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At least 685 records · Page 38Linked to original sources
PubMed2002

Fast recovery 3D fast spin-echo MR imaging of the inner ear at 3 T.

High-resolution MR imaging of the inner ear with a heavily T2-weighted 3D fast spin-echo sequence has been performed successfully at 1.5 T. However, at 3 T, the longer T1 time of CSF necessitates a longer TR, resulting in significantly prolonged imaging times. In this study, the fast recovery 3D fast spin-echo sequence, which permits the TR to be reduced while maintaining T2 contrast, was optimized at 3 T for imaging of the inner ear. The optimized sequence parameters are as follows: 1500/294 (TR/TE); echo spacing, 18.1 ms; bandwidth, 38 kHz at 512 readout; and imaging time, 13 minutes.

Ear, Inner↗
PubMed1990

Effect of arachidonic acid on the inner ear blood flow measured with a laser Doppler flowmeter.

The present study was undertaken to clarify the effect of arachidonic acid (AA) on the inner ear blood flow of rats as measured with a laser Doppler flowmeter. With the rats under anesthesia with sodium pentobarbital, the middle ear was approached ventrally and a laser Doppler probe was positioned over the lateral wall of the cochlea. Drugs were administered via the subclavicular artery. The dose range of each drug was determined so as not to affect the systemic blood pressure. The AA (20 to 70 micrograms) increased the inner ear blood flow dose-dependently; this effect was abolished by indomethacin (5 mg orally). Both prostaglandin E2 (PGE2; 1 to 50 ng) and CS-570, a PGI2 analogue (12.8 to 25.6 ng) caused a dose-dependent increase in the inner ear blood flow. The response of PGI2 was shorter than that of PGE2. On the other hand, a stable thromboxane A2 (STA2; 30 to 80 ng) decreased the inner ear blood flow dose-dependently. Administration of PGF2 alpha (0.2 to 3 micrograms) showed no effect on the inner ear blood flow. These results indicated that the effect of AA was mediated mainly via PGI2 and PGE2.

Animals↗
PubMed2000

C-type natriuretic peptide-like immunoreactivity in the rat inner ear.

C-type natriuretic peptide (CNP) is a member of the atrial natriuretic peptide family (ANP family). The family also includes ANP and brain natriuretic peptide (BNP). These peptides regulate the homeostasis of body fluid and blood pressure as a neuropeptide in the central nervous system as well as a cardiac hormone in the periphery. We have recently reported the expression of CNP mRNA in the inner ear. To assess the possible physiological role of CNP in the inner ear, we investigated the localization of CNP peptide in the rat inner ear by immunohistochemistry at the light and electron microscopic level. CNP-like immunoreactivity was widely distributed in the secretory and the neuronal portion of the inner ear, i.e. the spiral ligament, the dark cell region of the utriculus, the epithelium of the endolymphatic sac, the spiral ganglion cells and the vestibular ganglion cells. The results suggest that CNP may play a role in the homeostasis of the perilymph and endolymph and may also influence nerve activities in the inner ear.

Animals↗
PubMed1989

Ototoxic effects of a pseudodisaccharide aminoglycoside antibiotic, dactimicin, on the inner ears of guinea pigs.

The effect of dactimicin on the inner ear of guinea pigs was investigated by comparing it with the effects of ribostamycin, astromicin and amikacin. At doses of 200 and 400 mg/kg/day for 4 weeks, no pinna reflex loss was observed, but 2 animals receiving 400 mg dactimicin/kg/day showed unilateral loss of the outer hair cells in the cochlea and very scattered loss of the hair cells in the vestibular organ. At doses of 400 and 500 mg dactimicin/kg/day for 5 weeks, all surviving animals showed no abnormality of the outer hair cells, the inner hair cells and the spiral ganglion cells in the cochlea except for scattered unilateral loss of the outer hair cells and loss of the stria vascularis. Based on these observations, it is concluded that the ototoxicity of dactimicin on the inner ear of guinea pigs is the same as or a little stronger than that of ribostamycin, weaker than or the same as that of astromicin and weaker than amikacin.

Amikacin↗
PubMed1998

Cell fate choices and the expression of Notch, Delta and Serrate homologues in the chick inner ear: parallels with Drosophila sense-organ development.

The sensory patches in the vertebrate inner ear are similar in function to the mechanosensory bristles of a fly, and consist of a similar set of cell types. If they are truly homologous structures, they should also develop by similar mechanisms. We examine the genesis of the neurons, hair cells and supporting cells that form the sensory patches in the inner ear of the chick. These all arise from the otic epithelium, and are produced normally even in otic epithelium cultured in isolation, confirming that their production is governed by mechanisms intrinsic to the epithelium. First, the neuronal sublineage becomes separate from the epithelial: between E2 and E3.5, neuroblasts delaminate from the otocyst. The neuroblasts then give rise to a mixture of neurons and neuroblasts, while the sensory epithelial cells diversify to form a mixture of hair cells and supporting cells. The epithelial patches where this occurs are marked from an early stage by uniform and maintained expression of the Notch ligand Serrate1. The Notch ligand Delta1 is also expressed, but transiently and in scattered cells: it is seen both early, during neuroblast segregation, where it appears to be in the nascent neuroblasts, and again later, in the ganglion and in differentiating sensory patches, where it appears to be in the nascent hair cells, disappearing as they mature. Delta-Notch-mediated lateral inhibition may thus act at each developmental branchpoint to drive neighbouring cells along different developmental pathways. Our findings indicate that the sensory patches of the vertebrate inner ear and the sensory bristles of a fly are generated by minor variations of the same basic developmental program, in which cell diversification driven by Delta-Notch and/or Serrate-Notch signalling plays a central part.

Animals↗
PubMed2004

Developmental expression of otoconin-22 in the bullfrog endolymphatic sac and inner ear.

In amphibians, calcium carbonate crystals are present in the endolymphatic sac and the inner ear. The formation of these crystals is considered to be facilitated by a protein called otoconin-22. We examined the spatial and temporal expression of otoconin-22 during the development of the bullfrog (Rana catesbeiana) using RT-PCR, in situ hybridization (ISH), and immunofluorescence techniques. By RT-PCR, otoconin-22 mRNA was first detected in embryos at Shumway stage 20, and this expression pattern continues in late stages. The first otoconin-22 mRNA-positive reaction was detected in stage 22 embryos in the placode of the endolymphatic sac. Otoconin-22 protein was observed in the epithelial cells of the endolymphatic sac at stage 24. On the other hand, a whole-mount ISH technique showed the first expression of otoconin-22 mRNA in the inner ear, in addition to the endolymphatic sac, at the mid-phase of Shumway stage 25. We discuss the role of otoconin-22 in the formation of calcium carbonate crystals in the endolymphatic sac and inner ear.

Animals↗
PubMedDate not supplied

Development of melanosomes and cytochemical observation of tyrosinase activity in the inner ear.

The ultrastructure and tyrosinase activity of melanocytes in the inner ear of pigmented guinea pigs were observed. Melanocytes/melanocyte-like cells were seen in the stria vascularis, the vestibular dark cell area and the endolymphatic sac. In the stria vascularis, melanosomes in several stages of maturation were seen in the cytoplasm of the intermediate cells and melanin-laden endosomes existed in the basal cells. Only the intermediate cells contained tyrosinase-positive cytoorganelles; Golgi sacs and neighboring small vesicles. Numerous melanocytes containing many melanosomes were observed under the epithelium of the vestibular dark cell area, and they showed tyrosinase activity. Melanocytes were seen in the endolymphatic sac, and they also showed tyrosinase activity. However, the epithelial cells of the endolymphatic sac, which had vacuoles containing melanin, did not show tyrosinase activity. Based on these findings, it can be said that (1) most of the intermediate cells of the stria vascularis must be melanocytes, (2) melanogenesis is vigorous in melanocytes of the inner ear, and (3) melanin in the epithelial cells of the endolymphatic sac is transferred in from melanocytes and is never synthesized in the epithelial cells.

Animals↗
PubMed2004

The development of semicircular canals in the inner ear: role of FGFs in sensory cristae.

In the vertebrate inner ear, the ability to detect angular head movements lies in the three semicircular canals and their sensory tissues, the cristae. The molecular mechanisms underlying the formation of the three canals are largely unknown. Malformations of this vestibular apparatus found in zebrafish and mice usually involve both canals and cristae. Although there are examples of mutants with only defective canals, few mutants have normal canals without some prior sensory tissue specification, suggesting that the sensory tissues, cristae, might induce the formation of their non-sensory components, the semicircular canals. We fate-mapped the vertical canal pouch in chicken that gives rise to the anterior and posterior canals, using a fluorescent, lipophilic dye (DiI), and identified a canal genesis zone adjacent to each prospective crista that corresponds to the Bone morphogenetic protein 2 (Bmp2)-positive domain in the canal pouch. Using retroviruses or beads to increase Fibroblast Growth Factors (FGFs) for gain-of-function and beads soaked with the FGF inhibitor SU5402 for loss-of-function experiments, we show that FGFs in the crista promote canal development by upregulating Bmp2. We postulate that FGFs in the cristae induce a canal genesis zone by inducing/upregulating Bmp2 expression. Ectopic FGF treatments convert some of the cells in the canal pouch from the prospective common crus to a canal-like fate. Thus, we provide the first molecular evidence whereby sensory organs direct the development of the associated non-sensory components, the semicircular canals, in vertebrate inner ears.

Animals↗
PubMed1981

Inner ear pathology in deaf mutism.

This is a report of the inner ear pathology found in a pair of temporal bones from a deaf mutism case. This patient's spouse and four of six children were deaf mutes. Some members in the succeeding generation were also known to be deaf mutes. The temporal bones (horizontally sectioned) showed the cochleo-saccular degeneration with exactly similar extent bilaterally. The scala media and the saccular space were atrophied, and displaced membranes were attached onto the degenerated sensory epithelia in many areas, but some portion of the scala media exhibited an ectatic view. The cochlear and saccular nerves were severely reduced. In addition to the pathology found in the pars inferior, the internal auditory canal and the cochlear aqueduct were enlarged. All end organs and nerves in the pars superior were intact.

Aged↗
PubMed1982

[Inner ear and diabetes mellitus experimental streptocotocin diabetes in rats].

The histological changes in the inner ear were compared with the hearing ability in insulin deficiency diabetes of rats. 38 LEW-Han-rats were treated with streptocotocin; 34 of these became diabetic, as proved by the glucose tolerance test. 22 rats served as controls. The diabetes was not treated. For a period of up to 440 days the weight, blood glucose and auditory function were controlled in the living animals. Auditory function was tested by means of pinnal reflex of Preyer for a frequency range between 1000 and 20000 cps. With regard to the mean values of frequency, neither a decrease nor a difference between normal controls and diabetic rats was found to any substantial degree. Histological examinations of sacrificed diabetic rats meanwhile showed the well-known changes in the kidneys with microaneurism, thickened basal lamina, mesangial proliferation, and hyaline bodies. The changes in the inner ear, especially in the region of the stria vascularis and lamina spiralis ossea to the ganglion cochleae, were rather discrete, so that no pronounced diminution of the auditory function as a result of restricted metabolism was to be expected. A loss of ganglion cells was seen in the spiral ganglion of the cochlea in correlation with ageing. There was no clear difference between diabetic rats and normal controls. Insulin deficiency diabetes causes severe changes in the vessels, as demonstrated in the kidney. In the inner ear, however, there were no comparable changes, the hearing ability of diabetic rats remaining practically normal.

Animals↗
PubMed1996

Endolymphatic duct/sac enhancement on gadolinium magnetic resonance imaging of the inner ear: preliminary observations and case reports.

Twelve patients with auditory and/or vestibular symptoms were examined with a gadolinium magnetic resonance imaging (Gd-MRI) study. They all were found to have enhancement of only the endolymphatic duct/sac structures of the inner ear. Most of these findings were unilateral, but a few were bilateral. The patients underwent auditory, vestibular, and blood tests in an attempt to clarify the reason for this abnormal enhancement. Several specific etiologies were identified, but several cases had unknown causes. In this article we review the concept of inflammation of the inner ear structures with particular attention to the role of the endolymphatic duct/sac in the immune response of the inner ear. The idea of an inflammatory response of the inner ear leading to endolymphatic hydrops (Meniere's disease) is discussed, but these patients did not follow a clear path from inflammation of the endolymphatic duct/sac to endolymphatic hydrops. However, the longest follow-up was only 4 years, and our observations remain preliminary. Finally, the authors have found that Gd-MRI study of the inner ear provides valuable information in the investigation of patients with new auditory and/or vestibular symptoms.

Adult↗
PubMed1982

The laser microprobe mass analysis technique in the studies of the inner ear.

Laser microprobe mass analysis (LAMMA) has been used to investigate cation and anion concentration in shock frozen, freeze-dried and plastic embedded inner ear tissue. Dissected inner ear specimens were prepared in various media of known ionic compositions and the influence on the K/Na ratio was measured in the lateral cochlea wall (spiral ligament, stria vascularis). For control purposes of the various procedures employed, muscle specimens (external standard) were processed in parallel. It was found that there is a good correlation between the K/Na ratio and the preservation of the tissue fine structure by comparing the results in tissues with different degrees of freezing damage.

Cochlea↗
PubMed2006

Developmental expression and localization of KCNJ10 K+ channels in the guinea pig inner ear.

The inward rectifier Kir4.1, composed of KCNJ10 K channel subunits, plays an essential role in inner ear K homeostasis. We have investigated the developmental expression and localization of KCNJ10 (Kir4.1) in the guinea pig inner ear using semi-quantitative reverse transcription polymerase chain reaction and immunohistochemistry. Kcnj10 was expressed at low levels from embryonic day 30 (E30), increased from E45, and persisted from E50 to adulthood. KCNJ10 channel protein was detected in spiral ganglion satellite cells of the basal turn at E40, and at E45 its expression proceeded with a base-to-apex gradient along the cochlear spiral. KCNJ10 protein was enriched in the myelin sheath around the cochlear nerve between E40 and E45 and disappeared gradually with age. In the strial intermediate cells, KCNJ10 channel expression was first observed at E50, and lagged behind that of the spiral ganglion. In addition, KCNJ10 channel protein was expressed and localized in vestibular transitional cells. Differential expression of KCNJ10 channel protein suggests roles for KCNJ10 channels in inner ear development and onset of auditory function.

Animals↗
PubMed1997

[Immune-mediated inner ear disease: report of clinical cases].

Many clinical and experimental studies have obtained evidence of immune-mediated inner ear disease. Discrepancies between theories of the mechanisms of injury to the inner ear and the laboratory tests that identify it mean that the diagnosis is based on clinical symptoms and a positive response to treatment. We report four cases of immune-mediated inner ear disease characterized by endolymphatic hydrops, fluctuating hearing loss, sudden deafness (first symptom of primary Sjögren's syndrome), and rapidly progressive sensorineural hearing loss.

Adult↗
PubMed1999

Otx1 and Otx2 activities are required for the normal development of the mouse inner ear.

The Otx1 and Otx2 genes are two murine orthologues of the Orthodenticle (Otd) gene in Drosophila. In the developing mouse embryo, both Otx genes are expressed in the rostral head region and in certain sense organs such as the inner ear. Previous studies have shown that mice lacking Otx1 display abnormal patterning of the brain, whereas embryos lacking Otx2 develop without heads. In this study, we examined, at different developmental stages, the inner ears of mice lacking both Otx1 and Otx2 genes. In wild-type inner ears, Otx1, but not Otx2, was expressed in the lateral canal and ampulla, as well as part of the utricle. Ventral to the mid-level of the presumptive utricle, Otx1 and Otx2 were co-expressed, in regions such as the saccule and cochlea. Paint-filled membranous labyrinths of Otx1-/- mutants showed an absence of the lateral semicircular canal, lateral ampulla, utriculosaccular duct and cochleosaccular duct, and a poorly defined hook (the proximal part) of the cochlea. Defects in the shape of the saccule and cochlea were variable in Otx1-/- mice and were much more severe in an Otx1-/-;Otx2(+/)- background. Histological and in situ hybridization experiments of both Otx1-/- and Otx1-/-;Otx2(+/)- mutants revealed that the lateral crista was absent. In addition, the maculae of the utricle and saccule were partially fused. In mutant mice in which both copies of the Otx1 gene were replaced with a human Otx2 cDNA (hOtx2(1)/ hOtx2(1)), most of the defects associated with Otx1-/- mutants were rescued. However, within the inner ear, hOtx2 expression failed to rescue the lateral canal and ampulla phenotypes, and only variable rescues were observed in regions where both Otx1 and Otx2 are normally expressed. These results suggest that both Otx genes play important and differing roles in the morphogenesis of the mouse inner ear and the development of its sensory organs.

Animals↗
PubMedDate not supplied

Cytokeratin diversity in epithelia of the human inner ear.

The expression of cytokeratins (Cks) nos. 5, 7, the combination 5 and 8, 8, 10, 17, 18 and 19 was analysed in the inner ear of 14-24-week-old human fetuses, using 10 different well characterized monoclonal antibodies (mAbs). A complex pattern of Ck immunoreactivity was found. Cks 8 and 18 were identified in both cochlear and vestibular hair cells as well as in all other epithelia. Epithelia involved in fluid regulation (stria vascularis, Reissner's membrane and dark cell epithelium) revealed the same pattern of Ck immunoreactivity in spite of morphological differences in cell configuration. A specific Ck, no. 10 as detected with the mAbs RKSE 60, was found in the endolymphatic duct and sac. The expression of Cks in the human inner ear is in principle similar to that found in the labyrinth of other animal species, for instance in the mouse. However, the human inner ear had a more complex pattern than any inner ear so far known in animal species.

Antibodies, Monoclonal↗