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PubMed2001

[Detection of humoral immune response to inner ear proteins in patients with sensorineural hearing loss].

BACKGROUND: The precise mechanism of inner ear disease is still unknown. An autoimmune reaction could be one of several possible pathogenic factors involved in progressive sensorineural hearing loss. Heat shock protein 70 is suggested to play an important role in the development of autoimmune diseases. The aim of this study is the investigation of humoral immune reactivity to inner ear components in patients with sensorineural hearing loss. METHODS: The presence of antibodies to inner ear components was determined by immuno-blotting extracted bovine or human inner ear proteins. Study groups consisted of patients with idiopathic progressive sensorineural hearing loss (group A), patients with Menière's disease (group B), patients with sudden hearing loss (group C), patients with otosclerosis (group D), patients with Cogan's disease (group E), and individuals without hearing problems (group F). RESULTS: 40% of the patients with progressive sensorineural hearing loss showed reactivity against a 68-kDa protein extracted from bovine inner ear. In contrast to this, only 5% of healthy individuals and 10% with Menière's disease showed reactivity against the 68-kDa protein from bovine inner ear or against bovine heat shock protein 70. Some of the patients who showed reactivity against bovine inner ear proteins were tested with human inner ear and human heat shock protein 70; all of these showed reactivity. Approximately 6% of the patients with sudden hearing loss (group C), otosclerosis (group D), and Cogan's disease (group E) showed reactivity to inner ear proteins. A non-specific humoral immune reaction against inner ear proteins with molecular weights of 30, 40, 50, 60, and 220 kDa was observed in all patients. DISCUSSION: These results indicate a humoral immune reactivity against heat shock protein 70, which might be responsible for the pathogenesis of progressive sensorineural hearing loss.

Adult↗
PubMed2001

Estrogen receptors in the normal adult and developing human inner ear and in Turner's syndrome.

The influence of estrogens, the female sex hormone, on the ear and hearing is yet not fully investigated, though some studies have suggested that estrogens may influence hearing functions. The presence of estrogen receptors alpha and beta has earlier been shown in the inner ear of mice and rats. The aim of this study was to map possible estrogen receptors in the human inner ear. Inner ear tissue from human adults, aborted human normal fetuses and fetuses with Turner's syndrome were collected. Paraffin embedded sections of adult and fetal inner ears were immunostained with antibodies against estrogen receptors alpha and beta. Estrogen receptor alpha containing cells were found in the adult human inner ear only in the spiral ganglion, and estrogen receptor beta in the stria vascularis solely. The human fetal inner ear tissue from both normal and Turner fetuses showed a very weak staining of estrogen receptor alpha in the spiral ganglion cells, but no specific labeling of the Kölliker's organ of Corti at 13, 14 and 18 weeks of age. No staining of estrogen receptor beta was seen in the fetal inner ear.

Adult↗
PubMed1991

Distribution of glycoconjugates in ion transport cells of gerbil inner ear.

Ion transport cells in gerbil inner ear were differentiated histochemically by staining glycoconjugates (GCs) with a battery of horseradish peroxidase-conjugated lectins. Strong staining with PSA and LCA showed a high content of N-linked oligosaccharides in transport cell GCs. Reactivity with PHA-L and PHA-E identified GC with triantennary and with bisected biantennary N-linked oligosaccharides, respectively, in these cells. High affinity for DSA and PWM demonstrated abundant N-acetyl lactosamine in N-linked side chains. Ion transporting epithelial cells reacting with lectins specific for N-linked oligosaccharides included strial marginal cells and outer sulcus cells of the cochlea and dark cells, transitional cells, and planum semilunatum cells of the vestibular system. In general, all of the inner ear transport epithelial cells revealed a similar lectin binding profile, with the one exception that SBA reacted strongly with ion transporting cells in the vestibular system but only weakly with those in the cochlea. Fibrocytes specialized for ion transport located in distinct areas in the suprastrial and inferior regions of the spiral ligament also stained with lectins that demonstrate N-glycosylation. However, transport fibrocytes differed from transport epithelial cells in two ways. First, they reacted e with HPA, DBA, VVA, and SJA specific for O-linkages and second, they failed to react with UEA I. The staining pattern for N-glycosylated GC resembled that for Na+, K(+)-ATPase in inner ear, suggesting a relationship between these constituents.

Animals↗
PubMed1992

[Comparison of vulnerability between avian and mammalian inner ears--electrophysiological and morphological studies].

In order to assess the vulnerability of the inner ear, auditory function and morphology of the inner ear were compared between adult budgerigars and adult guinea pigs. Budgerigars have been considered to have an excellent auditory-vocal system. Two experimental conditions were produced in each species; one by acoustic hyperstimulation (1500 Hz, 120 dBSPL) for 96 hours, the other by administration of kanamycin (200 mg/kg) for 7 weeks. Measurement of auditory evoked potentials (AEP) and observation of hair cells by electron microscopy were performed both immediately and 14 days after exposure. In the acoustic hyperstimulation experiment, AEPs of budgerigars showed less damage and better recovery than those of guinea pigs, probably because of morphological differences between the two species in hair and supporting cells. Electron microscopic observation on the budgerigars showed that a small part of the hair cell area was damaged and that regeneration of hair cells had occurred in this area 14 days after exposure. Such observations in guinea pigs revealed that outer hair cells had been damaged and replaced by supporting cells 14 days after exposure. In the kanamycin administration experiment, AEPs showed the same degree of damage and recovery in both species. This suggests that blood supply and drug transport to the inner ear are almost the same although the structure of the inner ear differs markedly between the two species. Electron microscopic observation did not show an apparent regeneration of hair cells 14 days after administration in the budgerigars. Guinea pigs had a tendency to show progressive damage of both auditory function and inner ear morphology even after the cessation of administration. Regeneration of hair cells in the budgerigar differed under both experimental conditions, suggesting that there is a difference in the mode of auditory disturbance between acoustic hyperstimulation and administration of kanamycin. In conclusion, resistance to acoustic hyperstimulation is higher in the avian inner ear than in the mammalian inner ear, while resistance to administration of kanamycin does not differ significantly between the two species.

Acoustic Stimulation↗
PubMed2000

Monitoring inner ear pressure changes in normal guinea pigs induced by the Meniett20.

The inner ear fluid pressure of guinea pigs was measured during a series of complex oscillating middle ear pressure changes induced by the Meniett20 (Pascal Medical, Sweden), a possible therapeutic pressure generator to be used by patients with Meniere's disease. Middle ear pressure changes were transferred instantly to the inner ear, although inner ear pressure declined while middle ear pressure stayed relatively stable. An average undershoot of -1.0 cm H2O with respect to the steady-state pressure was seen after application of a pressure pulse, which was released in a few seconds. The results did not fully comply with a simple linear model in which a constant flow resistance between the inner ear and cerebrospinal space was assumed.

Animals↗
PubMed1990

[Detection of immunoglobulin in the inner ear tissue by PAP method].

The distribution of immunoglobulins IgG, IgA and IgM in the inner ear tissue from a patient who died of lung bleeding followed after sepsis was studied, and also the normal guinea pig inner ears and the inner ear disorders induced by Kanamycin injection were studied for the distribution of IgG. The temporal bones were fixed in formaldehyde, decalcified in EDTA and embedded in paraffin. The PAP method was used for the demonstration of the immunoglobulins. In both the human inner ear tissue and the normal control inner ear tissue of the guinea pigs deposits of IgG were found in the sensory organs and the endolymphatic sac, however, in the stria vascularis was slight. The severe damaged inner ears induced by Kanamycin the remarkable decreased deposits of IgG were found in the cochlea, but in the endolymphatic sac the remarkable increased deposits of IgG were found. No IgA and IgM were found in the human inner ear tissue.

Animals↗
PubMed1989

Theoretical and practical implications for plasmapheresis in autoimmune inner ear disease.

Immune-mediated inner ear disease, by convention called autoimmune inner ear disease (AIED), has established clinical profile guidelines for diagnosis. Treatment consists of steroid and/or cytotoxic drug immunosuppression. The role of plasmapheresis (PMP) in the treatment of AIED has not been defined. Lack of a precise serological marker prevents accurate immunological understanding. Definition is, of course, difficult in a disease whose natural history is not well delineated. Successful use of PMP in one steroid and cytotoxic drug intolerant patient with AIED led to its use in a total of eight patients. The rationale for PMP was based on its known effectiveness in other autoimmune diseases and thus, its potential use in AIED. Improved auditory function occurred in 6 of the 8 patients, 3 of whom have been followed for over 3 years. Three of the six no longer require immunosuppressant medication. PMP can be used as an alternative or adjunctive therapy in AIED. These preliminary results suggest PMP can stabilize or improve auditory and vestibular symptoms in selected patients. Its use as a first line therapy followed by cytotoxic immunosuppressants bears consideration.

Adult↗
PubMed1988

Frequency and localization of congenital anomalies of the middle and inner ears: a human temporal bone histopathological study.

This study investigated congenital anomalies occurring in the middle and the inner ears, with particular attention to their features, localizations, and frequencies. One hundred human temporal bones obtained from 73 individuals, aged 31 gestational weeks to 39 years, each of whom had anomalies of the middle ear and/or inner ear, were used for this study. The temporal bones had been removed at autopsy, fixed, dehydrated, embedded in celloidin, and sectioned horizontally or vertically at 20 microns. Every 10th horizontal section or every 20th vertical section was stained with hematoxylin and eosin, mounted and studied under a light microscope. In the middle ear the structure most often found to be anomalous was the facial nerve; in the inner ear it was the lateral semicircular canal. The implications of the anomalies observed are discussed as they relate to fetal development, dysfunction of the ear, and clinical interpretation of diagnostic radiological studies.

Adolescent↗
PubMed2004

Expression of the connexin43- and connexin45-encoding genes in the developing and mature mouse inner ear.

Intercellular communication through gap junctions is crucial for proper functioning of the inner ear. Indeed, mutations in several connexin genes have been found to cause hearing loss. In the inner ear, only the cell distributions of connexin30 and connexin26 have been well documented. We took advantage of the lacZ reporter gene in Cx43 and Cx45 knock-out mice to study the expression of the connexin43 and connexin45 genes during the inner ear development. Expression of Cx43 and Cx45 in the inner ear was detected from embryonic days 15.5 and 17.5, respectively. Until the 1st week of life, Cx43 was highly expressed in the connective tissues, and weakly expressed in the immature sensory epithelium of the cochlea. From postnatal day 8, however, Cx43 was almost exclusively expressed in the bone of the otic capsule. During embryogenesis, Cx45 was expressed in epithelial and connective inner ear tissues. From birth onwards, Cx45 expression could be detected in some inner ear capillaries. Vascular expression thereafter increased and persisted in the adult. In the mature inner ear, Cx45 was expressed in the entire vasculature. These results indicate that connexin43 and connexin45 play a role in the otic capsule bone and the inner ear vascular system, respectively.

Animals↗
PubMed1997

Isolation of human ear specific cDNAs and construction of cDNA libraries from surgically removed small amounts of inner ear tissues.

We have used representational difference analysis (RDA) for subtractive hybridization of oligo dT primed directionally cloned cDNA libraries from human inner ear tissue and a B-lymphoblast cell line. Two rounds of subtraction-amplification, followed by differential hybridization of selected clones led to the isolation of genes which were specific to the ear. Sequence analysis of randomly chosen clones revealed the presence of a histidine rich Ca2+ binding protein, human dynamin, collagen type 1A1, collagen type 2A1, SPARC, human growth hormone, and several specific genes which had no sequence homology in the data base. Furthermore, to apply these techniques for isolating genes specific to distinct inner ear structures and/or cell types of inner ear for which the starting tissue material is limiting, we have used a modified PCR based protocol to construct representative cDNA libraries. We have characterized a cDNA library constructed from small amounts of inner ear tissues recovered by ablative surgical procedure involving labyrinthectomy. The potential application of these protocols for isolating genes involved in hearing and deafness is discussed.

Adult↗
PubMed2006

The Notch ligand JAG1 is required for sensory progenitor development in the mammalian inner ear.

In mammals, six separate sensory regions in the inner ear are essential for hearing and balance function. Each sensory region is made up of hair cells, which are the sensory cells, and their associated supporting cells, both arising from a common progenitor. Little is known about the molecular mechanisms that govern the development of these sensory organs. Notch signaling plays a pivotal role in the differentiation of hair cells and supporting cells by mediating lateral inhibition via the ligands Delta-like 1 and Jagged (JAG) 2. However, another Notch ligand, JAG1, is expressed early in the sensory patches prior to cell differentiation, indicating that there may be an earlier role for Notch signaling in sensory development in the ear. Here, using conditional gene targeting, we show that the Jag1 gene is required for the normal development of all six sensory organs within the inner ear. Cristae are completely lacking in Jag1-conditional knockout (cko) mutant inner ears, whereas the cochlea and utricle show partial sensory development. The saccular macula is present but malformed. Using SOX2 and p27kip1 as molecular markers of the prosensory domain, we show that JAG1 is initially expressed in all the prosensory regions of the ear, but becomes down-regulated in the nascent organ of Corti by embryonic day 14.5, when the cells exit the cell cycle and differentiate. We also show that both SOX2 and p27kip1 are down-regulated in Jag1-cko inner ears. Taken together, these data demonstrate that JAG1 is expressed early in the prosensory domains of both the cochlear and vestibular regions, and is required to maintain the normal expression levels of both SOX2 and p27kip1. These data demonstrate that JAG1-mediated Notch signaling is essential during early development for establishing the prosensory regions of the inner ear.

Alleles↗
PubMed1995

De novo synthesis of glucocorticoid hormone regulated inner ear proteins in rats.

Changes of rat inner ear de novo protein synthesis in response to dexamethasone (DEX), a synthetic glucocorticoid, have been analyzed by high resolution two-dimensional sodium dodecyl sulfate polyacrylamide gel electrophoresis (2D-SDS-PAGE) and fluorography. Two proteins (M(r) 41,000 and 35,000) were amplified and one protein (M(r) 47,000) was suppressed by DEX in a cochlear culture medium. In the culture medium conditioned by vestibular tissue, three proteins (M(r) 67,000, 57,000 and 50,000) were amplified after DEX administration. In cochlear and vestibular tissues, glucocorticoid-responsive protein synthesis was down-regulated by DEX, including two proteins (M(r) 39,000 and 35,000) in the cochlea and five proteins (M(r) 80,000, 64,000, 59,000, 56,000 and 40,000) in the vestibule. The regulation of these inner ear proteins by DEX suggests that glucocorticoid may play an important role in normal inner ear microhomeostasis, as well as in the treatment of some inner ear disorders.

Animals↗
PubMed2001

Origins of inner ear sensory organs revealed by fate map and time-lapse analyses.

The inner ear develops from a simple ectodermal thickening called the otic placode into a labyrinth of chambers which house sensory organs that sense sound and are used to maintain balance. Although the morphology and function of the sensory organs are well characterized, their origins and lineage relationships are virtually unknown. In this study, we generated a fate map of Xenopus laevis inner ear at otic placode and otocyst stages to determine the developmental origins of the sensory organs. Our lineage analysis shows that all regions of the otic placode and otocyst can give rise to the sensory organs of the inner ear, though there were differences between labeled quadrants in the range of derivatives formed. A given region often gives rise to cells in multiple sensory organs, including cells that apparently dispersed from anterior to posterior poles and vice versa. These results suggest that a single sensory organ arises from cells in different parts of the placode or otocyst and that cell mixing plays a large role in ear development. Time-lapse videomicroscopy provides further evidence that cells from opposite regions of the inner ear mix during the development of the inner ear, and this mixing begins at placode stages. Lastly, bone morphogenetic protein 4 (BMP-4), a member of the transforming growth factor beta (TGF-beta) family, is expressed in all sensory organs of the frog inner ear, as it is in the developing chicken ear. Inner ear fate maps provide a context for interpreting gene expression patterns and embryological manipulations.

Animals↗
PubMed2005

Sudden sensorineural hearing loss associated with inner ear anomaly.

OBJECTIVE: This study was conducted to evaluate the frequency of inner ear anomaly in patients with sudden sensorineural hearing loss and in control subjects. STUDY DESIGN: Retrospective case review. SETTING: A tertiary referral center. PATIENTS AND INTERVENTION: We evaluated 366 patients (165 men and 201 women; age range, 3-91 yr) with sudden sensorineural hearing loss and 228 control subjects without sensorineural hearing loss using magnetic resonance imaging. Three hundred fifty-six patients had unilateral and 10 patients had bilateral sudden sensorineural hearing loss. RESULTS: Eleven (2.9%) of 376 ears with sudden sensorineural hearing loss had inner ear anomaly. Nine patients (2.5%) had inner ear anomaly associated with sudden sensorineural hearing loss, but none of the 228 control subjects had the anomaly. The current study demonstrated that the frequency of inner ear anomaly in patients with sudden sensorineural hearing loss was significantly higher than in control subjects. CONCLUSION: Our study reveals that inner ear anomaly may be associated with sudden sensorineural hearing loss in 2.5% of patients.

Acoustic Impedance Tests↗
PubMed2005

[Apoptosis and dynamic caspase-3 expression during the immune response of inner ear].

OBJECTIVE: To investigate whether apoptosis is involved in the pathogenesis of the immune response of inner ear, and relation between signal transportation of Caspase-3 and apoptosis. METHOD: Forty-five healthy, female white guinea pigs were employed in this study. Sensitized systematically with keyhole limpet hemocyanin (KLH), the KLH-immunized animals were inoculated with the same antigen, and the control animals were injected PBS through cochlea basal turn. All animals were sacrificed respectively at 1st, 3rd, 5th, 7th and 14th day after inner ear vaccination. The auditory brainstem response (ABR) was measured before the KLH injection to the inner ear and just before sacrificing the animal. Paraffin sections of cochleas from animals were stained using a TUNEL assay to identify inner ear cells undergoing apoptosis,and immunohistochemistry method was used to detect the expression of Caspase-3 in the inner ears. RESULT: After immunization, the ABR thresholds of the KLH-challenged ears were significantly elevated by comparing with the preimmunization (P < 0.05), but after injection, there was no significant difference in the ABR thresholds of the PBS-injected ears compared with preinjection. TUNEL-positive cells were found in the KLH immunized inner ears but no TUNEL-positive cells were observed in the control inner ears except for a few positive cells in the supporting cells, the stria vascularis cells and the spiral ganglion cells. The positive cells are the outer hair cells in Cortis organ, and the marginal cells in the stria vascularis and the neurons in the spiral ganglion. And, under morphological analysis by light microscope, these cells have the features characteristic of apoptosis. Apparent Caspase-3 immunoreactivity expression could be detected in Corti's organ, the lateral wall and the neurons of the spiral ganglion in the KLH-immunized inner ears from 5th day after inner ear vaccination, but no cells staining positive for Caspase-3 were found in the control inner ears. CONCLUSION: Apoptosis is induced by the immune response of inner ear; Caspase-3 cascade has important effect on the course of apoptosis.

Animals↗
PubMed2000

Developmental expression of aquaporin 2 in the mouse inner ear.

OBJECTIVES: The maintenance of endolymph homeostasis is critical for the inner ear to perform its functions of hearing and maintaining balance. The identification and cloning of aquaporins (a family of water channel proteins) has allowed the study of a novel cellular mechanism potentially involved in endolymph homeostasis. The objective of the present study was to define the developmental temporal and spatial expression pattern of aquaporin 2 (Aqp2) in the developing mouse inner ear. STUDY DESIGN: A systematic immunohistochemical study of Aqp2 protein expression was performed on embryonic mouse inner ears ranging from embryonic day 10 (otocyst stage) to embryonic day 18 (just before birth). METHODS: Serial cryosections of embryonic mouse inner ears were used for immunohistochemical experiments. A rabbit polyclonal antisera raised against a synthetic Aqp2 peptide was used with a standard nickel intensified 3,3-diaminobenzidine reaction protocol for immunolocalization of Aqp2 in tissue sections. RESULTS: Aquaporin 2 is expressed diffusely in the early otocyst, then becomes progressively restricted as the inner ear matures. During early cochlear duct formation (embryonic days 12 and 13), expression of Aqp2 is homogeneous; later, it becomes restricted to specific regions of the endolymphatic compartment (embryonic days 15 and 18). Similar restriction of expression patterns could be noted for the vestibular structures. Endolymphatic duct and sac and stria vascularis expression of Aqp2 was noted to occur fairly late during development but demonstrated a distinct pattern of immunolabeling. CONCLUSIONS: Aquaporin 2 shows an early and specific pattern of expression in the developing mouse inner ear, suggesting a significant role for this water channel protein in the development of endolymph homeostasis and meriting further functional studies of Aqp2 in the inner ear.

Animals↗
PubMed1987

[Sample distribution of inner ear fluids in the submicroliter range].

Biochemical analysis of inner ear fluids is fraught with numerous problems. After developing accurate techniques to measure inorganic and organic substances in fluid amounts of 0.1 microliter the problem of measuring and handling series of samples arose. It became necessary to develop methods to handle inner ear fluid taken without sophisticated techniques, i.e. to measure, to store and to dispatch inner ear fluid samples. The fluid volume is measured with a "nanocap" technique and is then transferred to cellulose acetate membranes. A 3 mm long glas capillary tube held by a special device is dipped into the inner ear fluid sample. The capillary tube is then placed on a membrane piece that adheres to the tube. The higher capillary forces of the membrane transfer the fluid out of the glass tube into the membrane which is put into a plastic reaction tube and stored. The reproducibility of the method was tested by flame photometric assays of standard sodium solutions and of perilymph from the scala tympani of guinea pigs. The variation coefficient is below 3% for a standard solution and below 5% for perilymph. The method developed to measure and handle inner ear fluids with the aid of "nanocap" and membrane pieces is easier and faster than the conventional techniques.

Animals↗
PubMed1982

[Therapeutic considerations in vascular diseases of the inner ear].

I propose an analogy between vascular diseases of the inner ear and those of other organs like brain, heart or peripheral vessel diseases in which functional and organic alteration can be objectively demonstrated. Symptomatic disturbances of inner ear circulation are monoform in its clinical appearance and the term of 'otangina' is proposed for the functional result. Three types of vascular distribution are discussed for the different regulatory entities, (I) the proximal cerebral vascular type, (II) the predistal innervated regulatory type and the (III) capillary regulatory type. The formal etiology of inner ear vascular diseases is is developed on the base of organic vascular lesions, i.e. arteriosclerosis, functional alterations, i.e. vasospastic disease, and finally change in the microcirculation by alterations of the rheology of the blood. Hypertension is portrayed as a main example for cardiovascular risk factors with respect to inner ear circulatory damage but diabetes mellitus, cigarette smoking and other metabolic diseases leading to vascular disturbances have to be considered. From these considerations I have developed a basic program for the diagnosis of vascular metabolic risk factors which should be realized before any treatment is advocated. I have critically evaluated the benefit and possible hazardous effects of so called 'vasoactive' and 'cephalotropic' drugs. For most inner ear circulatory disease such therapy is contraindicated. The models of drug treatment of acute deafness and the chronic or persistent inner ear deafness should be evaluated in prospective studies.

Arteriosclerosis↗