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At least 739 records · Page 41Linked to original sources
PubMed1986

Early morphological and chemical changes induced by cisplatin in the guinea pig organ of Corti.

Guinea pigs were treated with a single dose of Cisplatin (5 mg IP). After 2-4 days the cochleas were prepared for morphological analysis by scanning electron microscopy and chemical analysis by X-ray dispersive microanalysis. Following Cisplatin, the bundles of stereocilia on the hair cells were found to be rough, disarrayed, fused, and finally absorbed. Significant increases were found in the levels of calcium, sulphur, and phosphorus in the abnormal hair cells. It is suggested that the high calcium levels might be due to the inhibition of enzymes which normally keep cytoplasmic calcium low, and that some of the changes in the stereocilia might be secondary to this.

Animals↗
PubMed1998

Effect of membrane tension on gap junctional conductance of supporting cells in Corti's organ.

The effects of turgor pressure-induced membrane tension on junctional coupling of Hensen cell isolates from the inner ear were evaluated by input capacitance or transjunctional conductance measurement techniques. Turgor pressure was altered by changing either pipette pressure or the osmolarities of extracellular solutions. Both positive pipette pressure and extracellular applications of hypotonic solutions, which caused cell size to concomitantly increase, uncoupled the cells as indicated by reduced input capacitance and transjunctional conductance. These changes were, in many cases, reversible and repeatable. Intracellular application of 50 microM H-7, a broad-based protein kinase inhibitor, and 10 mM BAPTA did not block the uncoupling effect of positive turgor pressure on inner ear gap junctions. The transjunctional conductance at a holding potential of -80 mV was 53.6 +/- 5.8 nS (mean +/- SEM, n = 9) and decreased approximately 40% at a turgor pressure of 1.41 +/- 0.05 kPa. Considering the coincident kinetics of cell deformation and uncoupling, we speculate that mechanical forces work directly on gap junctions of the inner ear. These results suggest that pathologies that induce imbalances in cochlear osmotic pressure regulation may compromise normal cochlear homeostasis.

Animals↗
PubMedDate not supplied

Immunoelectron-microscopic localization of synaptophysin in the organ of Corti of the guinea pig.

Synaptophysin has been localized previously in the mammalian cochlea at the light-microscopic level and in few reports by electron microscopy using either a preincubation procedure or the avidin-biotin reaction. Here we present results of the electron-microscopic analysis for postembedding immunoreactivity of synaptophysin in the cochlea of the guinea pig of LR-White-embedded samples. Strong synaptophysin immunoreactivity is located in the cytoplasm of the efferent nerve endings at the base of inner and outer hair cells. Besides this, some antibodies to synaptophysin were also identified in the cytoplasm of outer hair cells. To get more information about the cellular content of synaptophysin, the density of the immunoreaction per square micrometer was determined for the outer hair cells of the second turn of the cochlea counting the gold particles in numerous ultrathin sections. The role of synaptophysin identified in the cytoplasm of outer hair cells is discussed.

Animals↗
PubMed1987

[Calcium antagonists and damage to the organ of Corti in acoustic trauma].

The protective effect of Ca2+ antagonists in acoustic trauma was evaluated by morphometric analysis of the guinea pig cochlea. Damage to the outer and inner hair cells was significantly reduced. Ca2+ antagonists may exert a beneficial influence on the cellular membrane of the sensory cell or on the cochlear vasculature if given in advance and in the early post-traumatic phase.

Animals↗
PubMed1996

Type II collagen-induced autoimmune ear disease in mice: a preliminary report on an epitope of the type II collagen molecule that induced inner ear lesions.

To identify the epitope on the type II collagen molecule that induced autoimmune ear disease, electrophysiological and histological studies were carried out in DBA/1J mice immunized with native chick type II collagen (Clln) and cyanogen bromide (CNBr) peptide 1I (CB-I1 peptide) that was cleaved from chicken type II collagen with CNBr digestion. Four months after immunization, three of six Clln-immunized mice and five of six CB-I1 peptide-immunized mice developed moderate hearing loss. No control animals showed hearing loss. The pattern of hearing loss was characteristic of progressive deafness. Furthermore, the immunized mice showed temporal lesions involving atrophy of the Corti organ and degeneration of the spiral ganglion, in proportion to the level of the hearing loss. Because similar inner ear lesions were induced by immunization with Clln and CB-I1 peptide, CB-I1 peptide contains at least one epitope that induces autoimmune inner ear disease in collagen II-induced disease on the chick type II collagen molecule involved in pathogenesis of autoimmune ear disease. CB-I1 peptides were concluded to contain the epitope that induces autoimmune inner ear disease in collagen IIn-induced disease.

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↗
PubMed1992

Peripheral and central target-derived trophic factor(s) effects on auditory neurons.

In the developing inner ear, a naturally occurring programmed cell death of cochleovestibular ganglion (CVG) neurons as well as peripheral and central target-derived trophic effects on survival of embryonic CVG neurons are known. To further analyze these target derived trophic interactions, spiral ganglion explants obtained from 5 day postpartum (P5) rat pups were cultured with an intact organ of Corti and in the absence of Corti's organ. Both neuronal survival and neurite extension were influenced by the presence of this peripheral target tissue. Local destruction of Corti's organ caused both neuritic retraction and neuronal cell death to occur in a corresponding portion of the spiral ganglion. This peripheral target-derived neurotrophic effect may be mediated by a diffusible factor(s) since organ of Corti conditioned medium also had a neurotrophic effect on the survival of auditory neurons in cell cultures of dissociated spiral ganglia from P5 rat pups. A component of central target tissue, i.e. astrocytes, was also shown to release a diffusible factor(s) that supported the survival of dissociated P5 rat spiral ganglion neurons. The neurotrophic effects on the in vitro survival of spiral ganglion neurons by both of these conditioned medium factors were concentration dependent.

Animals↗
PubMed1983

The pattern of sensorineural degeneration in the cochlea of the deaf shaker-1 mouse: ultrastructural observations.

Experiments were done to extend existing knowledge on the nature and course of postnatal sensory and neural changes in the inner ear of shaker-1 mutant mice. Mice, 3-, 6-, 10-, 12-, 18-, and 30 days old, homozygous for the sh-1 gene, were studied using transmission electron microscopy. The data indicate retarded development coupled with the early onset of progressive degeneration in Corti's organ its nerve supply, and the cells of the spiral ganglion. Especially noteworthy are the following: in 3-day-old mice both outer hair cells and spiral ganglion cells are already abnormal. The latter are especially loosely ensheathed by glial cells and are in direct contact with nerve fibers. Outer hair cells contain vacuoles and lysosomes. By 6 days of age inner hair cells come to be similarly affected. By 18 days most of the afferent nerve supply of the organ of Corti has degenerated. The behavior of efferents within the organ is complex. Efferents arrive late (day 12) at the outer hair cells, they are few in number, form only immature synapses with the cell, and they subsequently degenerate. In contrast, the efferent nerve supply of the inner hair cell appears normal, if not over-abundant. The simultaneous occurrence of organ of Corti and spiral ganglion cell anomalies is discussed in terms of the role of sensorineural interactions in the expression of genetic defects affecting the inner ear. The selective degeneration of efferents to outer hair cells is viewed as being consistent with the hypothesis that there are two independent efferent systems which innervate the two types of cochlear sensory hair cells.

Animals↗
PubMed1980

Organ of Corti-specific polypeptides: OCP-I and OCP-II.

Two polypeptides, OCP-I and OCP-II, specific to the organ of Corti of the quinea pig and the rate, were detected by two-dimensional polyacrylamide gel electrophoresis. They were neither present in other inner ear structures, nor in other organs tested. The two polypeptides constitute a substantial portion of the total protein of the organ of Corti. Both inner and outer layer of the organ of Corti contained approximately equal amounts of OCP-I and OCP-II. The molecular weights of OCP-I and OCP-II are 37,000 and 22,500 daltons, respectively. The corresponding pI values are 4.9 and 5.1, respectively. in addition, actin and tubulin were detected in both layers of the organ of Corti.

Animals↗
PubMed2005

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

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

Animals↗
PubMed2004

RNA expression induced by cisplatin in an organ of Corti-derived immortalized cell line.

Cisplatin [cis-diamminedichloroplatinum(II)] (CDDP) is an organic compound that is widely used for the treatment of a large number of tumors. Its clinical use is limited by the presence of some undesired side effects, like as oto- and nephro toxicity, whose mechanisms of action are not understood. One of the possible CDDP toxicity mechanism seems to involve the generation of reactive oxygen species (ROS), that can impair morphology and function of hair cells (HC) in the organ of Corti. To test this hypothesis we evaluated the effect of CDDP treatment on RNA steady-state levels of 15,000 genes by microarray analysis, using, as a experimental model, the OC-k3 cell line, obtained from the organ of Corti of transgenic mice and constitutively expressing the large SV40 T antigen. We have found overexpression of several genes related to arachidonate mobilization including phospholipase A2, group IV and V, phospholipase A2 activating protein and lysophospholipase I and III, as well as lipoxygenation like arachidonate 12-lipoxygenase and arachidonate 5-lipoxygenase activating protein. In addition, we found significant transcription of genes regulating cell respiration, including cyt c oxidase, as well as genes involved in xenobiotic detoxification and lipid peroxidation such as cyt P450, and other oxidases including spermine oxidase and monoamine oxidase. As a whole, overexpression of the group of different genes seems to indicate that an oxidative burst could take place during cisplatin administration. We therefore searched for evidences of superoxide anion and hydrogen peroxide by means of electron paramagnetic resonance (EPR) spectroscopy and flow cytometry, but failed to detect them. On the other hand, we found an increase of malondialdehyde (MDA) synthesis and protein carbonylation products, indicating the occurence of lipid peroxidative degradation. When we tested the effectiveness of butylated hydroxytoluene (BHT), dithiothreitol (DTT) and N-acetylcysteine (N-Ac) as cytoprotectants, all of them reduced protein carbonylation to control levels and significantly protected OC-k3 from CDDP-induced cell death, with an higher protection when using the lipophylic antioxidant BHT. The same antioxidants prevented also the onset of protein carbonylation, which extent was decreased to basal levels. These data indicate that CDDP is able to stimulate gene expression up to 12 h after the beginning of the treatment. This increase in gene transcription involves a large number of genes potentially able to increase the level of cell ROS. Consistently, cells survival is improved by cotreatment with antioxidants, in particular lipophilics.

Acetylcysteine↗
PubMed1994

Cellular retinol-binding protein type I is prominently and differentially expressed in the sensory epithelium of the rat cochlea and vestibular organs.

To understand the possible role of retinoic acid during inner ear development and cellular regeneration, we have examined the expression pattern of two intracellular retinoid-binding proteins, the cellular retinol- and retinoic acid-binding proteins of type I in the developing and mature rat inner ear. Expression of cellular retinol-binding protein type I was seen in the supporting cells of the organ of Corti and vestibular organs as soon as the first signs of differentiation of the adjacent hair cells were seen. In the developing organ of Corti, the expression pattern followed the basal-to-apical coil differentiation gradient. After the 1st postnatal week, detectable expression of cellular retinol-binding protein type I disappeared from the organ of Corti, but persisted in the supporting cells of vestibular organs throughout life. Expression of cellular retinoic acid-binding protein type I was not found in the inner ear sensory epithelia. Cellular retinol-binding protein type I has previously been shown to act as a substrate carrier in the synthesis of retinoic acid from its precursor, retinol. Our data suggest that retinoic acid is synthesized in the developing sensory epithelium of the cochlear and vestibular organs and that a concentration gradient formed by retinoic acid may have a role in differentiation of the cochlear sensory epithelium. Furthermore, retinoic acid may have a role in damage-induced hair cell regeneration in the developing and mature vestibular organs as well as in the developing auditory organ. The absence of cellular retinol-binding protein type I from the supporting cells of the mature organ of Corti may be associated with the inability of this organ to regenerate hair cells after damage.

Aging↗
PubMed1983

Transplacental kanamycin ototoxicity in the guinea pig.

The effect of kanamycin on the cochlear sensory epithelium of albino guinea pig fetuses was studied histologically following the administration of 200 or 400 mg/kg body weight kanamycin sulfate to the pregnant mothers for 8 consecutive days at different stages of gestation. Surface view analysis of Corti's organ revealed slight damage following treatment in the middle trimester of gestation and marked damage due to treatment in the last trimester. The pattern of hair cell loss induced during and after the functional differentiation of the cochlea resembled the pattern of ototoxic lesions in the adult ear. The assumed mechanisms for induction of teratogenesis by kanamycin in the fetal organ of Corti are discussed.

Animals↗
PubMed1976

Detection of ototoxicity from drugs applied topically to the middle ear space.

This paper summarizes data obtained from two separate studies done in our laboratory. Both studies were done to investigate the possibility that drugs commonly applied to the middle ear space could be the cause of sensori-neural hearing loss. The two drugs that were felt to be the most likely candidates for the studies were neomycin and polymyxin B. In the neomycin study, the various drug concentrations were administered three times a day for four weeks. In the polymyxin B study, the administration was three times a day for two weeks. Cochlear function was evaluated electrophysiologically and by examination of surface preparations of the organ Corti. The data show that both neomycin and polymyxin B can, in concentrations similar to those found in commercially available otic drops, induce cochlear damage when they are applied to the middle ear space of guinea pigs. The degree of damage produced is related. In the case of neomycin, it was shown that the effect worsens as the duration of the dosage administration is extended...

Animals↗