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At least 325 records · Page 18Linked to original sources

Long-term effect of acoustic trauma on distortion product otoacoustic emissions in chickens.

Distortion product otoacoustic emissions (DPOAE), 2F1-F2, were measured in chickens before and after exposure to a 1.5-kHz pure tone presented at 120-dB sound-pressure level for 48 h. The low-level component of the DPOAE input/output function was shifted to the right at all frequencies immediately after the exposure with the greatest effect occurring at and above the exposure frequency. The slope of the high-level component of the input/output also increased significantly for test frequencies close to and above the exposure frequency so that the amplitude of the DPOAE was equal to or greater than normal at high stimulus levels. DPOAE obtained at the highest and lowest frequencies were almost normal after 8 weeks of recovery; however, the input/output functions near the exposure frequency showed almost no improvement over the 8-week recovery period. The lack of recovery could conceivably be due to residual damage to hair cells that survived the exposure or to incomplete regeneration of the tectorial membrane.

Acoustic Stimulation↗

The stretching nonlinearity of the basilar membrane in a cochlear model.

Recently it has been suggested that the stretching nonlinearity of the basilar membrane might be responsible for the observed nonlinear behaviour of basilar membrane motion. In the present study this type of nonlinearity is investigated, both by estimating its influence in an analytical manner, and by calculating its effect numerically, using a regular pertubation method. The conclusion reads that the stretching nonlinearity does not explain the observed nonlinear phenomena; not only is stretching negligible at normal sound levels, but it also fails to fit the data qualitatively, because of its typical hard-spring effect. In consequence, the origin of cochlear nonlinearity is not to be sought in the macromechanics of the inner ear, but in the more detailed processes in th organ of Corti-tectorial membrane complex.

Basilar Membrane↗

The ultrastructure of the basilar papilla of the budgerigar's inner ear.

The basilar papilla in the inner ear of the adult budgerigar was studied by scanning and transmission electron microscopy. The sickle-shaped basilar papilla has short hair bundles on the proximal tip and long ones on the distal tip. The tectorial membrane shows a honeycomb-like pattern and enclosed a hair bundle in its alveolus. The papilla consists of two different types of hair cells; short and tall hair cells. The short hair cells with large efferent nerve endings are located on the free basilar membrane in the inferior part. The tall hair cells with large afferent nerve endings are located in the superior part. The similarity and difference of the structure are discussed between the budgerigar and other birds, and between birds and mammals.

Animals↗

Retardation of cochlear maturation and impaired hair cell function caused by deletion of all known thyroid hormone receptors.

The deafness caused by early onset hypothyroidism indicates that thyroid hormone is essential for the development of hearing. We investigated the underlying roles of the TRalpha1 and TRbeta thyroid hormone receptors in the auditory system using receptor-deficient mice. TRalpha1 and TRbeta, which act as hormone-activated transcription factors, are encoded by the Thra and Thrb genes, respectively, and both are expressed in the developing cochlea. TRbeta is required for hearing because TRbeta-deficient (Thrb(tm1/tm1)) mice have a defective auditory-evoked brainstem response and retarded expression of a potassium current (I(K,f)) in the cochlear inner hair cells. Here, we show that although TRalpha1 is individually dispensable, TRalpha1 and TRbeta synergistically control an extended array of functions in postnatal cochlear development. Compared with Thrb(tm1/tm1) mice, the deletion of all TRs in Thra(tm1/tm1)Thrb(tm1/tm1) mice produces exacerbated and novel phenotypes, including delayed differentiation of the sensory epithelium, malformation of the tectorial membrane, impairment of electromechanical transduction in outer hair cells, and a low endocochlear potential. The induction of I(K,f) in inner hair cells was not markedly more retarded than in Thrb(tm1/tm1) mice, suggesting that this feature of hair cell maturation is primarily TRbeta-dependent. These results indicate that distinct pathways mediated by TRbeta alone or by TRbeta and TRalpha1 together facilitate control over an extended range of functions during the maturation of the cochlea.

Animals↗

Structure of the hairs on cochlear sensory cells.

A study of cochlear sensory hairs has been made using transmission and scanning electron microscopy. The structure of the hairs and the relation to the hair cells and to the tectorial membrane is described. A number of micrographs demonstrate both the inner structure of the hairs and their relation to the surrounding structures.

Animals↗

Spatiotemporal expression of otogelin in the developing and adult mouse inner ear.

Using a PCR-based subtractive method on cDNA from 2-day-old mouse cochlea, we identified a gene encoding otogelin, Otog, an inner ear specific glycoprotein expressed in all acellular structures. Here, we provide evidence that otogelin is detected as early as embryonic day 10 in the otic vesicle. At this stage, otogelin is detected in the epithelial cells which do not overlap with the myosin VIIA-expressing cells, namely the precursors of the hair cells, thus arguing for an early commitment of the two cell populations. Analysis of otogelin spatiotemporal cell distribution allows a molecular tracing for the contribution of the cochlear and vestibular inner ear supporting cells to the formation of the acellular structures. Throughout embryonic and adult life, the expression of the otogelin gene as monitored by LacZ inserted into Otog, and the abundance of the protein are greater in the vestibule than in the cochlea. In adult, otogelin is still produced by the vestibular supporting cells, which argues for a continuous process of otogelin renewal in the otoconial membranes and cupulae. In contrast, in the tectorial membrane, otogelin should be a long-lasting protein since both the otogelin gene and protein were almost undetectable in adult cochlear cells. The data are consistent with the requirement for otogelin in the attachment of the otoconial membranes and cupulae to their corresponding sensory epithelia as revealed in Otog -/- mice.

Aging↗

Distribution of glycoconjugates during cochlea development in mice: light microscopic lectin study.

During development, different epithelial cells in the mouse cochlea express different cell surface glycoconjugates, which may reflect membrane specialization. Some of the lectins tested in this study (SBA, succ-WGA, and PSA) labeled the sensory cells of the cochlea around birth. Other lectins (WGA, Con A, RCA-II, and PHA-E) labeled surfaces of the sensory cells, particularly the stereocilia, from early stages of development (gestation day (GD) 16) through 21 days after birth. These may be adhesion molecules needed to attach the newly forming tectorial membrane (TM) to the stereocilia. Lectin staining of the developing TM revealed that the substructures of the TM are biochemically distinct. Lectin staining also showed the temporal sequence of the expression of cytoplasmic glycoconjugates of the cochlear epithelium during development. Biochemical changes during development are probably the result of different cells being involved in the production of glycoconjugates, and may have functional significance, specifically with regard to the expression of adhesion and/or signaling molecules.

Animals↗

Finite element micromechanical modeling of the cochlea in three dimensions.

A new cochlear modeling technique has been developed in which the number of assumptions required in model formulation is significantly less than in previous modeling studies. The main new feature of the method is that it allows individual cellular and membrane components of the organ of Corti to be embedded within the model fluid in their true structural positions, with connections to neighboring elements reflecting anatomical geometry. The cochlea is divided into a three-dimensional finite element (3-D FE) network of nodes, connected by branches representing the local mechanical properties. The model system of simultaneous equations, obtained by applying continuity at each node, is solved iteratively using a variant of the conjugate gradient method. Here the formulation and implementation of the 3-D FE method are described. Force generation by outer hair cells is included and results are presented which demonstrate the effect of tectorial membrane and Deiters' cell mechanical properties on the effectiveness of the cochlear amplifier.

Animals↗

The etiology of idiopathic sudden sensorineural hearing loss. Experimental herpes simplex virus infection of the inner ear.

HYPOTHESIS: Experimentally induced herpes simplex virus type 1 (HSV-1) labyrinthitis provides a suitable model for idiopathic sudden sensorineural hearing loss (ISSHL). BACKGROUND: Viral labyrinthitis has been postulated to play a role in the pathophysiology of ISSHL. Circumstantial evidence is pointing at members of the herpes virus family. Experimental viral labyrinthitis elicited by various virus families leaves a virus-specific pattern of cochlear damage. Herpes viruses provide the best matching pattern in the distribution of cochlear damage when compared with ISSHL postmortem cochlear histopathology. METHODS: Herpetic viral labyrinthitis was induced in guinea pigs using perilymphatic inoculation with HSV-1. A control group was inoculated with the culture medium only. Infection was confirmed by the measurement of HSV antibodies. Hearing was monitored. Cochlear damage was evaluated by light and electron microscopy. RESULTS: In all HSV-1 inoculated animals, rapid loss of hearing occurred. Seroconversion took place, but no systemic manifestations of herpetic infection were observed. The control group showed no cochlear or systemic symptoms. When comparing cochlear histopathology in ISSHL to experimental viral HSV-1 labyrinthitis, strong similarities were found: degeneration of the stria vascularis, destruction of the organ of Corti, loosening of the tectorial membrane, and inflammatory changes in neural structures. CONCLUSIONS: Based on clinical and histopathologic characteristics, experimental HSV-1 labyrinthitis provides a suitable model of ISSHL.

Animals↗

Modifications of cochlear microphonic frequency responses following transient changes of hydrostatic pressure in the perilymph.

Cochlear microphonic potential was recorded with differential electrodes implanted in the various turns of the guinea-pig cochlea. Isointensity frequency responses were plotted in normal conditions and after excessive displacements of the cochlear partition. These displacements were provoked by changes of hydrostatic pressure in the perilymph of scala tympani or scala vestibuli. Typical modifications of the frequency response were observed. The most noticeable was a division in two parts of the response zone which suggested the existence of two resonance peaks. Scanning electron microscopy revealed that changes of hydrostatic pressure provoked alterations of the stereocilia in the outer rows of external hair cells, probably in relation with a decoupling of the tectorial membrane from the organ of Corti. These results are discussed in terms of possible alterations of cochlear micromechanics.

Animals↗

Elemental composition of the mature inner ear.

An X-ray energy dispersive analysis was performed on the mature serial sectioned freeze-dried mammalian labyrinth (CBA/CBA mouse). The elemental distribution in the endolymphatic and perilymphatic spaces revealed similar results as have been reported in the literature when withdrawing fluid for microanalysis. The cupulae of the vestibular organs showed only minimal relative peak intensities of chlorine and potassium in contrast to the tectorial membrane in the cochlea with elemental identification also of sodium, sulphur and calcium. A difference in structural composition is therefore likely between these two tissues.

Animals↗

Distortion product otoacoustic emissions provide clues hearing mechanisms in the frog ear.

2f1-f2 and 2 f2-f1 distortion product otoacoustic emissions (DPOAEs) were recorded from both ears of male and female Rana pipiens pipiens and Rana catesbeiana. The input-output (I/O) curves obtained from the amphibian papilla (AP) of both frog species are analogous to I/O curves recorded from mammals suggesting that, similarly to the mammalian cochlea, there may be an amplification process present in the frog AP. DPOAE level dependence on L1-L2 is different from that in mammals and consistent with intermodulation distortion expectations. Therefore, if a mechanical structure in the frog inner ear is functioning analogously to the mammalian basilar membrane, it must be more broadly tuned. DPOAE audiograms were obtained for primary frequencies spanning the animals' hearing range and selected stimulus levels. The results confirm that DPOAEs are produced in both papillae, with R. catesbeiana producing stronger emissions than R. p. pipiens. Consistent with previously reported sexual dimorphism in the mammalian and anuran auditory systems, females of both species produce stronger emissions than males. Moreover, it appears that 2 f1-f2 in the frog is generated primarily at the DPOAE frequency place, while 2 f2-f1 is generated primarily at a frequency place around the primaries. Regardless of generation place, both emissions within the AP may be subject to the same filtering mechanism, possibly the tectorial membrane.

Acoustic Stimulation↗

Cochlea of the human fetus: a scanning electron microscope study.

Fine structures of the human fetal cochlea were observed by scanning electron microscopy. The study aimed to make the knowledge on the developmental microanatomy of the cochlea more accurate. The temporal bones of fetuses were removed and the membranous portions of the cochleas were prepared for observation. In a 14-week 6-day old fetus, the hair cells were arranged mainly in four rows. The sensory hairs differed in appearance from those in the adults. The innermost or first row hair cells corresponded to the inner hair cells and revealed certain characteristic structures. From the second to the third or outermost row, a rather uniform hair pattern with a bud-like appearance was noted. Neither W nor V letter formation of sensory hairs was found. One strong kinocilium was identified with its thick base; it was located lateral to the outermost stereocilia. With older fetuses, 22 weeks 2 days and 24 weeks 0 day of age, the hair patterns closely resembled those of the adult with the exception of the presence of a short kinocilium on the outer hair cells and a slim kinocilium on the inner hair cells. The present study indicates that structures including the sensory hairs and their attachment to the tectorial membrane, the Reissner's membrane and the stria vascularis essentially complete their morphologicjal development in 6 months after gestation.

Cochlea↗

Mechanics and nonlinearity of hair cell stimulation.

Many nonlinear auditory phenomena are described with a BPNL model, which consists of a nonlinear element preceded and followed by a linear filter. We aim at identifying these elements with cochlear processes. The directional sensitivity of the hair cell is assumed to provide a basis for the second filter. The nonlinearity is hypothesized at the level of mechanical impedance of the hair cell. On the basis of an approximate solution for the cochlear traveling wave, we determine radial and longitudinal components of the driving force on the hair cell. It is shown that appropriate two-tone suppression and sharpening can be obtained only if radial tuning is sharper than longitudinal tuning. This imposes severe constraints on the model. It requires specific assumptions about physical properties of, for example, the tectorial membrane. For instance, if this has significant stiffness in a direction at a small angle with the radial direction, and if stretch in this direction is nonuniform, then sharpening and two-tone suppression are explainable in terms of cochlear mechanics.

Biomechanical Phenomena↗

Vibration pattern of the organ of Corti up to 50 kHz: evidence for resonant electromechanical force.

Electromechanical force derived from the soma of the outer hair cell has long been postulated as the basis of the exquisite sensitivity of the cochlea. The problem with this postulate is that the electrical source and mechanical load for the electromechanical outer hair cell might be severely attenuated and phase-shifted by the electrical impedance of the cell and the mechanical impedance of the organ of Corti, respectively. Until now, it has not been possible to experimentally derive the high-frequency electrically induced force at the reticular lamina when the cells are embedded within the organ of Corti. In the study reported here, we succeeded in determining the frequency spectrum of the force up to 50 kHz. This was achieved by measuring both the electrically induced velocity and the mechanical impedance at different radial positions on the reticular lamina without tectorial membrane and with clamped basilar membrane. Velocity was measured with a laser interferometer and impedance, with a magnetically driven atomic force cantilever. The electromechanical force, normalized to the electric current density, exhibited a broad amplitude maximum at 7-20 kHz with a quality factor, Q(3dB), of 0.6 - 0.8. The displacement response was independent of frequency up to 10-20 kHz. The force response compensates for the viscoelastic impedance of the organ of Corti, extending the amplitude response of the organ to high frequencies. It is proposed that the electrical phase response of the cell is compensated with Zwislocki's original mechanism of a parallel resonance in the tectorial membrane-stereocilia complex.

Animals↗

Endotoxin induced damage to the cochlea in guinea pigs.

An apparently unique form of cochlear damage was produced in guinea pigs by perfusing the cochlea or injecting the cerebrospinal fluid with bacterial endotoxin. This developed rapidly (within two hours) and was characterised by swelling of the tectorial membrane and damage to both inner and outer hair cells, with parallel functional damage demonstrable electrophysiologically. All these changes could be attenuated by pretreatment with dexamethasone. Such endotoxin mediated lesions may be the mechanism by which hearing loss occurs in bacterial meningitis.

Action Potentials↗

Hypothyroidism and the ear: electrophysiological, morphological, and chemical considerations.

There is both clinical and laboratory evidence that hearing loss can result from congenital and acquired hypothyroidism. The reversibility of this process, however, and its incidence and pathophysiology are not universally agreed upon. Laboratory animals rendered hypothyroid with radioactive iodine 131 or propylthiouracil demonstrated normal perilymph sodium and potassium levels but increased auditory thresholds for N1N2 response and brain stem evoked audiometry as well as a crystallized consistency of the bone of the bullae and cochleae, ossicular abnormalities, obliteration of the oval and round window, large dark staining lipid accumulations in Hensen's cells, large intercellular spaces in the stria vascularis with degeneration of the marginal and intermediate cells, inner and outer hair cell degeneration, debris in the cochlear duct, and tectorial membrane irregularity. Otic capsule biochemical alterations were identified which may account for the osseous changes observed morphologically. The morphological, biochemical, and electrophysiological findings in this study support the hypothesis that the cochlea is a site of lesion for sensorineural hearing loss in hypothyroidism. Middle ear changes identified could be responsible for the conductive component.

Animals↗

Pathological specimens of rat temporal bone--comparison between different fixative solution.

We investigated the difference in temporal bone specimens fixated by three sorts of fixative solution (10% formalin fixative, Wittmaack's fixative and Heidenhein-SuSa fixative). 1. 10% Formalin's fixative solution We found many pinkish precipitates, which are stained by hematoxy-eosin, in the scala media of the cochlea. Same substance is found in the perilymphatic space and endolymphatic space in the vestibulum. The fusion of the cells is indicated in the tectorial membrane, inner sulucus cell, outer sulucus cell especially in the apical turn of the cochlea. 2. Wittmaack's fixative solution The detachment of inner and outer sulucus cells are found from basilar membrane at the basal turn of the cochlea. The tendency in convex and concave form of the Reissner's membrane is most remarkable in these three fixative solution. 3. Heidenhein-SuSa fixative solution In this solution, no precipitates, no fusion of cells are found. No detachment of the inner or outer sulucus cells is also found. This study indicates that Heidenhein-SuSa fixation is most excellent fixative method.

Animals↗