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At least 991 records · Page 55Linked to original sources
PubMed2000

Treatment with all-trans-retinoic acid decreases levels of endogenous TGF-beta(1) in the mesenchyme of the developing mouse inner ear.

BACKGROUND: Previous studies have shown that in utero exposure of the mouse embryo to high doses of all-trans-retinoic acid (atRA) produces defects of the developing inner ear and its surrounding cartilaginous capsule, while exposure of cultured periotic mesenchyme plus otic epithelium to high doses of exogenous atRA results in an inhibition of otic capsule chondrogenesis. METHODS: In this study, we examine the effects of atRA exposure on the endogenous expression of transforming growth factor-beta(1) (TGF-beta(1)), a signaling molecule that mediates the epithelial-mesenchymal interactions that guide the development of the capsule of the inner ear. RESULTS: Our results demonstrate a marked reduction in immunostaining for TGF-beta(1) in the periotic mesenchyme of atRA-exposed embryos of age E10.5 and E12 days in comparison with control specimens. Consistent with these in vivo findings, high-density cultures of E10.5 periotic mesenchyme plus otic epithelium, treated with doses of atRA that suppress chondrogenesis, showed significantly decreased levels of TGF-beta(1), as compared with TGF-beta(1) levels in untreated control cultures. Furthermore, we demonstrate a rescue of cultured periotic mesenchyme plus otic epithelium from atRA-induced chondrogenic suppression by supplementation of cultures with excess TGF-beta(1). CONCLUSIONS: Our results support the hypothesis that TGF-beta(1) plays a role in mechanisms of atRA teratogenicity during inner ear development.

Animals↗
PubMed1998

Autoregulation of human inner ear blood flow during middle ear surgery with propofol or isoflurane anesthesia during controlled hypotension.

UNLABELLED: We used controlled hypotension to obtain a bloodless cavity during middle ear surgery under an optical microscope. No previous study has assessed the effect of controlled hypotension on inner ear blood flow (IEF) autoregulation in humans receiving propofol or isoflurane anesthesia. In the present study, the IEF autoregulation was determined using laser Doppler flowmetry in combination with transient evoked otoacoustic emissions (TEOAEs) during controlled hypotension with sodium nitroprusside in 20 patients randomly anesthetized with propofol or isoflurane. A coefficient of IEF autoregulation (Ga) was determined during controlled hypotension, with a Ga value ranging between 0 (no autoregulation) and 1 (perfect autoregulation). During controlled hypotension with propofol, IEF remained stable (1%+/-6%; P > 0.05) but decreased by 25%+/-8% with isoflurane (P < 0.05). The Ga was higher during propofol anesthesia (0.62+/-0.03) than during isoflurane anesthesia (0.22+/-0.03; P < 0.0001). Under propofol anesthesia, there were individual relationships between TEOAE amplitude and change in IEF in four patients. Such a correlation was not observed under isoflurane anesthesia. These results suggest that human IEF is autoregulated in response to decreased systemic pressure. Furthermore, isoflurane has a greater propensity to decrease cochlear autoregulation and function than propofol. IMPLICATIONS: The present study shows that inner ear blood flow is autoregulated under propofol, but not isoflurane, anesthesia during controlled hypotension in humans during middle ear surgery. Further studies are needed to explore the postoperative auditory functional consequences of the choice of the anesthetic drug used in middle ear surgery.

Adult↗
PubMedDate not supplied

Evaluation of hyperactive caloric responses in patients with inner ear diseases.

Twenty-three patients with various types of inner ear diseases, who showed hyperactive caloric responses (21 patients showed unilateral hyperactive caloric responses, and 2 patients showed bilateral hyperactive caloric responses) were monitored during 2-10 years and underwent caloric tests repeatedly (2-7 times). None of them showed continuous hyperactivity of the labyrinth throughout their clinical courses. It seems that hyperactive caloric responses in patients who suffer from inner ear disease may be a transient phenomenon, caused by fluctuations of the vestibular condition, central compensation, age and/or mental state of the patients.

Adult↗
PubMed2005

Osteoprotegerin in the inner ear may inhibit bone remodeling in the otic capsule.

OBJECTIVES: To elucidate factors that may be responsible for the inhibition of remodeling of bone within the otic capsule. METHODS: Expression of osteoprotegerin (OPG), receptor activator of nuclear factor kappa B (RANK), and RANK ligand (RANKL) were assayed in samples of bone obtained from the otic capsule, calvarium, and femur, and from the soft tissue within the cochlea using semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR) in mice. Immunostaining was used for histologic localization of the gene products. An enzyme-linked immunosorbent assay (ELISA) was used to quantify the amount of OPG within perilymph, serum, and cerebrospinal fluid. The micro-anatomy of the interface between the otic capsule and the fluid spaces of the cochlea was investigated by brightfield and phase-contrast microscopy and by three-dimensional reconstruction in the mouse and human. RESULTS: OPG, a powerful inhibitor of bone remodeling, was expressed at extremely high levels within the soft tissue of the cochlea and was present in the perilymph at very high concentrations. The OPG produced within the inner ear may diffuse into the surrounding otic capsule, where it may be responsible for inhibition of bone turnover. Our anatomic studies revealed an extensive system of interconnected canaliculi within the otic capsule that had direct openings into the fluid spaces of the inner ear, thus providing a possible anatomic route for the diffusion of OPG from the inner ear into the surrounding bone. CONCLUSION: OPG, a potent inhibitor of osteoclast formation and function, is expressed at high levels within the inner ear and is secreted into the perilymph and the surrounding bone and may serve to inhibit active bone remodeling within the otic capsule, especially immediately adjacent to the cochlea. By this means, the cochlear soft tissue may control the nature of the surrounding petrous bone.

Animals↗
PubMed2002

Three-dimensional fast recovery fast spin-echo imaging of the inner ear and the vestibulocochlear nerve.

The aim of this study was to assess the performance of three-dimensional fast recovery fast spin-echo (3DFRFSE) for imaging of the inner ear as well as the facial and vestibulocochlear nerves. We evaluated 3DFRFSE sequences, comparing it with 3D fast spin-echo (3DFSE) in a water phantom and in 12 normal volunteers. We also examined 66 patients using 3DFRFSE sequence and assessed the visualization of their pathologies. In a water phantom study, signal intensity (SI) on 3DFRFSE was higher than that on 3DFSE at the same TR ranging from 1,500 to 6,000 ms. In normal volunteers, 3DFRFSE with TR of 2,800 ms showed comparable SI, and signal-to-noise ratio (SNR) and contrast-to-noise ratio (CNR) superior to those on 3DFSE with TR of 5,000 ms. In clinical setting, 3DFRFSE was useful in demonstrating anatomic details in the labyrinth and pathologic findings of inner ear. The 3DFRFSE can provide high-resolution heavily T2-weighted images (T2WI) with shorter scan time than 3DFSE without significant disadvantage. The 3DFRFSE is a beneficial technique for evaluation of lesions in the inner ear as well as the facial and vestibulocochlear nerves.

Ear, Inner↗
PubMed2006

Evaluation of vascular endothelial growth factor addition in vitro on mouse inner ear progenitor cell cultures.

We analyzed progenitor cell cultures of inner ear tissue from newborn mice, and found proliferating cells, morphologically differentiating cells and subpopulations of cells expressing either neuronal or glial markers. In addition, we observed the expression of fetal liver kinase-1, a receptor for the vascular endothelial growth factor in a subpopulation of the cultured cells. Consistent with the expression of fetal liver kinase-1, addition of vascular endothelial growth factor at a dose of 10 ng/ml increased the expansion rate of inner ear-derived progenitor cells. Together with other published data, these results suggest that the vascular endothelial growth factor might be involved in inducing or supporting cochlear repair processes.

Alanine↗
PubMed1983

Ototoxic effect of an aminoglycoside drug on an immature inner ear.

In order to investigate to what extent an immature inner ear is injured by external causes, the effect of Kanamycin on an immature cochlea was studied in mice by using scanning and transmission electron microscopes. Our results showed that immature cochleae are more highly susceptible to injury than mature cochleae, especially when the Nuel's space and the Corti tunnel open. It is suggested that in humans, during the stage corresponding to the above period, that is, in about the third gestational month, the inner ear is highly susceptible to injury by external causes.

Animals↗
PubMed1995

[Effect of variations in middle ear pressure on ruptures of the round window membrane of the inner ear of the guinea pig (Cavia porcellus)].

The electrical activity of the inner ear before and after rupture of the round window membrane was monitored in guinea pigs under different pressure conditions with the aid of electrocochleography. Following studies were conducted weekly over a period of 4 weeks. Findings showed that overpressure below the pressure needed to open the Eustachian tube caused strong temporary functional disturbance of the cochlea, especially at high frequencies. Irreversible changes that were pressure-dependent were observed and occurred mainly at high frequencies. Application of low pressure to the round window membrane caused a functional loss comparable to changes after overpressure. Animals with a predamaged cochlea reacted to overpressure that was below opening pressure of the tube and to corresponding low pressure with a longer lasting functional loss than did animals with an undamaged cochlea.

Acoustic Impedance Tests↗
PubMed1994

Identification of hair cell progenitors and intermitotic migration of their nuclei in the normal and regenerating avian inner ear.

Postembryonic production of sensory hair cells occurs in both normal and aminoglycoside-damaged avian inner ears. The cellular source and mechanism that results in new differentiated hair cells were investigated in the avian vestibular epithelia using three distinct cell-cycle-specific labeling methods to identify proliferating sensory epithelial cells. First, immunocytochemical detection of the proliferating cell nuclear antigen, an auxiliary protein of DNA polymerase, allowed labeling of cells in late G1, S, and early G2 phases of the cell cycle. Second, a pulse-fix tritiated thymidine autoradiographic protocol was used to identify cells in S phase of the cell cycle. Finally, Hoechst 33342, a fluorescent DNA stain, was used to identify epithelial cells in mitosis. The distribution of cells active in the cell cycle within the normal and ototoxin-damaged vestibular epithelium suggests that supporting cells within the sensory epithelia are the cellular precursors to the regenerated hair cells. Differences between the proliferation marker densities in control and damaged end organs indicate that the upregulation of mitotic activity observed after streptomycin treatment is due primarily to an increase in the number of dividing progenitor cells. The differences between the extent of ototoxic damage and the level of reparative proliferative response suggest a generalized stimulus, such as a soluble chemical factor, plays a role in initiating regeneration. Finally, after DNA replication is initiated, progenitor cell nuclei migrate from their original location close to the basement membrane to the lumenal surface, where cell division occurs. This pattern of intermitotic nuclear migration is analogous to that observed in the developing inner ear and neural epithelium.

Aminoglycosides↗
PubMed1998

Development of the mouse inner ear and origin of its sensory organs.

The molecular mechanisms dictating the morphogenesis and differentiation of the mammalian inner ear are largely unknown. To better elucidate the normal development of this organ, two approaches were taken. First, the membranous labyrinths of mouse inner ears ranging from 10.25 to 17 d postcoitum (dpc) were filled with paint to reveal their gross development. Particular attention was focused on the developing utricle, saccule, and cochlea. Second, we used bone morphogenetic protein 4 (BMP4) and lunatic fringe (Fng) as molecular markers to identify the origin of the sensory structures. Our data showed that BMP4 was an early marker for the superior, lateral, and posterior cristae, whereas Fng served as an early marker for the macula utriculi, macula sacculi, and the sensory portion of the cochlea. The posterior crista was the first organ to appear at 11.5 dpc and was followed by the superior crista, the lateral crista, and the macula utriculi at 12 dpc. The macula sacculi and the cochlea were present at 12 dpc but became distinguishable from each other by 13 dpc. Based on the gene expression patterns, the anterior and lateral cristae may share a common origin. Similarly, three sensory organs, the macula utriculi, macula sacculi, and cochlea, seem to arise from a single region of the otocyst.

Animals↗
PubMedDate not supplied

An inner ear anomaly in golden hamsters.

A new mutation of the inner ear was discovered in golden hamsters raised in our laboratories. Although scanning electron microscopy showed a normal arrangement of individual stereocilia on the first row of outer hair cells, the entire bundle of stereocilia were irregular in orientation and scattered in several directions. Seventy per cent to 85% of the stereociliary bundles were found to be abnormal throughout the cochlea, with no apparent difference between the right and left sides. Transmission electron microscopy showed that the cuticles of the first row of the outer hair cells were dislocated, but no dislocation due to this mutation was apparent in the lower portions. This mutation of the inner ear was already present in the basal turn four days after birth. The kinocilium was located outside of the stereocilia in the first row of outer hair cells, but sensory hairs were scattered in every direction, as in the adult animals. A comparison of auditory brainstem response tests revealed no difference between the abnormal and normal hamsters.

Animals↗
PubMed2003

The opioid receptors in inner ear of different stages of postnatal rats.

There is increasing evidence that the opioid system has a role in hearing. To provide further evidence for such a role, the expression of opioid receptor mRNAs and proteins in the inner ear of rats was studied during development from birth (P0) to postnatal day 16 (P16). A semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) was employed to detect changes in the expression of delta- (DOR) kappa- (KOR) and mu- (MOR) opioid receptor mRNAs in rat cochleae at P0, P4, P8 and P16. Expression of DOR mRNA levels steadily increased from P0 to P8 with no further increases by P16. KOR mRNA was expressed at a relatively high level at P0 and P4 followed by a decrease while MOR mRNA was expressed at a low level at P0 and P4 followed by an increase by P8 and P16. Immunocytochemical labelling of inner ear sections revealed unique developmental and distribution patterns of opioid receptors. In the organ of Corti DOR immunoreactivity (DOR-IR) was detected in hair cells from P4. In contrast MOR-IR was present only in supporting cells at P0-P16. In the spiral ganglion all three receptor subtypes were expressed from P0 on nerve cell soma and qualitatively appeared to increase with age. Also DOR-IR and MOR-IR were detected at P8 and P16 in nerve fibers within the spiral ganglion. In the limbus DOR-IR was detected at P8 and P16 on cells proximal to the tectorial membrane while MOR-IR was detected more distally. In general these findings demonstrate that within the inner ear each receptor subtype follows specific temporal and spatial developmental patterns, some of which may be associated to the onset of hearing. The data provide further evidence that the opioid system may play a role in the development and functioning of the inner ear.

Aging↗
PubMed1986

[Evaluation of risk factors in various forms of inner ear hearing loss].

As in cardio-vascular diseases certain risk factors are held responsible for the genesis of inner ear affections. We thoroughly examined 205 patients, suffering from various kinds of internal ear disorders. Examinations included audiometric tests, medical, neurological and ophthalomological consultations and laboratory findings. Evaluation showed a significant increase of certain risk factors in our patients compared to the normal population. 50.2% of our patients were overweight, 29.3% had a high blood cholesterol, 28.8% had anaemia, and 22.4% had hypertension. These lesions of the auditory system thus share the same risk factors as the coronary and cerebral circulations. In the second stage of the study we looked for correlations between individual parameters and certain variations of inner ear disturbances, eg. sudden hearing loss, progressive or non-progressive hearing loss, low or high frequency disorders. It was not possible to distinguish between the forms of inner ear disease mentioned on the basis of the prevalence of certain risk factors.

Arteriosclerosis↗
PubMed1999

Corticosteroid pharmacokinetics in the inner ear fluids: an animal study followed by clinical application.

OBJECTIVE: Autoimmune disease (e.g., Cogan syndrome) and other inflammatory inner ear diseases may ravage the labyrinth if not treated aggressively with antiinflammatory medication. Corticosteroids are the mainstay of treatment, yet, partly because of the existence of the blood-labyrinthine barrier, the ideal drug, dose, and route of administration are currently unknown. STUDY DESIGN: In the present study, we established cochlear fluid pharmacokinetic profiles of hydrocortisone, methylprednisolone, and dexamethasone in the guinea pig following oral, intravenous, and topical (intratympanic) administration. High-performance liquid chromatography was used to determine the drug concentrations, and comparisons were made with simultaneous pharmacokinetic profiles from blood and cerebrospinal fluid. RESULTS: Our findings demonstrated a much higher penetration of all three drugs into the cochlear fluids following topical application as compared with systemic administration, with methylprednisolone showing the best profile. DISCUSSION: The results suggested that intratympanic administration of corticosteroids might be more efficacious while avoiding high blood levels and therefore the deleterious side effects of systemic use. CLINICAL APPLICATION: Thirty-seven patients with various inner ear disorders causing sensorineural hearing loss were subsequently treated using intratympanic corticosteroids, 20 with dexamethasone, and 17 with methlyprednisolone. Patients with immune-mediated hearing losses showed the best results, with notable improvement also seen in several cases of a "sudden deafness." No benefit was seen in patients with cochlear hydrops or those with sudden deterioration of a preexisting hearing loss. Three patients developed a transient otitis media related to the treatments, easily controlled with antibiotics. There were no cases of treatment-induced hearing loss and no permanent tympanic membrane perforations. CONCLUSIONS: Overall injection of intratympanic corticosteroids for the treatment of hearing loss in inner ear disorders appears to be both safe and highly effective for certain disorders. The concept of this technique is supported by animal experimental data. The findings from the present study warrant further clinical application and experimental investigation.

Administration, Oral↗
PubMed1991

Platelet storage pool deficiency associated with inherited abnormalities of the inner ear in the mouse pigment mutants muted and mocha.

Several inherited human syndromes have combined platelet, auditory, and/or pigment abnormalities. In the mouse the pallid pigment mutant has abnormalities of the otoliths of the inner ear together with a bleeding abnormality caused by platelet storage pool deficiency (SPD). To determine if this association is common, two other mouse pigment mutants, muted and mocha, which are known to have inner ear abnormalities, were examined for hematologic abnormalities. Both mutants had prolonged bleeding times accompanied by abnormalities of dense granules as determined by whole mount electron microscopy of platelets and by labeling platelets with mepacrine. When mutant platelets were treated with collagen, there was minimal secretion of adenosine triphosphate and aggregation was reduced. Lysosomal enzyme secretion in response to thrombin treatment was partially reduced in muted platelets and markedly reduced in mocha platelets. Similar reductions in constitutive lysosomal enzyme secretion from kidney proximal tubule cells were noted in the two mutants. These studies show that several mutations that cause pigment dilution and platelet SPD are associated with abnormalities of the inner ear. Also, these mutants, like previously described mouse pigment mutants, are models for human Hermansky-Pudlak syndrome and provide additional examples of single genes that simultaneously affect melanosomes, lysosomes, and platelet dense granules.

Animals↗
PubMed2001

Damage to the vestibular inner ear causes long-term changes in neuronal nitric oxide synthase expression in the rat hippocampus.

The vestibular inner ear detects head acceleration and initiates compensatory eye movement and postural reflexes that help keep the visual image of the world stable on the retina, and maintain balance, during unexpected head movement. The most primitive vestibular systems are estimated to have evolved more than 500 million years ago and in mammalian and submammalian species the vestibular reflexes are mediated by basic brainstem pathways (see Wilson and Melvill Jones, 1979 for review). Although the contributions of the vestibular system to higher cognitive function have generally received less attention than its reflexive roles, vestibular sensory information is transmitted to higher centres in the brain and humans with vestibular damage are known to experience debilitating perceptual illusions (see Curthoys and Halmagyi, 1995; Berthoz, 1996 for reviews). Increasing behavioural and neurophysiological evidence suggests that the hippocampus uses information from the vestibular inner ear in order to build up maps of space that can be used in the development of spatial memory during learning tasks (McNaughton et al., 1991; Chapuis et al., 1992; Wiener and Berthoz, 1993; O'Mara et al., 1994; Wiener et al., 1995; Gavrilov et al., 1995; Stackman and Taube, 1996; Vitte et al., 1996; Taube et al., 1996; Save et al., 1998; Peruch et al., 1999; Cuthbert et al., 2000; Russell et al., 2000). However, to date, there has been no indication of the long-term neurochemical effects of the loss of vestibular input on hippocampal function. Since nitric oxide has been implicated in the mechanisms of hippocampal synaptic plasticity associated with the development of short-term memory (e.g. Schuman and Madison, 1991; Schuman et al., 1994; Arancio et al., 1996; Wu et al., 1997; Lu et al., 1999), we examined whether changes occur in the activity and expression of the enzymes responsible for nitric oxide production (nitric oxide synthases) in subregions of the rat hippocampus at different times following unilateral peripheral vestibular lesions, using western blotting and radioenzymatic assays. We found a decreased expression of neuronal nitric oxide synthase in the ipsilateral dentate gyrus at 2 weeks following the vestibular damage and not before, that may be related to the long-term effects of the loss of vestibular input on hippocampal function. These results support the hypothesis that head movement and position information derived from the vestibular inner ear may be important for the normal function of the hippocampus.

Afferent Pathways↗
PubMed1997

Induction of cell proliferation by fibroblast and insulin-like growth factors in pure rat inner ear epithelial cell cultures.

Proliferation of supporting cells in the inner ear is the early major event occurring during hair cell regeneration after acoustic trauma or aminoglycoside treatment. In the present study, we examined the possible influence of 30 growth factors on the proliferation of pure rat utricular epithelial cells in culture. Utricular epithelial sheets were separated and partially dissociated from early postnatal rats via a combined enzymatic and mechanical method. The cultured utricular epithelial cells expressed exclusively epithelial cell antigens, but not fibroblast, glial, or neuronal antigens. With tritiated thymidine incorporation assays, we found that several fibroblast growth factor (FGF) family members, insulin-like growth factor-1 (IGF-1), IGF-2, transforming growth factor-alpha (TGF-alpha), and epidermal growth factor (EGF), stimulated proliferation of the utricular epithelial cells. In contrast, neurotrophins and other growth factors did not elicit any detectable mitogenic effects. Among all of the growth factors examined, FGF-2 was the most potent mitogen. When FGF-2 was added in combination with IGF-1 or TGF-alpha to the medium, combined effects were seen. These results were confirmed with BrdU immunocytochemistry. Thus, the present culture system provides a rapid and reliable assay system to screen novel growth factors involved in proliferation of mammalian inner ear supporting cells. Furthermore, immunostainings revealed that the cultured utricular epithelial cells expressed FGF and IGF-1 receptors, and utricular hair cells produced FGF-2 in vivo. The addition of neutralizing antibodies against FGF-2 or IGF-1 to the cultures significantly inhibited the utricular epithelial cell proliferation. This work suggests that FGF-2 and IGF-1 may regulate the proliferation step during hair cell development and regeneration.

Animals↗