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PubMed1985

The ferret as a model for inner ear research.

Viral infections have long been suspected to be causative agents in a number of inner ear dysfunctions. With few exceptions, the virus has not been demonstrated as the direct agent leading to hearing loss and/or vertigo. Selective inner ear changes have been observed recently in sensory and nonsensory epithelial cells in the ferret model for Reye's syndrome after intranasal inoculation with influenza B combined with aspirin administration and the creation of an arginine deficiency. Such findings suggest that these agents act synergistically on the inner ear, particularly on cells that are metabolically active, and that the ferret may now be a useful model to examine the role of certain upper respiratory tract viruses implicated in inner ear disorders, singly and in combination with other agents that may cause metabolic alterations.

Animals↗

PubMed1997

Clinical Experiences of Steroid Targeting Therapy to Inner Ear for Control of Tinnitus.

We summarize our long-term clinical experiences with an inner-ear drug delivery system (DDS) for control of tinnitus. The inner-ear DDS consist of transtympanic perfusion of 2 or 4 mg dexamethasone to the round window via the middle ear. Therapeutic results of steroid targeting therapy to the inner ear were evaluated in 3,978 ears of 3,041 patients. Tinnitus improved in 75% of these patients immediately after treatment and in 68% after 6 months. The effects of such therapy on tinnitus varied depending on the underlying diseases. The improvement of tinnitus in the presence of labyrinthine hydrops was good, whereas the effects on noise- or drug-induced tinnitus were poor. Our results indicate that in high-tone tinnitus, the effects were poor, but they were good for low-pitched tinnitus. No correlation existed between the efficacy of management and loudness of the tinnitus. The dangers of perforating the eardrum and of inciting the discomfort of vertigo as a result of the transtympanic injection of dexamethasone are minimal. We believe that the transtympanic infusion technique is an effective DDS for control of inner-ear diseases and symptoms. This technique may be performed by any neurootologist in an outpatient clinic.

Journal Article↗

PubMed2002

Nitric oxide in the inner ear.

During the past year significant advances have been made in our understanding of the functional significance of nitric oxide (NO) in the inner ear. NO synthase and the NO production site have now been localized using immunohistochemistry and a new fluorescence indicator for NO. The functional significance of NO in the inner ear, in particular as a neurotransmitter, is becoming increasingly clear. Increasing evidence suggests that excessive NO production may play an essential role in inner ear disorders. The production of an inducible form of NO synthase may be closely related to this phenomenon. Based on the mechanisms of inner ear disorders, new pharmacological strategies for preventing or treating inner ear disorders have been suggested.

Animals↗

PubMed1992

A new model of equilibrium dysfunction in the rat induced by photochemical damage to the inner ear's microcirculation.

A new photochemical method was employed to damage the inner ear microcirculation in the rat. Under pentobarbital anesthesia, the middle ear was exposed by a ventral approach and the tympanic membrane and the malleus and incus were removed. The vestibule was then illuminated by a filtered xenon light (wave length: 540 nm) while rose bengal was infused intravenously. Microscopic examination revealed disintegration of the hair cells in the vestibule. Changes could be prevented by pretreatment with intravenous acetylsalicylic acid (ASA) or heparin. Twenty-four hours after the completion of photo-illumination the rats exhibited nystagmus toward the intact ear and showed rolling during the swimming test, both signs of equilibrium dysfunction. These findings were inhibited by ASA or heparin pretreatment. Our present results indicate that our method causes a photochemically induced occlusion in the rat's inner ear microcirculation and may be useful for evaluating the various effects of drugs on the inner ear.

Animals↗

PubMed1993

Effect of ibudilast on microcirculation thrombosis in rat inner ear.

The effect of ibudilast (0.1, 0.3 mg/kg), which has cerebral vasodilating and antiplatelet effects, was evaluated in two models of rat inner ear microcirculation thrombosis by using the photochemical reaction between green light (wave length: 540 nm) and intravenous injection of rose bengal. Furthermore, the inner ear blood flow was measured by a laser-Doppler flowmeter. In the hearing disturbance model, under anesthesia, the compound action potential of the cochlear nerve (AP) was measured by an electrocochleogram. The sound stimulus was an 8-kHz sine wave at 80 dB SPL. The AP was calculated 128 times. In the controls, the AP disappeared about 4 min after the intravenous injection of rose bengal (20 mg/kg). The time required to completely suppress the AP in the animals treated with ibudilast (0.1, 0.3 mg/kg) was significantly prolonged as compared with that in the controls. In the equilibrium dysfunction model, ibudilast (0.1, 0.3 mg/kg) reduced the time of abnormal swimming in the swimming test 24 hr after the completion of photo-illumination. Ibudilast (0.3 mg/kg) increased the inner ear blood flow during the 10-min observation period as compared with the controls, while it did not affect the mean blood pressure. In conclusion, ibudilast increased the inner ear blood flow and was effective in two models of rat inner ear microcirculation thrombosis.

Animals↗

PubMed2005

Cisplatin ototoxicity to the rat inner ear: a role for HMG1 and iNOS.

Cisplatin is a chemotherapeutic agent that causes toxic damage to the inner ear (ototoxicity). Although much attention has been directed at identifying ways to protect the inner ear against cisplatin ototoxicity, little is known about the mechanisms by which cisplatin causes damage to the inner ear. Binding of high-mobility group (HMG1) protein to cisplatin-modified DNA participates in mediating the antitumor effects of cisplatin. This study seeks to determine if HMG1 may also participate in the ototoxicity of cisplatin. To address this, patterns and levels of expression of HMG1 have been evaluated in the rat cochlea in response to cisplatin chemotherapy. Our findings demonstrate a marked upregulation of HMG1 protein in the spiral (auditory) ganglion cells of cisplatin-treated rats in comparison to levels of expression of HMG1 in the spiral ganglion cells of untreated control animals. Increased levels of HMG1 were observed in the cisplatin-treated kidney, a peripheral target tissue of cisplatin, but not in the heart, a tissue not typically affected by cisplatin chemotherapy, suggesting HMG1 specificity in cisplatin toxicity. Furthermore, levels of inducible nitric oxide synthase (iNOS), an HMG-regulated enzyme associated with cochlear pathology, are increased in the spiral ganglion cells of cisplatin-treated rats 1 day post the cisplatin-mediated upregulation in HMG1. This increase in HMG1 and iNOS can be prevented in the cochleae of cisplatin-treated rats by administration of l-methionine, an established method of protection against cisplatin ototoxicity. Our results support a role for HMG1 and iNOS in mechanisms of cisplatin ototoxicity in the rat inner ear.

Animals↗

PubMedDate not supplied

The role of the endolymphatic sac in inner ear immunity.

The present study further assessed the role of the endolymphatic sac (E.S.) in the generation of inner ear immune responses. Guinea pigs underwent unilateral endolymphatic sac obliteration (Rt) and the opposite ears (Lt) served as controls. The animals were then systemically sensitized to KLH and both inner ears were subsequently challenged with KLH. Absence of the E.S. significantly reduced perilymph anti-KLH levels and greatly reduced cellular infiltration within the cochlea as compared to the control ears (Lt). Control studies demonstrated that neither surgical trauma to the semicircular canal nor the chemical effects of silver nitrate caused immunosuppression of the normal inner ear immune response. From these findings, the E.S. appears to be the main site of antigen processing in the inner ear and a site analogous to the gut with respect to absorptive and immunologic functions.

Animals↗

PubMed1997

[A study of inner ear autoantibodies in patients with sensorineural hearing loss].

In order to identify the inner ear autoantibodies, sera from 277 patients with sensorineural hearing loss and/or vertigo were reacted with bovine inner ear antigen by the western blotting method. We examined the relationships between the rate of the inner ear autoantibodies and clinical symptoms, course, diagnosis, age and positive tests for antinuclear antibodies. The rate of the autoantibodies which reacted with the 68-kD protein determinant, however, tended to increase with the elevation of hearing threshold. These of autoantibodies also tended to have a high incidence in patients with a fluctuating hearing threshold. Antibody against the 68-kD protein was detected in serum from 64.3% of patients with progressive sensorineural hearing loss. These results indicate that autoimmunological mechanisms involving the 68-kD protein may be one of the causes of sensorineural hearing loss.

Adult↗

PubMed1995

Surface-coil magnetic resonance imaging of the internal auditory canal and the inner ear. Preliminary report.

Parasagittal surface-coil magnetic resonance imaging of the internal auditory canal and the inner ear was performed. We used T2-weighted fast spin-echo sequences to visualize the inner ear and the individual nerves in the internal auditory canal with high contrast in a short acquisition time. Computer-assisted quantitative measurement of the nerves was performed to estimate the cross-sectional areas and the diameters of the nerves. The average diameters of the facial nerve, the cochlear nerve, and the vestibular nerve of normal-hearing individuals were, respectively, 1.1 +/- 0.2 mm (mean +/- SD), 1.2 +/- 0.2 mm, and 1.5 +/- 0.2 mm. In the cerebellopontine angle, the average diameter of the eighth nerve was 1.8 +/- 0.2 mm. Two patients with unilateral and bilateral hearing loss were also presented. In the patient with unilateral deafness, the cochlear nerve of the diseased side was not identified and the eighth cranial nerve diameter was smaller than that of the normal side. In the patient with bilateral deafness, fibrosis of the inner ear and atrophy of the eight nerve were demonstrated in the ear with posttraumatic deafness. The present method may represent a new approach to the assessment of pathologic processes involving the inner ear and the nerves in the internal auditory canal.

Adult↗

PubMed1998

Effect of increased inner ear pressure on middle ear mechanics.

Velocity of malleus, umbo, and stapes footplate in response to stepwise increases up to +400 mm H2O in hydrostatic pressure of the inner ear was investigated in 10 fresh human temporal bones by using a laser Doppler interferometer. The sound-pressure input was 114 dB SPL, and the frequency range was 0.4 to 5.0 kHz. Static displacement of these sites was also measured by a video measuring system. When the inner ear pressure was increased, the malleus and stapes moved outward. Amplitude of umbo velocity decreased below 1.0 kHz with a slight increase around 2.0 kHz, whereas stapes velocity decreased at all frequencies with the major effect below 1.0 kHz. The phase angle of malleus umbo velocity advanced markedly in response to the increased inner ear pressure between 1.0 and 1.4 kHz. Change in the vibration of the umbo was thought to be primarily caused by an increased stiffness of the middle ear conduction system, and that of the stapes was caused by distention of the annular ligament and increased cochlear impedance produced by the increased inner ear pressure. These changes in TM vibration and its phase angle may help detect indirectly an elevation of inner ear pressure.

Aged↗

PubMed2005

BMP4 signaling is involved in the generation of inner ear sensory epithelia.

BACKGROUND: The robust expression of BMP4 in the incipient sensory organs of the inner ear suggests possible roles for this signaling protein during induction and development of auditory and vestibular sensory epithelia. Homozygous BMP4-/- animals die before the inner ear's sensory organs develop, which precludes determining the role of BMP4 in these organs with simple gene knockout experiments. RESULTS: Here we use a chicken otocyst culture system to perform quantitative studies on the development of inner ear cell types and show that hair cell and supporting cell generation is remarkably reduced when BMP signaling is blocked, either with its antagonist noggin or by using soluble BMP receptors. Conversely, we observed an increase in the number of hair cells when cultured otocysts were treated with exogenous BMP4. BMP4 treatment additionally prompted down-regulation of Pax-2 protein in proliferating sensory epithelial progenitors, leading to reduced progenitor cell proliferation. CONCLUSION: Our results implicate BMP4 in two events during chicken inner ear sensory epithelium formation: first, in inducing the switch from proliferative sensory epithelium progenitors to differentiating epithelial cells and secondly, in promoting the differentiation of hair cells within the developing sensory epithelia.

Animals↗

PubMed1997

Detection of C-type natriuretic peptide (CNP) and atrial natriuretic peptide (ANP-B) receptor mRNAs in rat inner ear.

C-Type natriuretic peptide (CNP) is the third member of the natriuretic peptide family which plays an important role in body fluid homeostasis. To determine a possible role of CNP in regulation of an inner ear fluid, we investigated the expression of CNP and atrial natriuretic peptide B receptor (ANP-B receptor) mRNAs in rat inner ear using a reverse transcription polymerase chain reaction (RT-PCR) method. Amplification products with sizes expected for CNP and ANP-B were detected in the inner ear. After cloning and analysis, the sequences for PCR products were identical to those of CNP or ANP-B receptor in the brain. These results indicate that both CNP and ANP-B receptor are expressed in the inner ear of the rat and suggest that CNP may play a role in inner ear function (such as regulation of inner ear fluid) in an autocrine and/or paracrine manner.

Animals↗

PubMed2001

[The orientation and its significance of water channel protein in the mouse inner ear].

OBJECTIVE: To examine the distribution of various subtypes of water channel protein (aquaporin, Aqp) in various structures of the mouse inner ear. METHODS: Thirty mice with white color were used in this study and were cardiacally perfused. The temporal bones were taken out and were processed and sectioned by paraffin-embedded technique. The sections were labeled with fluorescent antibody by immunohistochemical method. The distribution of Aqp1, 3, 4, 5, 7, 9 were confirmed in the inner ear of mouse. RESULTS: The constant and clear fluorescent reaction could be observed in the inner ear tissue with the first antibody concentration of 1:200 for Aqp-1 and 1:100 for Aqp-3, 7, 9. But the reaction of Aqp-4 and 5 could not be found with the concentration of 1:50, even 1:30. Aqp-1 was labeled in the round window membrane, spiral ligament, endolymphatic sac and duct, utricle and saccule and the wall of inner ear blood vessel; Aqp-3 in the spiral limb, vestibular lip, internal and external sulci, basilar membrane and basilar membrane crest, endolymphatic sac and duct, membranous semicircular canal and utricle and saccular macula; Aqp-7 in the stria vascularis, basilar membrane, Reissner's membrane, utricle and saccule and their maculae; Aqp-9 in the spiral limb, vestibular lip internal and external sulci, Reissner's membrane, membranous semicircular canal, saccule and its macula. CONCLUSION: Aqp-1, 3, 7, 9 were extensively distributed in various tissues of mouse inner ear. Their distribution sites and reaction degree were different, and mainly located in the structures related to the endolymph.

Animals↗

PubMed2004

Cochlear implantation in children with congenital inner ear malformations.

OBJECTIVE/HYPOTHESIS: To assess the audiologic and surgical outcomes for pediatric cochlear implant patients with inner ear malformations. STUDY DESIGN: Retrospective review of 315 pediatric cochlear implant cases from 1994 to 2002. METHODS: Twenty-eight pediatric cochlear implant patients with known inner ear malformations determined on high-resolution computed tomography (HRCT) of the temporal bone were the subjects of review. Results of HRCT findings, intraoperative findings, postoperative complications, and objective measures of both closed- and open-set testing of speech perception were analyzed. RESULTS: Patients with the constellation of an incompletely partitioned (IP) cochlea, enlarged vestibular aqueduct (EVA), and a dilated vestibule (i.e., Mondini's malformation) as well as those with an isolated EVA or partial semicircular canal aplasia have relatively good levels of speech perception. Patients with total semicircular canal aplasia, isolated IP, cochlear hypoplasia, or common cavity demonstrated lower levels of performance. Poor performance may be related to associated developmental delays rather than labyrinthine anatomy alone. Complications of surgery were relatively limited. CONCLUSIONS: Cochlear implantation can be successfully performed in children with inner ear malformations. These children and their parents can expect significant auditory benefits from this intervention. The various types of inner ear malformations may have quite different prognoses for good auditory performance.

Adolescent↗

PubMed2006

Pharmacodynamics of adenovector distribution within the inner ear tissues of the mouse.

Recent studies have demonstrated that delivery of genes to the inner ear can achieve a variety of effects ranging from support of auditory neuron survival to protection and restoration of hair cells, demonstrating the utility of vector based gene delivery. Translation of these findings to useful experimental systems or even clinical applications requires a detailed understanding of the pharmacokinetics of gene delivery in the inner ear. Ideal gene delivery systems will employ a well tolerated vector which efficiently transduces the appropriate target cells within a tissue, but spare non-target structures. Adenovectors based on serotype 5 (Ad 5) are commonly used vectors, are easy to construct and have a long track record of efficacious gene transfer in the inner ear. In this study we demonstrate that distribution of Ad5 vector occurs in a basal to apical gradient with rapid distribution of vector to the vestibule after delivery via a round window cochleostomy. Transduction of the vector and expression of the delivered transgene occurs by 10 min post vector delivery. At 24 h post delivery only 16% of vector that was initially detectable within the inner ear by quantitative PCR remained. Perilymph sampling was used to determine that vector concentrations in perilymph peaked at 30 min post delivery and then declined rapidly. Understanding these basic distribution patterns and parameters for delivery are important for the design of gene delivery vectors and vital for modeling dose responses to achieve safe efficacious delivery of a therapeutic agent.

Adenoviridae↗

PubMed2000

FGF/FGFR-2(IIIb) signaling is essential for inner ear morphogenesis.

Interactions between FGF10 and the IIIb isoform of FGFR-2 appear to be crucial for the induction and growth of several organs, particularly those that involve budding morphogenesis. We determined their expression patterns in the inner ear and analyzed the inner ear phenotype of mice specifically deleted for the IIIb isoform of FGFR-2. FGF10 and FGFR-2(IIIb) mRNAs showed distinct, largely nonoverlapping expression patterns in the undifferentiated otic epithelium. Subsequently, FGF10 mRNA became confined to the presumptive cochlear and vestibular sensory epithelia and to the neuronal precursors and neurons. FGFR-2(IIIb) mRNA was expressed in the nonsensory epithelium of the otocyst that gives rise to structures such as the endolymphatic and semicircular ducts. These data suggest that in contrast to mesenchymal-epithelial-based FGF10 signaling demonstrated for other organs, the inner ear seems to depend on paracrine signals that operate within the epithelium. Expression of FGF10 mRNA partly overlapped with FGF3 mRNA in the sensory regions, suggesting that they may form parallel signaling pathways within the otic epithelium. In addition, hindbrain-derived FGF3 might regulate otocyst morphogenesis through FGFR-2(IIIb). Targeted deletion of FGFR-2(IIIb) resulted in severe dysgenesis of the cochleovestibular membraneous labyrinth, caused by a failure in morphogenesis at the otocyst stage. In addition to the nonsensory epithelium, sensory patches and the cochleovestibular ganglion remained at a rudimentary stage. Our findings provide genetic evidence that signaling by FGFR-2(IIIb) is critical for the morphological development of the inner ear.

Animals↗

PubMed2000

Clinical course of pediatric congenital inner ear malformations.

OBJECTIVE: To determine any factors that could improve the early detection and management of congenital inner ear malformations. STUDY DESIGN: A retrospective review was performed of all patients with a diagnosis of inner ear malformation at Loyola University Medical Center (LUMC) and the Hospital for Sick Children (HSC) between 1987 and 1995. Clinical records and audiometric data were accumulated. One neuroradiologist reviewed every temporal bone computed tomography (CT) scan. METHODS: Forty-six pediatric patients with congenital inner ear anomalies evaluated at two tertiary care hospitals. RESULTS: The average patient age at initial assessment was 25.7 months. A family history of hearing loss was noted in only five patients (12.8%). A major nonotological deformity was seen in 41% of patients. The average hearing threshold was 88 dB. All three patients with sudden hearing loss had vestibular aqueduct enlargement. Two of the three patients with common cavity anomalies had a history of recurrent meningitis. Twenty-seven patients had a vestibular aqueduct deformity, the most frequent radiographic abnormality in the series. CONCLUSIONS: Because inner ear malformation was diagnosed after 24 months of age in a significant percentage of patients, we recommend increased parental education and vigilance by primary care practitioners. Universal newborn screening may be the key to earlier detection of these infants. For children with idiopathic sensorineural hearing loss, we recommend a temporal bone CT scan. Patients with vestibular aqueduct enlargement must be counseled about the risk of progressive sensorineural hearing loss, meningitis, and the need to avoid contact sports. Patients with common cavity abnormalities should be considered for exploratory tympanotomy and also educated about the risk for meningitis.

Acoustic Impedance Tests↗

PubMed1987

Neuroactive substances in inner ear extracts.

To identify the neurotransmitter released by sensory hair cells, as well as to find other substances that might influence neural function of the inner ear, we have prepared extracts from inner ears of fishes (which have large numbers of hair cells), fractionated the extracts, and studied the effects of the fractionated extracts on the discharge rate of afferent fibers innervating hair cells in the lateral line organ of the African clawed frog Xenopus laevis. The extracts contain active substances that do not bind to a cation-exchange resin at neutral pH. Gel-permeation chromatography suggests that at least 2 unidentified excitatory substances are present in the extracts: one of low molecular weight (Mr about 200) and one of high molecular weight (Mr less than or equal to 5000). Some extracts also contain a high-molecular-weight inhibitory substance (Mr greater than 5000). The low-molecular-weight active substance is detected in extracts of inner ear, but not in brain or muscle. The high-molecular-weight excitatory substance is present both in brain and in inner ear.

Action Potentials↗