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PubMed1990

Immunohistochemistry and histochemistry of the inner ear gelatinous membranes and statoconia of the chick (Gallus domesticus).

This study was undertaken to investigate whether the gelatinous membranes (GMs) of the chick (Gallus domesticus) inner ear contain glycoproteins and proteoglycans, as is the case in mammals, and whether or not the relative concentrations of glycoproteins and proteoglycans change during development. We used electron-microscopic histochemistry with tannic acid, Alcian blue and ruthenium red and immunoperoxidase with monoclonal antibodies to fibronectin and keratan sulfate. Both techniques were applied to material from newly hatched chicks in various developmental stages. In hatchlings, tannic acid, which precipitates mainly proteoglycans, stained the mineralizing GMs of the utricle, saccule and lagenar macula darker than it did the nonmineralizing GMs of the cristae and tectorial membrane of the basilar papilla, while Alcian blue and ruthenium red stained all GMs in the vestibule and basilar papilla almost to the same degree. Antikeratan sulfate (a proteoglycan marker) stained the GMs intensively, while antifibronectin (glycoprotein monoclonal marker) stained them less intensively. In the mineralizing GMs of the embryos, the immunoreactivity (density) of keratan sulfate almost doubles between days 7 (stages 31) and 21 (stage 46), while the density of fibronectin does not seem to change as much. Different concentrations of glycoproteins and proteoglycans in each GM may impart to it the capacity to remain unmineralized, as is the case for cupulae of the vestibule and tectorial membrane of the basilar papilla, or mineralized, as is the case for the statoconial membrane of the maculae.

Animals↗
PubMed1992

The structural and functional aspects of hair cell regeneration in the chick as a result of exposure to intense sound.

This paper summarizes the structural and functional damage caused by intense sound exposure in neonatal chicks. Scanning electron microscopy has been used to follow the structural changes to the papilla and their subsequent repair. Pure-tone exposures produced a localized lesion consisting of tectorial membrane destruction, changes in surface organization of the papilla, and hair cell loss. The papilla underwent significant repair following the exposure and new hair cells could be identified on the sensory surface after 4 days of recovery. In addition, various evoked-potential methods provided an objective assessment of auditory function and demonstrated that the peripheral ear was severely impaired by overstimulation. Auditory function returned to near normal levels within 3 days postexposure. The inescapable conclusion from these observations was that hair cell regeneration had little to do with the functional recovery observed during the first 3 days. Tectorial membrane regeneration and the restoration of cochlear micromechanics were combined to form a hypothesis to account for the restoration of auditory function.

Acoustic Stimulation↗
PubMed1999

Constitutive expression of GlyCAM-1 core protein in the rat cochlea.

Glycosylation-dependent cell adhesion molecule-1 (GlyCAM-1) is a mucin-like glycoprotein previously identified on high endothelial venules (HEV) of lymph nodes and also in lactating mammary glands. A specifically glycosilated form of GlyCAM-1 on HEV has been shown to be a ligand for a leukocyte L-selectin, which plays an important role in leukocyte rolling along the inflamed endothelium. Here we report that GlyCAM-1 is also expressed in the cochlea. Immunohistochemistry revealed the lateral wall of the cochlea, tectorial membrane, modiolus, organ of corti, and spiral modiolar vein (SMV) to be strongly stained with polyclonal anti-GlyCAM-1 antibody. Moreover, RT-PCR of the cochlear tissue by the use of specific oligonucleotide primers for rat GlyCAM-1 generated a 378 bp product which was then verified by nucleotide sequencing to represent GlyCAM-1. Electron microscopic investigation revealed the presence of GlyCAM-1 over the entire lumenal surface of the vessels, and the basolateral infoldings in stria vascularis. However, soluble L-selectin or mAb MECA-79 which recognizes a carbohydrate epitope on functional L-selectin ligands bound only to the spiral ligament, tectorial membrane and modiolus. These observations suggest that GlyCAM-1 expressed in the cochlear region is heterogenous in terms of its glycosylation.

Animals↗
PubMed1999

Comparing in vitro, in situ, and in vivo experimental data in a three-dimensional model of mammalian cochlear mechanics.

Normal mammalian hearing is refined by amplification of the motion of the cochlear partition. This partition, comprising the organ of Corti sandwiched between the basilar and tectorial membranes, contains the outer hair cells that are thought to drive this amplification process. Force generation by outer hair cells has been studied extensively in vitro and in situ, but, to understand cochlear amplification fully, it is necessary to characterize the role played by each of the components of the cochlear partition in vivo. Observations of cochlear partition motion in vivo are severely restricted by its inaccessibility and sensitivity to surgical trauma, so, for the present study, a computer model has been used to simulate the operation of the cochlea under different experimental conditions. In this model, which uniquely retains much of the three-dimensional complexity of the real cochlea, the motions of the basilar and tectorial membranes are fundamentally different during in situ- and in vivo-like conditions. Furthermore, enhanced outer hair cell force generation in vitro leads paradoxically to a decrease in the gain of the cochlear amplifier during sound stimulation to the model in vivo. These results suggest that it is not possible to extrapolate directly from experimental observations made in vitro and in situ to the normal operation of the intact organ in vivo.

Acetylcholine↗
PubMedDate not supplied

Mutation in the zonadhesin-like domain of alpha-tectorin associated with autosomal dominant non-syndromic hearing loss.

A gene responsible for autosomal dominant non-syndromic hearing impairment in two families (DFNA8 and DFNA12) has recently been identified as TECTA encoding alpha-tectorin, a major component of the tectorial membrane. In these families, missense mutations within the zona pellucida domain of alpha-tectorin were associated with stable severe mid-frequency hearing loss. The present study reports linkage to DFNA12 in a new family with autosomal dominant high frequency hearing loss progressing from mild to moderate severity. The candidate region refined to 3.8 cM still contained the TECTA gene. A missense mutation (C1619S) was identified in the zonadhesin-like domain. This mutation abolishes the first of the vicinal cysteines (1619Cys-Gly-Leu- 1622Cys) present in the D4 von Willebrand factor (vWf) type D repeat. These results further support the involvement of TECTA mutations in autosomal dominant hearing impairment, and suggest that vicinal cysteines are involved in tectorial membrane matrix assembly.

Extracellular Matrix Proteins↗
PubMed1988

Cholecalcin (28-kDa CaBP) in the rat cochlea. Development in normal and hypothyroid animals. An immunocytochemical study.

The distribution of cholecalcin (28-kDa calcium-binding protein) in the cochlea of developing rats was followed by immunocytochemistry. In normal animals, the protein first appeared in utero in the cells of Kölliker's organ, a structure involved in the secretion of the tectorial membrane. The inner hair cells, followed by the outer hair cells, then became immunoreactive from the base of the cochlea to the apex. Their cuticular plate, the anchoring structure for stereocilia, was particularly labeled. The cells of Kölliker's organ lost their immunoreactivity after the first postnatal week, the time when they lose their secretory activity. During the same period, when the tunnel of Corti and the space of Nuel open, labeling appeared in the supporting cells. The neurons of the spiral ganglion were stained from the second postnatal week and the fibers of the cochlear nerve after the end of the first month. No difference was induced by thyroid deficiency until the second postnatal week. Thereafter, Kölliker's organ did not transform and its cholecalcin immunoreactivity persisted, together with the secretory activity. As a result, the tectorial membrane was greatly distorted and the mechanical properties of the organ of Corti were dramatically impaired. The supporting cells were labeled although the tunnel of Corti and the space of Nuel did not open. Staining of the spiral ganglion neurons was delayed. All the nervous structures of the cochlea were, however, stained at the end of the first postnatal month, as in normal animals, despite the irreversible complete deafness. Cholecalcin is thus present during development of the cochlea in both non-neuronal and neuronal structures, and is probably involved in very different processes in various types of cells.

Aging↗
PubMed2004

Spontaneous otoacoustic emissions in monitor lizards.

Monitors (all of which belong to the genus Varanus) make up a very uniform family of often large lizards. They have a large auditory papilla that is not highly specialized, but is divided into two unequal sub-papillae. All hair cells are covered by a tectorial membrane. Spontaneous otoacoustic emissions (SOAE) were examined in Cape monitor lizards (Varanus exanthematicus) and found between 1.08 and 2.91 kHz (at 32 degrees C) and with levels between -2.8 and 25.8 dB SPL. The frequency of SOAE was temperature dependent, with a maximal shift of 0.07 octaves/degrees C. All SOAE could be suppressed by external tones, most easily by tones near the center frequency and thus suppression tuning curves were V-shaped. In addition, SOAE could be facilitated by external tones, the amplitude increasing up to 10 dB. The most effective tones were generally those between 0.33 and 0.75 octaves above the respective center frequency of the SOAE. External tones could also change the center frequency of SOAE by up to several hundred Hz, most tones causing frequency 'pushing'. Compared to SOAE of other lizards, Varanus SOAE have larger amplitudes and show larger frequency shifts with temperature. Both of these features may be the result of the coupling of large numbers of hair cells via the continuous tectorial membrane.

Acoustic Stimulation↗
PubMed1996

Tuning, spontaneous activity and tonotopic map in chicken cochlear ganglion neurons following sound-induced hair cell loss and regeneration.

Adult chickens were exposed for 48 h to a 525 Hz, 120 dB SPL tone that destroyed the hair cells and tectorial membrane in a crescent-shaped patch along the abneural edge of the basilar papilla. Single-unit recordings were obtained from cochlear ganglion neurons 0-1, 5, 14 and 28 days post-exposure to determine what effect the cochlear lesion had on neural discharge patterns and if the discharge patterns fully recovered. Immediately after exposure, the tuning curves were extremely broad and CF thresholds were elevated by 30-40 dB. In addition, the average spontaneous rate and percentage of neurons with interspike interval histograms with preferred intervals were greatly reduced. Tuning curves and spontaneous activity started to recover by 5 days post-exposure; however, some W-shaped tuning curves with two distinct tips and a hypersensitive tail were observed at this time. W-shaped tuning curves disappeared and spontaneous activity recovered to normal levels 14-28 days post-exposure. However, the CF thresholds of the most sensitive neurons were still slightly elevated, tuning curve slopes below CF were shallower than normal, and thresholds in the low-frequency tail of the tuning curves were often hypersensitive. These functional deficits were most closely associated with residual damage to the upper fibrous layer of the tectorial membrane. To determine if the cochlear frequency-place map was altered by the cochlear lesion, four physiologically characterized neurons were labeled with biocytin at 5 days post-exposure. The CFs of the labeled neurons were consistent with the normal frequency-place map (Chen et al. (1994) Hearing Research 81, 130-136) indicating that the tonotopic map was not altered.

Acoustic Stimulation↗
PubMed1999

Non-coating fixation techniques or redundancy of conductive coating, low kV FE-SEM operation and combined SEM/TEM of biological tissues.

Non-coating fixation methods, in particular the tannic acid/arginine/osmium tetroxide procedure, are employed for a number of reasons on the guinea-pig organ of Corti hair cell stereocilia glycocalyx and the imprints of the stereocilia at the bottom side of the tectorial membrane, and on the rat and cat intestinal epithelial microvilli glycocalyx and mucus-producing goblet cells. These methods are used firstly to confirm that non-coating prepared specimens can be embedded for TEM observation at 60-100 kV without loss of detail information, and these images can be compared with cryo-FE-SEM images of the same structure/tissue. Secondly, they show that specimens treated according non-coating techniques become optimally preserved and electrically conductive, so that no external conductive coating is required. In this way a comparison of images of subsequent fresh fracture faces is possible without a decrease in information on detail, which otherwise could happen after subsequent coating layers required after standard fixation. Thirdly, they show that non-coating methods can be used quite well with low accelerating voltages because the osmium-tannic acid complex in the specimen surface produces a large number of backscattered and secondary electrons in the surface layer, showing in particular surface phenomena. Fourthly, they show that with an optimal non-coating preservation, in combination with a well-balanced pre-fixation mixture, preparation artefacts due to extraction and even dehydration and drying are minimized. This is compared with images of the organ of Corti hair cells treated with a so-called three-aldehyde pre-fixation mixture, which causes disrupted stereocilia to cling onto the bottom side of the tectorial membrane.

Animals↗
PubMed2003

Time course of inner ear degeneration and deafness in mice lacking the Kir4.1 potassium channel subunit.

The Kir4.1 gene (KCNJ10) encodes an inwardly rectifying K(+) channel subunit abundantly expressed in the CNS. Its expression in the mammalian inner ear has been suggested but its function in vivo in the inner ear is unknown. Because diverse human hereditary deafness syndromes are associated with mutations in K(+) channels, we examined auditory function and inner ear structure in mice with a genetically inactivated Kir4.1 K(+) channel subunit. Startle response experiments suggest that Kir4.1-/- mice are profoundly deaf, whereas Kir4.1+/- mice react like wild-type mice to acoustic stimuli. In Kir4.1-/- mice, the Reissner membrane is collapsed, the tectorial membrane is swollen, and type I hair cells and spiral ganglion neurons as well as their central processes degenerate over the first postnatal weeks. In the vestibular ganglia, neuronal cell death with apoptotic features is also observed. Immunostaining reveals that Kir4.1 is strongly expressed in stria vascularis of wild-type but not Kir4.1-/- mice. Within the spiral ganglion, Kir4.1 labeling was detected on satellite cells surrounding spiral ganglion neurons and axons. We conclude that Kir4.1 is crucial for normal development of the cochlea and hearing, via two distinct aspects of extracellular K(+) homeostasis: (1). in stria vascularis, Kir4.1 helps to generate the cochlear endolymph; and (2). in spiral and vestibular ganglia, Kir4.1 in surrounding glial cells helps to support the spiral and vestibular ganglion neurons and their projecting axons.

Animals↗
PubMedDate not supplied

Damage to the stria vascularis in the guinea pig by acute atoxyl intoxication.

The aim of the present study was to show the morphological degeneration at the ultrastructural level, after damaging the stria vascularis experimentally. The acute lesions, after acute atoxyl intoxication, occur after about 12 hours, and begin as a degeneration of both the marginal and the intermediate cells, whereas the basal cells remain mainly unaffected. The severely damaged marginal or intermediate cells may become loosened from the stria vascularis and rejected from it into the endolymphatic space. Under such conditions the basal cells may line the surface facing the endolymph, although this occurs very rarely. Intially, there may be a slight bulging of Reissner's membrane, but soon the membrane becomes depressed, and sometimes a total collapse occurs, with Reissner's membrane flattened over the tectorial membrane against the organ of Corti. It is only seldom that Reissner's membrane touches the strial surface. Mitochondrial degeneration with formation of intramitochondrial inclusion bodies is an interesting early finding in the damage pattern.

Animals↗
PubMed1985

Inner ear structure in the deaf and normally hearing Dalmatian dog.

Both cochleae of two 6-week-old Dalmatian dogs of the same litter were examined by means of surface specimens and histological section techniques. Basic quantitative data on the morphometry of the cochlear duct in the hearing (though hypopigmented) pup are presented. The cochlear ducts of the deaf (though normally coloured) pup exhibited in general the same alterations (collapse of the scala media) as described in the literature. In addition, we describe also the coalescence of membranous structures, projection of the tectorial membrane up to the spiral ligament and preservation of inner hair cells in the second (i.e. middle) cochlear coil. These new findings complement the previous data and indicate an alternative possible course of hereditary inner ear degeneration in the Dalmatian dog.

Animals↗
PubMed1991

The molecular and structural basis of hearing impairment in mice with the cpk mutant gene.

We studied hearing impairment and cochlear ultrastructure in C57BL/6J mice containing the cpk mutant gene. Heterozygous cpk/+ mutant mice, 6-8 months old, showed a marked hearing loss as demonstrated by auditory evoked potentials with some showing hearing loss at 90 db sound pressure. Ultrastructural studies of first cochlear turn disclosed the absence of organs of Corti, no tissues on the basilar membrane, scanty spiral ganglia, normal tectorial membrane, and vacuolation of the stria vascularis. Reissner's membrane is normal at the endolymphatic side, but transparent at the perilymphatic side. In the second turn the organ of Corti are normal but Nuel's space is full of debris. The cpk mutant mice have hearing impairment perhaps due to deficiencies of genes expressing vital basement membrane components.

Acoustic Stimulation↗
PubMed1992

Microstructures of the osseous spiral laminae in the bat cochlea: a scanning electron microscopic study.

The architecture and surface structures of the primary and secondary osseous spiral laminae in the cochlea of the bat, an animal able to hear high frequency sounds, were examined by scanning electron microscopy to understand the micromechanical adaptations of the bony supportive elements in the inner ear to the specific hearing function. The bat used was Myotis frater kaguyae. The myotis bat cochlea was seen to consist of a hook and a spiral portion with one and three-quarter turns and was characterized by: 1) a distinct ridge-like projection running spirally along the middle line on the vestibular leaf of the primary osseous spiral lamina; 2) a wide secondary osseous spiral lamina; and 3) a narrow spiral fissure between the primary and secondary osseous spiral laminae. The ridge on the primary osseous spiral lamina was 150 microns high in the hook and basal turn, then lowered toward apex, and flattened before the apical end. The surface structures appeared to provide a firm anchorage of the auditory teeth. The secondary osseous spiral lamina, which anchors the fibers of the basilar membrane, was sharply projected and measured 150 microns in width in the hook, and then narrowed gradually toward apex to disappear in the helicotrema. The spiral fissure for the basilar membrane was about 40 microns in width in the hook and about 120 microns in the apical turn. The findings suggest the presence of a narrow and rigid basilar membrane with a high amount of fibers and a strong bony support to the auditory teeth for scaffolding the tectorial membrane during intense vibration in response to high frequency sounds.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

Energy transduction in the cochlea.

Reasons are presented for considering that the properties of the travelling wave as described by von Békésy are inadequate by themselves to explain phenomena at the threshold of hearing as regards energetics and speed of acoustic transmission. The degree of "tuning" of the basilar membrane is also insufficient. Alternative propositions based on the physico-chemical properties and macromolecular physics of the tectorial membrane are offered. These proposals have both an experimental and theoretical basis. The final section indicates how several unresolved problems of cochlear function might be approached from this fresh standpoint.

Acoustics↗
PubMed1996

Distribution of beta-tectorin mRNA in the early posthatch and developing avian inner ear.

Expression of beta-tectorin mRNA in the inner ear of the embryonic and early posthatch (PH) chick was studied by in situ hybridisation. In the PH chick, beta-tectorin mRNA is expressed in the basilar papilla, in the clear and the cuboidal cells that lie either side of the papilla, in the striolar regions of the maculae, and in two small groups of cells lying adjacent to the midline in the cristae of the anterior and posterior ampullae. Expression of beta-tectorin is not observed in the lateral ampulla. In the sensory epithelia of the PH chick in which beta-tectorin mRNA is detected, expression is restricted to the supporting cell population. During development of the cochlear duct, beta-tectorin expression begins between embryonic (E) days 5 and 6. At E6, expression is observed throughout the length of the duct but is highest at the distal end. By E7, the pattern of expression is reversed and is highest at the proximal end of the cochlea, suggesting that a wave of high beta-tectorin expression passes disto-proximally along the papilla during E6 and E7. Expression of beta-tectorin mRNA is not detected in the homogene cells at any stage during the development of the cochlear duct, indicating that these cells do not synthesise one of the two major proteins of the avian tectorial membrane. The distribution of supporting cells expressing beta-tectorin mRNA in the different epithelia was compared with the distribution of sensory cells that have type B hair bundles, those with shaft links restricted to basal regions of their stereocilia, and sensory cells that have type A bundles, those with shaft links all over the entire surface of their stereocilia. Hair cells with type A hair bundles are never found in association with supporting cells expressing beta-tectorin. Although there is a correspondence in the basilar papilla and the maculae of the utriculus and lagena between the distribution of supporting cells expressing beta-tectorin mRNA and hair cells with type B bundles, this correlation does not generalise to the other sensory epithelia.

Animals↗
PubMedDate not supplied

Abnormal otoconia and calcification in the labyrinths of deaf Dalmatian dogs.

Abnormal mineral deposits from the membranous labyrinths of deaf Dalmatian puppies were examined microscopically. Most such deposits were located on the saccular otoconial membrane and were associated with collapse of the saccule and of Reissner's membrane. In both ears of one pup, crystals resembling otoconia were found on the surface of the stria vascularis. In two others, grossly abnormal crystals were seen on the utricular otoconial membrane, and in one of these crystals were also attached to the cupula of the left horizontal canal. In four animals the tectorial membrane was calcified. Most deposits consisted of apatite spherulites, but large multiple crystals (probably of calcite) were occasionally present. Some of the abnormal mineral deposits in the Dalmatian closely resemble those found in man, and they may originate in the same way.

Animals↗
PubMed2000

Targeted disruption of otog results in deafness and severe imbalance.

Genes specifically expressed in the inner ear are candidates to underlie hereditary nonsyndromic deafness. The gene Otog has been isolated from a mouse subtractive cDNA cochlear library. It encodes otogelin, an N-glycosylated protein that is present in the acellular membranes covering the six sensory epithelial patches of the inner ear: in the cochlea (the auditory sensory organ), the tectorial membrane (TM) over the organ of Corti; and in the vestibule (the balance sensory organ), the otoconial membranes over the utricular and saccular maculae as well as the cupulae over the cristae ampullares of the three semi-circular canals. These membranes are involved in the mechanotransduction process. Their movement, which is induced by sound in the cochlea or acceleration in the vestibule, results in the deflection of the stereocilia bundle at the apex of the sensory hair cells, which in turn opens the mechanotransduction channels located at the tip of the stereo-cilia. We sought to elucidate the role of otogelin in the auditory and vestibular functions by generating mice with a targeted disruption of Otog. In Otog-/- mice, both the vestibular and the auditory functions were impaired. Histological analysis of these mutants demonstrated that in the vestibule, otogelin is required for the anchoring of the otoconial membranes and cupulae to the neuroepithelia. In the cochlea, ultrastructural analysis of the TM indicated that otogelin is involved in the organization of its fibrillar network. Otogelin is likely to have a role in the resistance of this membrane to sound stimulation. These results support OTOG as a possible candidate gene for a human nonsyndromic form of deafness.

Acoustic Stimulation↗