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At least 865 records · Page 48Linked to original sources
PubMed1997

Effect of prostaglandin E1 on the rat inner ear microvascular thrombosis.

1. The effect of prostaglandin E1 was investigated with a two-rat model of hearing disturbance and equilibrium dysfunction associated with inner ear microvascular thrombosis. 2. The inner ear microvascular thrombosis was induced by photochemical reaction between Rose Bengal and transmural green light (540 nm). Photochemical reaction causes endothelial injury followed by platelet adhesion, aggregation, and formation of a platelet- and fibrin-rich thrombus. 3. Under anesthesia, the cochlea or the vestibule was irradiated with green light to induce hearing disturbance or equilibrium dysfunction. 4. In the hearing disturbance model, a compound cochlear nerve action potential was recorded by electrocochleography every minute after the beginning of photoirradiation in the presence of Rose Bengal. 5. In the equilibrium dysfunction model, the photoirradiation was applied for 10 min after Rose Bengal administration. The behavior of rats was observed in the swimming test, and nystagmus was observed 24 hr after the end of photoirradiation. 6. Prostaglandin E1 significantly (P < 0.05) prolonged the time required to suppress the action potential. In the swimming test, 3 of the 6 animals treated with prostaglandin E1 did not rotate about their longitudinal axes (equilibrium dysfunction) and the duration of well-balanced swimming was significantly prolonged (P < .001). Prostaglandin E1 significantly (P < 0.05) suppressed the appearance of nystagmus. 7. In conclusion, prostaglandin E1 potentially prevents hearing disturbance and equilibrium dysfunction due to inner ear microvascular disorders.

Action Potentials↗
PubMed1987

Reversible changes in inner ear function following hyaluronan application in the middle ear.

A safety study regarding the potential ototoxicity of 1.9% hyaluronan was performed in 20 rats. In all animals the middle ear was completely filled with hyaluronan three times at 2-day intervals between the administrations. Inner ear function was evaluated by computerized auditory brainstem response (ABR) measurements. ABR recordings were performed prior to exposure, after myringotomy (but prior to administration of hyaluronan), 5 days after the last administration (n = 15; these animals were then sacrificed for analysis of the middle ear), one month and 3 months later (n = 5). The hearing thresholds were improved in animals 5 days after the last administration of hyaluronan at 6-8 kHz, whereas the hearing thresholds were impaired at 12 and 20 kHz. After one month, ABR thresholds were even better than precontrol levels at 2, 4 and 6 kHz, whereas at all other frequencies the ABR threshold was normal. Three months after hyaluronan exposure, all ABR thresholds were normal, but viscous material was present in the middle ear in 3 of 5 animals. It is concluded that hyaluronan causes reversible changes in inner ear function but lacks ototoxic adverse effects.

Animals↗
PubMed2003

[The orientation and its significance of aquaporin-2 in the rat inner ear].

OBJECTIVE: To study the distribution of aquaporin-2(water channel protein; Aqp-2) in various structures of the SD rat inner ear. METHOD: Fifteen SD rat were used in this experiment and were cardically perfused. The temporal bones were taken out, fixed in 4% paraformaldehyde, processed and sectioned by paraffin-embedded technique. The expression and distribution of Aqp-2 in the rat inner ear were examined by SP immunohistochemical technique. RESULT: Aqp-2 were observed mainly in endolymphatic sac, stria vascularis and spiral ganglion. In addition, Aqp-2 were also labeled in Cortis organ, basilar membrane, vestibular lip and tympanic lip of spiral limus, tectorial membrane and spiral prominence. CONCLUSION: Aqp-2 distributed in the rat inner ear tissues closely related with endolymph metabolism: the endolymphatic sac and stris vascularis. Its expression in the Corti's organ gave another explanation for the handicap hearing along with endolymphatic hydrops, and the distribution of Aqp-2 in the spiral ganglion indicated its possible role in the maintenance of hearing.

Animals↗
PubMedDate not supplied

A reexamination of experimental type II collagen autoimmunity: middle and inner ear morphology and function.

Type II collagen autoimmunity has been reported to result in a number of middle and inner ear morphological and functional abnormalities. We investigated the immunological, electrophysiological, and anatomical effects of this autoimmune state in well-established Wistar-Furth rat models of type II collagen autoimmune arthritis. Seventeen animals immunized with bovine type II collagen were divided into short term (1-3 months postimmunization) and long term (9-11 months) groups. Thirty-three experimental ears were tested electrophysiologically and were compared to nine ears of unimmunized Wistar-Furth rats. No hearing loss was found in the immunized animals, except for four animals that showed middle ear abscess formation consistent with spontaneous, purulent otitis media. All immunized animals showed very significant serum and perilymph antibody titers to type II collagen. No morphological abnormalities of the external, middle, or inner ears could be identified in the noninfected experimental animals. These findings do not support previously reported observations that type II collagen autoimmunity results in ear disease.

Animals↗
PubMed1998

[The experimental research of inner ear metabolism and electrical physiology of autoimmune sensorineural hearing loss].

Inquire into the mechanism of inner ear pathological physiology in autoimmune sensorineural hearing loss (ASHL). With the auditory electric-physiological techniques and enzyme-histochemical method, the change of inner ear hearing function and enzyme activity were observed. These animals, which threshold of auditory nerve compound active potential (CAP) and cochlear microphonic potential(CM) heightening evidently, showed that the amplitude of endolymphatic potential(EP) (include-EP) bring down in various degrees, which was related to the change of the active of Na(+)-K(+)-ATPase and SDH in vascularis stria and endolymphatic sac. The abnormality of enzymes metabolism in inner ear tissues, which following autoimmune inflammation damage, is the pathological foundation of hearing dysfunction.

Action Potentials↗
PubMed1985

Primary culture of capillary endothelial cells from the spiral ligament and stria vascularis of bovine inner ear. Retention of several endothelial cell properties in vitro.

Methods for isolation and culture of microvascular endothelial cells of the inner ear were devised to provide an in-vitro system for studying endothelial functions in this tissue. Capillaries from the stria vascularis and spiral ligament were treated enzymatically to free them from surrounding tissue. Contamination by extraneous tissue was minimized by banding capillary segments in Percoll gradients and culture in plasma-derived serum on a fibronectin-coated substrate. Although only small amounts of inner ear tissue were available, tritiated thymidine autoradiography demonstrated that considerable growth in culture was possible. Addition of heparin and endothelial cell growth supplement to the medium enhanced proliferation. The endothelial origin of the cultured cells was confirmed by immunofluorescent demonstration of the presence of Factor VIII-related antigen and angiotensin-converting enzyme. In addition, tight junctions between cells were observed in both thin sections and platinum replicas obtained by freeze-fracture techniques. Endothelial cells from neither the stria vascularis nor the spiral ligament allowed passage of horseradish peroxidase across the monolayer during a 5-min period. However, endothelial cells from the stria vascularis exhibited a greater amount of pinocytotic activity than those of the spiral ligament, a difference that is also observed in vivo. Methods for expanding a small population of endothelial cells with retention of specialized properties into one of sufficient size for morphologic and biochemical studies have been demonstrated for the inner ear.

Animals↗
PubMed1976

[Pharmacologic aspects in the management of inner ear disease (author's transl)].

Our knowledge of the effects of drugs on the inner ear is extremely insufficient when compared to their effects on other organs. The role of drugs commonly recommended for therapy of inner ear disorders (such as, procaine, antihistaminics, diuretics, osmotics, corticoids and substances changing blood viscosity) has yet to be clarified since the clinical effects of these pharmaceuticals or vasoactive substances often cannot be confirmed by experimental study. Under present circumstances, the use of definitive therapy to prevent deafness has only limited application--as in thyroid hormone substitution to prevent deafness from cretinism.

Bicarbonates↗
PubMed1997

[Ongoing production of sensory epithelium cells in the avian inner ear].

Does the ongoing proliferation of sensory cells occur in the postnatal avian inner ear? This question still awaits further investigation. 5-bromodeoxyuridine (BrdU) is a thymidine analogue that is incorporated into DNA during S phase of the cell cycle. Chickens were given intraperitoneal injections of BrdU at 100 ml/kg body weight. Six hours after injection, they were sacrificed and the temporal bones were removed and prepared for BrdU immunohistochemistry to examine mitotic activity in the inner ear. A small number of labeled hair cells and supporting cells were seen in the basilar papilla (BP). There is a low rate of ongoing production in the postnatal avian vestibular epithelium. The ongoing, postnatal proliferation of vestibular epithelial cell suggests that this epithelium has the potential for repair after degeneration, trauma or ototoxic damage.

Animals↗
PubMed1993

Distribution of KHRI 3 epitopes in the inner ear.

Murine monoclonal antibodies against cochlear structures were previously generated to obtain probes for elucidating the function of cochlear cell subsets. Preliminary immunocytochemical characterization showed that the monoclonal antibody KHRI 3 binds to supporting cells but not sensory cells in the guinea pig cochlea. We have now investigated KHRI 3 epitopes in other species and other parts of the inner ear. The KHRI 3 epitope appears to be species-specific since no immunolabeling was seen in rat inner ear nor in chick inner ear. In immunocytochemical assays in the guinea pig vestibular tissues KHRI 3 stained saccular wall cells and transitional epithelial cells in the utricle and ampules as well as clusters of cells in the endolymphatic sac. In Western blots KHRI 3 stained a broad 70-75 kDa band in lanes loaded with guinea pig cochlea homogenates--as seen previously--as well as in lanes loaded with vestibular tissue homogenates. The immunolabeling patterns suggest that KHRI 3 epitopes are cell membrane components or related to membrane structures. Thus the monoclonal antibody KHRI 3 appears to define a nonsensory cell subset in the guinea pig inner ear that can be identified by expression of KHRI 3 epitopes.

Animals↗
PubMed1985

Recent advances in laser microprobe mass analysis (LAMMA) of inner ear tissue.

Maintenance of ionic gradients within the various fluids compartments of the inner ear requires transport active cellular systems at different locations. LAMMA analysis is ideally suited for detection of ions in microquantity on cellular levels overcoming many technical difficulties. The present paper summarizes the results of microprobe analysis obtained with laser induced mass spectrometry (LAMMA) supplemented by X-ray microprobe analysis of epithelial cell layers adjacent to the endolymphatic space in the cochlear duct, in the vestibular organ and in the endolymphatic sac. The possible role of inner ear as well as ocular melanin in the mechanisms of active ion transport is discussed.

Animals↗
PubMed1999

CT and MR findings of Michel anomaly: inner ear aplasia.

In 1863, Michel described a condition characterized by a total absence of differentiated inner ear structures associated with other skull base anomalies, including an abnormal course of the facial nerve and jugular veins. Michel aplasia clearly differs from Michel dysplasia, in which arrest of embryologic development occurs later. Recently, the role of otic capsule formation on mesenchymal differentiation was reported as well as the impact of the genetic deletion of the homeobox gene on the development of the ear, cranial nerves, and hindbrain. We report two patients with a total absence of inner ear structures bilaterally, illustrating the characteristic appearance of Michel aplasia and associated skull base anomalies.

Adolescent↗
PubMed1988

Endolymphatic sac surgery in congenital malformations of the inner ear.

A retrospective analysis of 40 patients (49 ears) with congenital progressive sensorineural hearing loss who underwent endolymphatic sac surgery was performed. The inner ears were radiographically abnormal in 57% of operated ears. In the remaining cases, subtle malformations beyond the resolving power of radiographic studies were suspected. Early postsurgical hearing loss (defined as a loss greater than 10 dB in three-tone average or greater than 15% in speech discrimination score) was found in 29% of operated ears (14/49). However, only two of these patients lost all of their residual hearing postoperatively (2/49 or 4%). An enlarged endolymphatic sac was noted at surgery in 50% of those with significant postoperative hearing losses. Longer-term stability of hearing was assessed in 22 patients with bilateral inner-ear pathology who underwent surgery on one side only. A comparison of the hearing fate of the operated and nonoperated ears suggested no benefit from the surgical intervention when compared to the natural history of the disease. Based upon this experience, endolymphatic sac surgery for the purpose of hearing stabilization in patients with congenital malformations of the inner ear is no longer recommended.

Adolescent↗
PubMed2000

Roles of beta-catenin in inner ear development in rat embryos.

We studied the roles of beta-catenin in inner ear development in rat embryos using immunostaining and antisense experiments. High levels of beta-catenin appeared transiently in the otic cup during inner ear development. While beta-catenin accumulation was not yet observed in the thickened surface ectoderm at the otic placode, it became to be detected at the apical surface of the otic cup. Then it disappeared from the otocyst. When embryos were treated with the beta-catenin antisense oligodeoxynucleotide (ODN), accumulation of beta-catenin in the otic cup was suppressed and the beta-catenin protein level was significantly less in treated embryos than in controls. The number of cells in the otic cup in treated embryos was smaller than in control embryos. Cells that incorporated bromodeoxyuridine (BrdU) in the otic placode were fewer in number in treated embryos than in controls. In control embryos, acoustic neurons were detected by 2H3 (anti-neurofilament 165 kDa antibody) staining within the acoustic neural crest complex, while only a little staining of 2H3 was observed in the complex of the treated embryos. These results suggested that beta-catenin plays a role in cell proliferation in the otic placodes and in differentiation of acoustic neurons within the acoustic neural crest complex.

Acoustic Maculae↗
PubMedDate not supplied

Intelligibility of sentences recorded from the uterus of a pregnant ewe and from the fetal inner ear.

The intelligibility of sentences recorded from the uterus of a pregnant ewe and from the near-term fetal sheep inner ear was judged by 30 listeners. Sentences were presented to the ewe at 95 and 105 dB SPL while sequential recordings of sound with a hydrophone and a cochlear microphonic (CM) with electrodes were made. Recordings were randomized and presented to listeners to judge the intelligibility of sentences processed through the ewe and fetal inner ear. Intelligibility scores were nearly 99% for air and uterus conditions, dropped to 73% for CM ex utero and to 41% for CM in utero. Results indicated that filtering provided by the tissues and fluids of the maternal abdomen did not affect sentence intelligibility significantly, but the filtering effects as the signal passed into the fetal inner ear resulted in much poorer intelligibility.

Animals↗
PubMed1983

[Effect of intravenous administration of micronomicin on the inner ear of guinea pigs].

The present experiment was made to clarify the effect of intravenous administration of micronomicin (sagamicin, MCR) on the inner ear of guinea pigs (300--350 g). MCR was given to the animals intravenously at dose of 25, 50 mg/kg and 100 mg/kg, respectively for 28 days. Pinna reflex test in frequency range from 20 kHz to 0.5 kHz was performed before, during and after the administration. The temporal bones were removed after intravital perfusion of the inner ears with neutral formation after the end of the administration. Histopathological examination was performed on the serial celloidin sections of the inner ears which had been stained with hematoxylin eosin. The following results were obtained. 1. MCR had a mild corti toxicity, which did not show remarkable dose dependent increase. 2. MCR had more affinity for the vestibular organs than for the organ of corti. The affinity for the vestibular organ increased with increase in dose. 3. MCR showed less increase in corti toxicity in intravenous administration than in intramuscular injection. However, the affinity of MCR for the vestibular organ showed little more increase in the intravenous administration than in the intramuscular injection.

Aminoglycosides↗
PubMed1988

The developing and senescent inner ear: selected topics and models.

Development and senescence are not mirror images, reversed, or opposite processes, but instead involve some common, as well as different mechanisms. In this review, we link the themes of development and senescence of the inner ear through the use of models. The inner ear develops in a highly coordinated series of stages. During development, each organ undergoes major structural changes prior to and during the onset of function. Thereafter, patterns of activity change as each sensory organ matures to its normal functional status. The remodeling continues at a slower pace after the onset of function. By comparison, the senescent inner ear loses its functional capacity and displays varying degrees of impairment. Cell degeneration and atrophy are commonly reported. However, in properly preserved specimens, senescent cells display few cytological markers aside from age pigment that can help to identify them.

Aging↗
PubMed2006

Progression of inner ear pathology in Ames waltzer mice and the role of protocadherin 15 in hair cell development.

The Ames waltzer (av) mouse mutant exhibits auditory and vestibular abnormalities resulting from mutation of protocadherin 15 (Pcdh15). Ames waltzer has been identified as an animal model for inner ear pathology associated with Usher syndrome type 1F. Studies correlating anatomical phenotype with severity of genetic defect in various av alleles are providing better understanding of the role played by Pcdh15 in inner ear development and of sensorineural abnormalities associated with alterations in Pcdh15 protein structure as a result of gene mutation. In this work we present new findings on inner ear pathology in four alleles of av mice with differing mutations of Pcdh15 as well as varying alterations in inner ear morphology. Two alleles with in-frame deletion mutations (Pcdh15 (av-J) and Pcdh15 (av-2J)) and two presumptive functional null alleles (Pcdh15 (av-3J) and Pcdh15 (av-Tg)) were studied. Light and electron microscopic observations demonstrated that the severity of cochlear and vestibular pathology in these animals correlates positively with the extent of mutation in Pcdh15 from embryonic day 18 (E18) up to 12 months. Electron microscopic analysis of immature ears indicated early abnormalities in the arrangement of stereocilia and the inner and outer hair cell cuticular plates, stereocilia rootlets, and the actin meshwork within the cuticular plate. In severe cases, displacement of the kinocilium and alterations in the shape of the cuticular plate was also observed. Mice harboring in-frame deletion mutations showed less disorganization of stereocilia and cuticular plates in the organ of Corti than the presumptive functional null alleles at P0-P10. A slower progression of pathology was also seen via light microscopy in older animals with in-frame deletions, compared to the presumptive functional null mutations. In summary, our results demonstrate that mutation in Pcdh15 affects the initial formation of stereocilia bundles with associated changes in the actin meshwork within the cuticular plate; these effects are more pronounced in the presumed null mutation compared to mutations that only affect the extracellular domain. The positive correlation of severity of effects with extent of mutation can be seen well into adulthood.

Alleles↗