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PubMed1975

Action of Corti's organ and the cochlea: a new theory.

An "engineer's model" of the labyrinth is derived from the monoclinic crystal and the avian egg. The anatomy of the human cochlea and of the semicircular canals is then related by diffraction theory and Fresnel's explanation of optic activity. Increased cochlear electric potential, which represents stored energy, is associated with mechanical translation of the basilar membrane and angular separation of Corti's rods and is effected by "pumping" by the endolymphatic sac and the muscles that act on the auditory ossicles. The semicircular canals function as valves; the utricular and saccular macules form holograms and reflect the energy into the cochlear duct. Incoming acoustic waves excite dipole resonance and stimulate emission of a fraction of the stored energy; further amplification is effected by the hair cells, which, together with the tectorial membrane, behave like a transistor. These findings lead to a new theory of static balance and the action of Corti's organ: the labyrinth functions as a traveling wave maser of which the cochlea is the slow wave structure. Cochlear geometry itself effects resolution of incoming sound pitch. Corti's organ corresponds to the melatopes of the crystal, and the inter-rod angle is critical for any particular frequency, since it is related to dispersion of the optic axes.

Acoustics↗
PubMed1987

Repeated TTS exposures in monkeys: alterations in hearing, cochlear structure, and single-unit thresholds.

The findings of a number of studies investigating the effects of excessive sound on hearing have indicated that the correspondence between behavioral, physiological, and histological measures of noise-induced hearing loss may be markedly dependent upon the sensitivity of the particular measure. Recent studies demonstrating significant changes in the responses of single auditory neurons following brief exposures to pure tones suggest that single-unit activity may be a sensitive indicator of physiological insult to the organ of Corti's sensory cells. In addition, the long-lasting nature of the changes in neural responsiveness suggests that each temporary threshold shift (TTS) episode may produce an increment of damage to the ear that eventually contributes to a measurable permanent threshold shift (PTS). A logical extension of this implication is the proposal that repeated episodes of TTS would first affect single-unit thresholds, and that such damage would eventually manifest itself as PTS. A test of this notion was performed by repeatedly exposing monkeys to short-lasting TTS sounds for many months. Behavioral thresholds were monitored using a reaction-time task before and after each inducement of TTS. Two subjects participated in exposure sessions for 18 months, while the remaining monkey was exposed to identical stimuli for 6 months. At the end of behavioral testing, the monkeys were prepared for chronic recording from single cells of the cochlear nucleus. Following the recording period, cochleas were prepared for examination as plastic-embedded whole mounts. Flat preparations of the cochlear duct were made and the position and extent of damage to the organ of Corti and myelinated nerve fibers were determined. No elevations in behavioral threshold were noted for the monkey receiving 6 months of sound-exposure experience, while for both subjects exposed for 18 months, a significant high-frequency hearing loss became apparent during the final months of exposure. For damaged ears, the thresholds of ipsilateral cochlear nucleus units were elevated for characteristic frequencies (CFs) corresponding to the frequency regions where behavioral thresholds were shifted. Thresholds for units with high-frequency CFs in the animal exposed for 6 months also demonstrated a loss in sensitivity. Histological examination of the cochleas of monkeys with permanent hearing losses revealed corresponding damage to the high-frequency region of the organ of Corti. The monkey exposed for 6 months, which demonstrated only elevated unit thresholds, also had high-frequency lesions.(ABSTRACT TRUNCATED AT 400 WORDS)

Acoustic Stimulation↗
PubMed2000

Cloning and expression of the alpha9 nicotinic acetylcholine receptor subunit in cochlear hair cells of the chick.

Hair cells of the vertebrate inner ear are subject to efferent control by the release of acetylcholine (ACh) from brainstem neurons. While ACh ultimately causes the hair cell to hyperpolarize through the activation of small conductance Ca(2+)-activated K(+) channels, the initial effect is to open a ligand-gated cation channel that briefly depolarizes the hair cell. The hair cell's ligand-gated cation channel has unusual pharmacology that is well matched to that of the nicotinic subunit alpha9 expressed in Xenopus oocytes. We used sequence-specific amplification to identify the ortholog of alpha9 in the chick's cochlea (basilar papilla). Chick alpha9 is 73% identical to rat alpha9 at the amino acid level. A second transcript was identified that differed by the loss of 132 base pairs coding for 44 amino acids near the putative ligand-binding site. RT-PCR on whole cochlear ducts suggested that this short variant is less abundant than the full length alpha9 mRNA. In situ hybridization revealed alpha9 mRNA in sensory hair cells of the chick cochlea. The pattern of expression was consistent with the efferent innervation pattern. The alpha9 label was strongest in short (outer) hair cells on which large calyciform efferent endings are found. Tall (inner) hair cells receiving little or no efferent innervation had substantially less label. The cochlear ganglion neurons were not labeled, consistent with the absence of axo-dendritic efferent innervation in birds. These findings suggest that alpha9 contributes to the ACh receptor of avian hair cells and supports the generality of this hypothesis among all vertebrates.

Alternative Splicing↗
PubMedDate not supplied

Calcium transport in the endolymphatic space of cochlea and vestibular organ.

Ca++ concentrations and d.c. potential within the endolymphatic space of the cochlear duct and the semicircular canal following acute anoxia or ethacrynic acid intoxication (100 mg/kg i.v.) were measured by means of double-barrelled microelectrodes. Ionic calcium content and d.c. potential were found to change in a roughly biphasic fashion after either intervention. The maximal increase in Ca++ concentration coincided with the decline in the d.c. potential, which after a rapid decline finally reached and maintained negative voltages. This phenomenon was more pronounced in the cochlear part than in the semicircular canal. A model of calcium homeostasis is proposed in an attempt to reconcile the data presented with earlier evidence.

Animals↗
PubMed2006

Molecular characterization and expression of maternally expressed gene 3 (Meg3/Gtl2) RNA in the mouse inner ear.

The pathways responsible for sound perception in the cochlea involve the coordinated and regulated expression of hundreds of genes. By using microarray analysis, we identified several transcripts enriched in the inner ear, including the maternally expressed gene 3 (Meg3/Gtl2), an imprinted noncoding RNA. Real-time PCR analysis demonstrated that Meg3/Gtl2 was highly expressed in the cochlea, brain, and eye. Molecular studies revealed the presence of several Meg3/Gtl2 RNA splice variants in the mouse cochlea, brain, and eye. In situ hybridizations showed intense Meg3/Gtl2 RNA staining in the nuclei of type I spiral ganglion cells and in cerebellum near the dorsal vestibular region of the cochlea. In embryonic mouse head sections, Meg3/Gtl2 RNA expression was observed in the otocyst, brain, eye, cartilage, connective tissue, and muscle. Meg3/Gtl2 RNA expression increased in the developing otocyst and localized to the spiral ganglion, stria vascularis, Reissner's membrane, and greater epithelial ridge (GER) in the cochlear duct. RT-PCR analysis performed on cell lines derived from the organ of Corti, representing neural, supporting, and hair cells, showed significantly elevated levels of Meg3/Gtl2 expression in differentiated neural cells. We propose that Meg3/Gtl2 RNA functions as a noncoding regulatory RNA in the inner ear and that it plays a role in pattern specification and differentiation of cells during otocyst development, as well as in the maintenance of a number of terminally differentiated cochlear cell types.

Animals↗
PubMed1978

Genesis of the round window rupture syndrome; some experimental observations.

Clinical and experimental evidence has revealed that rupture of the round window membrane, by itself, is not a major cause of sensorineural hearing loss. Eighteen guinea pigs underwent removal of the round window. The status of cochlear function was determined by recording the cochlear microphonic. An average loss of only about 6 db was observed after surgery. It is felt that there must commonly be more cochlear damage concurrent with window rupture to explain the significant and often relatively immediate hearing losses seen in clinical practice. The site(s) of this primary trauma has not yet been discovered, but it would seen reasonable in the light of recent reports that the perilymphatic vessels, the vas spirale, the stria vascularis and/or the intergrity of the cochlear duct might be involved in the genesis of this hearing loss. We propose that the term "round window rupture syndrome" be used as a more accurate description of this entity. The round window damage provides evidence of more devastating trauma within the cochlea. Thus, the clinician, being alerted, should not stop his therapeutic efforts with surgical closure of the RW. Better prognosis for the patient, as well as leading into new avenues for the investigation of cochlear function, would be the result.

Animals↗
PubMed1996

Chick cochlear efferent neurons are not immunoreactive for calcitonin gene-related peptide.

The fluorescent retrograde tracer, rhodamine dextran amine, was unilaterally injected into the cochlear duct of anesthetized chicks. Retrogradely labeled cells were found bilaterally in the brainstem ventromedial to the superior olivary nucleus and to the ventral facial nucleus, and in the caudal pontine reticular formation between the dorsal facial nucleus and the abducens nerve root. Tissue sections containing retrogradely labeled cells were incubated in an antiserum to calcitonin gene-related peptide (CGRP) and a fluorescently labeled secondary antiserum. No double-labeled neurons were found, suggesting that chick cochlear efferent neurons do not contain CGRP or that levels of CGRP in these cells may be too low to be detected immunohistochemically.

Animals↗
PubMed1998

Photochemically induced focal cochlear lesions in the guinea pig: I. DAB staining and SEM study.

A photochemical reaction was used to produce focal microcirculation disorders in the guinea pig cochlea. Temporal bones were removed at various intervals between 5 minutes and 1 month after infusion of rose bengal (RB) and illumination. Infused but unilluminated contralateral cochleae served as controls. Dissected cochlear structures were stained by 3,3'-diaminobenzidine (DAB) peroxidase substrate medium. After observation by light microscopy (LM), the same specimens were processed and observed by scanning electron microscopy (SEM). Dilation of strial capillaries and destruction of strial epithelial cells became apparent at 1 hour after illumination. Tightly packed red blood cells were found filling the severed end of markedly dilated strial capillaries at 24 hours after the procedure. DAB staining of the osseous spiral lamina indicated vascular change with vessel dilation in the illuminated area. At 1 week after illumination, the lesion area of the stria vascularis and spiral prominence was replaced by a layer of larger, flat cells. At 1 month after illumination, all vascular supply to the cochlear lateral wall disappeared at the site of illumination. All lesions remained focal and showed no sign of expansion or reduction throughout the observation period. The cochlear duct of the guinea pig appears to be segmentally nourished by the capillary system. Observation of DAB stained tissue by LM and SEM proved to be informative in the study of microcirculation disorders of the inner ear.

3,3'-Diaminobenzidine↗
PubMed1992

[Indications and results of cochlear implants in young children].

In order to determine the criteria for patient selection and the preoperative prognostic factors for hearing recovery after cochlear implants in young totally dead children, the results of hearing rehabilitation were studied in 15 children who had undergone cochlear implantation at from 2 to 9 years of age. The choice of implant is determined by the permeability of the cochlear duct. A multi-system should be used, except when the cochlea is totally ossified. The reliability and efficacy of mono and multi system implants make it possible to offer a solution to the urgent therapeutic problems posed by total deafness in the young child.

Age Factors↗
PubMed1995

Electromotile hearing: evidence from basilar membrane motion and otoacoustic emissions.

Electrical stimulation of the cochlea is known to cause auditory sensations in humans and other animals. It also has been shown to produce emissions of sound from the inner ear. In the current study we investigate the relationship between electrically induced motion of the basilar membrane (BM) and the production of otoacoustic emissions. We test the hypothesis that electrical current-induced movements of the outer hair cell (OHC electromotility) result in intracochlear acoustic pressure which causes traveling waves on the BM. Our results demonstrate that the dominant response of the guinea pig inner ear to electric stimulation, at the round window membrane (RW) or across the cochlear duct, is a mechanical response of the organ of Corti. We observed that electrical stimulation of the cochlea produced traveling wave activity on the BM, measured with a laser Doppler velocimeter. The BM motion was accompanied by sound emitted by the cochlea for frequencies up to at least 25 kHz. Furthermore, bipolar rectangular current stimulation produced steady, bipolar displacements of the BM (to 2 nm), indicating functional elongation or contraction of OHCs occurs depending on the polarity of the current pulse. All of the evoked responses were absent after drug treatments eliminated the OHCs. Our data indicate that OHCs undergo electrically evoked displacements capable of producing high-fidelity, high-frequency acoustic energy. The electrically evoked intra-cochlear energy results in conventional traveling waves within the cochlea, as well as emissions of sound from the cochlea. These data provide direct support for a mechanism of cochlear sensitivity and tuning involving high-frequency OHC electromotility. Moreover, the data also indicate that any intra- or extracochlear electric current which affects the electric polarization of OHCs could induce BM traveling waves and cause 'electromotile hearing'. This form of hearing would be one component under the more general definition of the electrophonic effect.

Animals↗
PubMed1997

Localization of endothelin-1 and endothelin-3 in the cochlea.

The distribution of endothelin-1 (ET-1) and endothelin-3 (ET-3) was studied by indirect immunostaining of decalcified guinea pig and rat cochleae. No species differences were observed. Perikarya and processes of spiral ganglion cells were highly reactive for both ET-1 and ET-3. The epithelial lining of the cochlear duct stained for ET-1 and ET-3, but reactivity for ET-1 was higher in the lining cells of the inner sulcus, Claudius', and Hensen's cells, while the tympanic covering layer of the basilar membrane stained stronger for ET-3 compared to ET-1. In the stria vascularis, all cell types stained for ET-3, while marginal cells were more reactive for ET-1. Spiral ligament fibroblasts were reactive for ET-1, but not for ET-3. Connective tissue cells of the spiral limbus stained for both endothelins. The region of synapses on outer hair cells reacted for ET-1 and ET-3 but sensory cells remained unstained. Endothelins are discussed to act as modulatory peptides, possibly interfering with nitric oxide, prostaglandins, and atrial natriuretic peptide in the lateral cochlear wall (lateral cochlear wall, i.e. stria vascularis and spiral ligament). The occurrence of endothelins in cochlear neurons suggest their potential role as neurotransmitters.

Animals↗
PubMed2003

Inner ear morphology in a bilaterally deaf Dogo Argentino pup.

Two bilaterally deaf and three unilaterally deaf pups were identified from a litter of 10 Dogo Argentino pups presented for hearing evaluation by electrophysiological investigation. One pup, a bilaterally deaf female aged 43 days, was available for histopathology. Examination of both inner ears revealed bilateral cochlear degeneration with atrophy of the stria vascularis, collapse of the cochlear duct, degeneration of the organ of Corti, and abnormal tectorial membrane. The left vestibule, including the sacculus, was normal. The spiral and vestibular ganglia were essentially normal. This is the first histopathological description of lesions associated with deafness in a Dogo Argentino, but abnormalities were similar to those previously described in deaf Dalmatian pups and in other white hair-coated breeds. The defect was classified as a cochleosaccular degeneration. It was probably congenital and genetic causes were suspected.

Animals↗
PubMed2006

COUP-TFI controls Notch regulation of hair cell and support cell differentiation.

The orphan nuclear receptor COUP-TFI (Nr2f1) regulates many aspects of mammalian development, but little is known about its role in cochlear hair cell and Deiter's support cell development. The COUP-TFI knockout (COUP-TFI(-/-)) has a significant increase in hair cell (HC) number in the mid-to-apical turns. The total number of hair cells is not increased over wild type, perhaps because of displaced hair cells and a shortened cochlear duct. This implicates a defect of convergent-extension in the COUP-TFI(-/-) duct. In addition, excess proliferation in the COUP-TFI(-/-) sensory epithelium indicates that the origin of the extra HCs in the apex is complex. Because loss-of-function studies of Notch signaling components have similar phenotypes, we investigated Notch regulation of hair cell differentiation in COUP-TFI(-/-) mice and confirmed misregulation of Notch signaling components, including Jag1, Hes5 and in a manner consistent with reduced Notch signaling, and correlated with increases in hair cell and support cell differentiation. The disruption of Notch signaling by a gamma-secretase inhibitor in an in vitro organ culture system of wild-type cochleae resulted in a reduction in expression of the Notch target gene Hes5 and an increase in hair cell differentiation. Importantly, inhibition of Notch activity resulted in a greater increase in hair cell differentiation in COUP-TFI(-/-) cochlear cultures than in wild-type cultures, suggesting a hypersensitivity to Notch inactivation in COUP-TFI(-/-) cochlea, particularly at the apical turn. Thus, we present evidence that reduced Notch signaling contributes to increases in hair cell and support cell differentiation in COUP-TFI(-/-) mice, and suggest that COUP-TFI is required for Notch regulation of hair cell and support cell differentiation.

Amyloid Precursor Protein Secretases↗
PubMed1994

Pathology of prelingual profound deafness: magnitude of labyrinthitis fibro-ossificans.

Quantitative histologic studies were performed on 15 temporal bones from eight adult persons who were known to have prelingual bilateral profound hearing loss. The pathologic changes are characterized by severe degeneration of the structures of the cochlear duct, often with degeneration of the vestibular sense organs, causing a reparative host response that features osteoneogenesis and fibrous proliferation followed by retrograde neuronal degeneration. The pathology is consistent with meningogenic bacterial or viral labyrinthitis that occurred subclinically or went undiagnosed. Bone and fibrous tissue are present in varying extent in the scala tympani of 12 of the 15 temporal bones. Six cochleae from four subjects with fibro-osseous proliferation in the scala tympani extending as far as the ascending part of the basal turn have neuronal populations ranging from 963 to 5,355 (mean 2,826, 8% of neonatal normal, 35,500). In three cochleae from two subjects with no fibro-osseous proliferation in any area of the scala tympani the neuronal population ranges from 11,322 to 20,484 (mean 15,438, 43% of neonatal normal). Relative to cochlear implantation, computed tomographic imaging provides a means for determining the extent of fibro-osseous proliferation in the scala tympani, which in turn alerts the surgeon to surgical obstacles to optimal implantation as well as providing a basis for judging the extent of loss of cochlear neuronal population.

Aged↗
PubMed2006

The widely patent cochleovestibular communication of Edward Cock is a distinct inner ear malformation: implications for cochlear implantation.

OBJECTIVES: In 1838, Edward Cock described the anatomic findings in 4 inner ears with a widely patent communication between the cochlea and the vestibule that is now frequently referred to as the "common cavity deformity" and is often confused with Michel's "otocyst deformity." Little is known about the anatomic characteristics, including the presence of neural elements in this malformation. METHODS: Light microscopy and 2-dimensional and computerized 3-dimensional reconstructions were used to determine the histopathology and spiral ganglion cell counts in 7 temporal bones with a widely patent cochleovestibular communication. RESULTS: In all 7 specimens, the cochlea, vestibule, and semicircular canals were distinguishable and a bony defect resulting in an abnormal communication of perilymphatic space between the cochlea and vestibule was present. The ductus reuniens was abnormally wide in all. The cochlear duct varied from less than 1 turn to up to 2 turns. The mean spiral ganglion cells were estimated as a percentage of age-matched normal controls at 2.3%, 16.5%, and 26.8% when the cochlea was approximately 1, 1(1/2), and 2 turns, respectively (p = .007). The cribrose area consisted of a thin membrane in 2 specimens, and Rosenthal's canal openly communicated with the cerebrospinal fluid space in 3 specimens. The stapes footplate was abnormal in all 7 specimens and consisted of a central defect bridged by a thin membrane in 4 specimens. The facial nerve was dehiscent in 5 specimens (71%) and also followed an anomalous course in 2 specimens (28%). CONCLUSIONS: The widely patent cochleovestibular communication is a distinct inner ear malformation, recognition of which may have important clinical implications. Estimates of spiral ganglion cells can be predicted from the number of cochlear turns. Although cochlear implantation is feasible in patients with this malformation, a higher risk of cerebrospinal fluid gushers, facial nerve injuries, meningitis, and poor performance would be predicted. A better understanding of the anatomy will allow more effective surgical planning and techniques and may have a significant impact in improving outcomes.

Aged, 80 and over↗
PubMed1989

Appearance of B and H blood group antigens in the developing cochlear hair cells.

The presence of human blood-group antigens was analyzed in the rat cochlea during its postnatal development, using anti-A, anti-B and anti-H antibodies. At no stage was reactivity with anti-A antibody observed. With the anti-H antibody, a strong reactivity was observed from 1 to 9 days after birth within hair cells and some other surface epithelial cells of the cochlear duct. After postnatal day 9, only a faint reactivity persisted in a few non-sensory cells. With the anti-B antibody, only hair cells were selectively labeled. At early stages (postnatal day 1 and 3), the reactivity was intense and observed both around the cell surface and within the supranuclear region of cytoplasm. Later on, the reactivity decreased; it was limited at postnatal day 9 to a reactive spot below the cuticular plate. Results are compared with a preliminary finding describing the first appearance of B and H antigens in the organ of Corti at a prenatal stage, and with data concerning other sensory and neural structures. The appearance and progressive disappearance of B and H antigens on sensory and non-sensory cells can be correlated with significant events in the development of the cochlea. The transient expression of B and H antigens in cochlear sensory cells may correspond to developmental changes in their surface glycoconjugates.

ABO Blood-Group System↗
PubMed1981

Changes in cation contents of stria vascularis with ouabain and potassium-free perfusion.

Perfusion of the perilymphatic space of guinea pig cochleae with K-free medium leads to a gradual decline of the endocochlear potential (EP) over 30-50 min to a negative value (mean: -12 mV). The input resistance of scala media does not decrease during this time. The ATP and K content of the stria vascularis are reduced by similar amounts (26 and 34%, respectively) during this period. Perfusion of 1 mM ouabain produces a different pattern of response: strial ATP remains normal while strial K content is strongly reduced (by 77%). Strial Na rises in a complementary way to the K loss. These results demonstrate that a reduction of the K concentration of the perilymph leads to an inhibition of the generator of the positive component of the EP rather than to a general increase of cochlear duct membrane conductance. In addition, they suggest, in concert with other considerations (such as the slower rate of decline of the EP during K-free vascular perfusion (Wada, J., Kambayashi, J., Marcus, D.C. and Thalmann, R (1979): Arch. Otorhinolaryngol. 225, 79-81)), that the mode of action may be different from that of ouabain. In spite of the lack of teleological support, we offer the hypothesis that the strial generator of the EP may primarily utilize K from perilymph and that vascular K may not have access to the generator.

Adenosine Triphosphate↗
PubMed2006

Immunohistochemical localization of G protein betagamma subunits in the lateral wall of the rat cochlea.

The role of G protein-mediated signal transduction in the production of endolymph, an extracellular fluid of unusual ionic composition, is beginning to be understood. The identity of Galpha subunits in the stria vascularis and the spiral ligament of the lateral wall of the cochlear duct is well established. However, little is known about the presence of betagamma subunits. This study used immunohistochemistry to investigate the distribution of G protein betagamma subunits in the lateral wall of the cochlea. Temporal bones of 6- to 8-week-old rats were fixed in 4% paraformaldehyde and 0.1% glutaraldehyde and processed for embedding in paraffin wax. The dewaxed, midmodiolar sections of the cochlea were incubated with subunit-specific polyclonal antibodies. The results show that the pattern of immunoreactivity varies for the G protein beta1-4 and gamma1-3, 5 and 7 subunits in the stria vascularis and spiral ligament. In the stria vascularis, immunoreactivity was detected for beta2, beta3, beta4, gamma1, gamma2 and gamma7 subunits. All five types of fibrocytes in the spiral ligament exhibited positive staining for gamma2 and gamma7. However, immunoreactivity for beta1-4 subunits was variable. Immunoreactivity for gamma3 and gamma5 subunits was not detected in the lateral cochlear wall. The expression pattern of G protein betagamma subunits in lateral wall provides a basis for interpreting the functions of G protein-coupled receptors in cochlear fluid homeostasis.

Animals↗