previous reports that Cx26 and Cx30 can solely and concertedly perform different functions in the cochlea.

Animals↗

PubMed2004

Survival of adult spiral ganglion neurons requires erbB receptor signaling in the inner ear.

Degeneration of cochlear sensory neurons is an important cause of hearing loss, but the mechanisms that maintain the survival of adult cochlear sensory neurons are not clearly defined. We now provide evidence implicating the neuregulin (NRG)-erbB receptor signaling pathway in this process. We found that NRG1 is expressed by spiral ganglion neurons (SGNs), whereas erbB2 and erbB3 are expressed by supporting cells of the organ of Corti, suggesting that these molecules mediate interactions between these cells. Transgenic mice in which erbB signaling in adult supporting cells is disrupted by expression of a dominant-negative erbB receptor show severe hearing loss and 80% postnatal loss of type-I SGNs without concomitant loss of the sensory cells that they contact. Quantitative RT-PCR analysis of neurotrophic factor expression shows a specific downregulation in expression of neurotrophin-3 (NT3) in the transgenic cochleas before the onset of neuronal death. Because NT3 is critical for survival of type I SGNs during development, these results suggest that it plays similar roles in the adult. Together, the data indicate that adult cochlear supporting cells provide critical trophic support to the neurons, that survival of postnatal cochlear sensory neurons depends on reciprocal interactions between neurons and supporting cells, and that these interactions are mediated by NRG and neurotrophins.

Animals↗

PubMed1991

[Experimental cochlear damage by neomycin ear drops].

Damage caused by neomycin sulphate solution, identical in concentration to that in ear drops, was tested on the cochleas of 28 guinea pigs. Neomycin sulphate with dexamethasone sodium, and physiologic salt solutions were also tested. Only neomycin solutions damaged the cochlea, and even after only a single exposure. The damage after a single exposure was to the supporting cells and not to the hair cells. However, because of the importance of the supporting cells for normal hearing and because destruction of supporting cells leads to shedding of hair cells, the resulting functional impairment is similar. As a result of further exposure to neomycin the hair cells themselves are damaged, and there is also loss of cell hair. Damage to either the cells or to the hair causes hearing loss. From our work it is clear that in guinea pigs neomycin is absorbed from the middle ear into the inner ear and damages the cochlea. Increased exposure to neomycin increases the damage.

Animals↗

PubMed2001

ATP-induced movement of the stalks of isolated cochlear Deiters' cells.

Deiters' cells, a type of supporting cell in the sensory epithelium of the cochlea, the organ of Corti, have been found to have P2X and P2Y adenosine triphosphate (ATP) receptors on their surfaces. Activation of these receptors may alter the mechanical properties of Deiters' cells and thus of the organ itself. ATP was applied to Deiters' cells isolated from guinea pig cochlea and the tip of the cells' stalk monitored for an ATP induced movement. Application of 100 microM ATP to the cell body of isolated Deiters' cells induced a small, reversible movement of the cells' stalk whereas application of bathing media did not. Results suggest that in vivo endogenous extracellular ATP released from unidentified locations could alter cochlear mechanics.

Adenosine Triphosphate↗

PubMed2006

Supporting cell proliferation after hair cell injury in mature guinea pig cochlea in vivo.

In cold-blooded animals, lost sensory hair cells can be replaced via a process of regenerative cell proliferation of epithelial supporting cells. In contrast, in mammalian cochlea, receptor (hair) cells are believed to be produced only during embryogenesis; after maturity, sensory or supporting cell proliferation or regeneration are thought to occur neither under normal conditions nor after trauma. Using bromodeoxyuridine (BrdU) as a proliferation marker, we have assessed cell proliferation activity in the mature organ of Corti in the cochlea of young guinea pigs following severe damage to the outer hair cells induced by kanamycin sulfate and ethacrynic acid. Although limited, we have found BrdU-labeled nuclei in the regions of Deiters cells when BrdU is given for 3 days or longer. When BrdU is given for 10 days, at least one labeled nucleus can be observed in the organ of Corti in approximately half of the ears; proliferating cells typically appear as paired daughters, with one nucleus being displaced away from the basement membrane to the position expected of the hair cells. Double-staining with antibodies to cytokeratin, vimentin, and p27 have shown that the BrdU-labeled nuclei are located in cells phenotypically similar to Deiters cells. Most of the uptake of BrdU occurs 3-5 days following ototoxic insult, and the number of BrdU-labeled cells does not decrease until 30 days following insult. These findings indicate that Deiters cells in the mature mammalian cochlea maintain a limited competence to re-enter the cell cycle and proliferate after hair cell injury, and that they can survive at least for 1 month.

Animals↗