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PubMed2001

Transcription factor GATA-3 alters pathway selection of olivocochlear neurons and affects morphogenesis of the ear.

Patterning the vertebrate ear requires the coordinated expression of genes that are involved in morphogenesis, neurogenesis, and hair cell formation. The zinc finger gene GATA-3 is expressed both in the inner ear and in afferent and efferent auditory neurons. Specifically, GATA-3 is expressed in a population of neurons in rhombomere 4 that extend their axons across the floor plate of rhombomere 4 (r4) at embryonic day 10 (E10) and reach the sensory epithelia of the ear by E13.5. The distribution of their cell bodies corresponds to that of the cell bodies of the cochlear and vestibular efferent neurons as revealed by labeling with tracers. Both GATA-3 heterozygous and GATA-3 null mutant mice show unusual axonal projections, such as misrouted crossing fibers and fibers in the facial nerve, that are absent in wild-type littermates. This suggests that GATA-3 is involved in the pathfinding of efferent neuron axons that navigate to the ear. In the ear, GATA-3 is expressed inside the otocyst and the surrounding periotic mesenchyme. The latter expression is in areas of branching of the developing ear leading to the formation of semicircular canals. Ears of GATA-3 null mutants remain cystic, with a single extension of the endolymphatic duct and no formation of semicircular canals or saccular and utricular recesses. Thus, both the distribution of GATA-3 and the effects of null mutations on the ear suggest involvement of GATA-3 in morphogenesis of the ear. This study shows for the first time that a zinc finger factor is involved in axonal navigation of the inner ear efferent neurons and, simultaneously, in the morphogenesis of the inner ear.

Animals↗
PubMed1995

The utriculo-endolymphatic valve in pediatric temporal bones.

The utriculo-endolymphatic valve (UEV) is located in the posterior wall of the utricle at its junction with the utricular duct and was first described in a human fetus by Bast in 1928. Although different theories about its normal position and function have been postulated, the function of the UEV remains unclear. In the present investigation we studied 118 temporal bones from 70 children to determine whether there were differences in the position of the valve and by inference, its function between children and adults. Premortem ages ranged from newborn to 10 years (mean age, 11.6 months). All temporal bones were fixed in 10% formalin, decalcified and processed by the celloidin technique. Specimens were sectioned in a horizontal plane at a thickness of 20 microns. Every tenth section was stained with hematoxylin-eosin and studied by light microscopy. The position of the UEV was then classified as closed or open. Valves damaged by preparation or having an uncertain position were classified as artifact. The chi-square test was used to determine a correlation between the position of the valve and the status of the rest of the endolymphatic system and whether or not endolymphatic hydrops was present in the cochlear and vestibular systems. The UEV was closed in 39 temporal bones (33.1%) and open in 13 (11.0%). Artifacts were found in 66 bones (55.9%). In the group of patients with a collapsed ductus reuniens the UEV was closed in 38% of the specimens, suggesting that the UEV prevented loss of endolymph from the pars superior, but these findings were not statistically significant.

Artifacts↗
PubMed1990

[Pathohistological study on active endolymphatic hydrops in guinea pig--with stress stimulations].

Recently Meniere's disease is believed to show a pathological features of endolymphatic hydrops, but the etiology of this disease has not yet been ascertained. Many investigators tried to create animal models with endolymphatic hydrops by obliterating endolymphatic sac and duct. However, these methods have not been adequate to explain the mechanism of development of Meniere's disease, because it gives mechanical damage to destroy endolymphatic sac and duct. On the other hand, Meniere's disease is thought to develop even as a result of stress. The present paper reported the conduction of an acute experiment, creating active endolymphatic hydrops by stress load, to study the occurrence rate of endolymphatic hydrops and the pathological findings of inner ears by a light microscope. This was followed by a light and electron microscopic study on the changes in permeability of the cochlear lateral wall with horseradish peroxidase and a study of the development mechanism of endolymphatic hydrops. Results obtained were as follows: 1. Although it was impossible to cause endolymphatic hydrops with a single stimulation, four kinds of stress stimulations could cause endolymphatic hydrops with the rate of 37.8%. 2. Judging from the different pathological findings between the group with four kinds of stress stimulations and the untreated control group, vessel permeability in the stria vascularis was highly changeable, while that in the spiral ligament was not. 3. It was found out that increased permeability of the stria vascularis vessels was by increased pinocytotic vesicular transport and through tight junctions from vessel lumen to basal lamina and that it was presumably only by increased pinocytotic vesicular transport beyond basal lamina. 4. It was assumed that increased permeability of the stria vascularis vessels was one of the causes of endolymphatic hydrops which were believed to be pathological features of Meniere's disease.

Animals↗
PubMed1990

Haircell forward and reverse transduction: differential suppression and enhancement.

Cochlear outer haircells are believed to play a significant role in an amplification process which greatly enhances inner ear sensitivity. Haircell forward (mechanical-to-electrical) and reverse (electrical-to-mechanical) transduction may be involved. We have produced decreases in cochlear microphonic and increases in electrically-evoked cochlear emissions using the drug, furosemide. The data indicate forward and reverse transduction are not a simple bi-directional process and suggest that the outer haircells are part of a negative feedback system.

Animals↗
PubMed1999

Morphological changes induced by administration of a Na+,K+-ATPase inhibitor in normal and hydropic inner ears of the guinea pig.

The objective of this study was to determine the effects of ouabain, a Na+,K+-ATPase inhibitor, in inner ears. Administering ouabain locally through the round window and vestibule, resulted in degenerative changes in cochlear and vestibular sensory cells and limbal fibrocytes, but the stria vascularis and spiral ligament were less affected. The position of Reissner's membrane was rarely changed. Vacuolar spaces in the sensory epithelia of cristae, maccula utriculi and macula sacculi increased in number. Nystagmus was a common occurrence with or without demonstrating degeneration of vestibular sensory cells. By administering ouabain systemically, the course of developing endolymphatic hydrops could not be altered in the ears with endolymphatic duct blockage. Edema of nerve endings of inner hair cells and vestibular sensory cells was frequently observed with administration of a high concentration of ouabain in both normal and hydropic ears, but edema was reversible. Degeneration of some vestibular sensory cells were observed in hydropic ears with a long survival time. The mechanism of selective sensitivity or non-sensitivity of inner ear tissues to ouabain is discussed.

Animals↗
PubMed1999

Inner ear transgene expression after adenoviral vector inoculation in the endolymphatic sac.

Gene transfer has been performed in a variety of organs. In the mammalian inner ear, viral vectors have been used to introduce exogenous reporter genes via the scala tympani into the cochlea. While scala tympani inoculation is clinically feasible, it is not without risks. Moreover, transgene expression has so far been restricted to the cochlear tissues in the perilymphatic spaces that are contiguous with the scala tympani. To achieve gene transfer of vestibular organs and cells surrounding the endolymphatic space, and to extend the clinical utility of inner ear gene therapy, we developed a new surgical approach for vector inoculation. A replication-deficient adenoviral vector, Ad.RSVntlacZ, was injected into the guinea pig endolymphatic sac. A large number of blue (LacZ-positive) cells was observed in the endolymphatic sac and duct, the vestibule, and the ampulla. Blue cells were also detected in the cochlea, mainly in cells bordering the endolymphatic space: marginal cells in the stria vascularis and supporting cells in the organ of Corti. These findings indicate that inoculation of viral vectors into the endolymphatic sac can provide efficient gene transfer into a variety of cell types that are not accessible via scala tympani inoculation.

Adenoviridae↗
PubMed1989

Does severe water deprivation affect the inner ear? An experimental study of the gerbilline endolymphatic sac.

Through an ultrastructural study of the endolymphatic duct (ED) and sac (ES) system, the effects of an impaired body fluid metabolism on the inner ear fluid environment in the mongolian gerbil has been evaluated. A dehydrative state has been determined depriving of water for both five and twelve days this desert animal, which is known to withstand long periods of water abstinence. The morphological changes of the ED and ES under these circumstances have been compared with those induced by ethacrynic acid intoxication. Although the cochlear partition did not show signs of damage, the ED and ES system seems to be negatively influenced by the dehydrative state and displays a marked imbibition of the subepithelial tissue, which at places shows accumulation of an organic matrix. A regulating role for the antidiuretic hormone on the inner ear fluids of the mongolian gerbil is also proposed and discussed.

Animals↗
PubMed1980

Anatomical studies of the posterior petrous apex with regard to hearing preservation in acoustic neuroma removal.

Some surgeons have shown that tumors of the internal auditory canal and cerebellopontine angle may be removed with preservation of hearing through the suboccipital approach. If hearing is to be conserved, the cochlear division of the VIIIth cranial nerve and blood supply of the labyrinth must be preserved. In addition, surgical entry into the labyrinth, upon removal of the posterior wall of the internal auditory canal, must be avoided since it is likely to result in permanent sensorineural hearing loss. Careful anatomic dissection of 20 human temporal bones has shown that exposure of the lateral-most recess of the internal auditory canal from a suboccipital approach is impossible without injury to the endolymphatic duct, common crus, vestibule or ampulla of the posterior semicircular canal. Previous authors have suggested that exposure of the horizontal crest may be used as a safe landmark in avoiding labyrinthine injury. However, our study has shown that exposure of the horizontal crest usually leads to labyrinthine injury. In 19 out of 20 cases, the labyrinth would have been entered had the horizontal crest been used as a landmark for the lateral limit of bone removal. The application of the anatomical relationship quantified in this study may improve our ability to avoid labyrinthine injury in the suboccipital removal of acoustic neuromas.

Ear Canal↗
PubMed1994

Changes in immunostaining of cochleas with experimentally induced endolymphatic hydrops.

Cochleas with experimentally induced endolymphatic hydrops were immunostained for Na+,K(+)-ATPase, intracellular Ca(++)-ATPase, carbonic anhydrase, aldehyde dehydrogenase, calcium-binding proteins, vimentin, and the gap junction protein, connexin 26. No changes in immunostaining of hydropic ears were observed 1 week after blockage of the endolymphatic duct. Two weeks to 1 month after the operation, immunostaining of type I fibrocytes in the spiral ligament, which are positive for all but Na+,K(+)-ATPase, was slightly decreased on the operated side. These changes became more pronounced 3 months after the operation. However, staining for Na+,K(+)-ATPase of the stria vascularis and of type II fibrocytes of the spiral ligament was not reduced until 6 months postoperative. The reduction of enzymes and other cell constituents that may be involved in ion balance of cochlear fluids indicates that cells in the spiral ligament play an important role in cochlear homeostasis and that they merit further study in animal and human otopathology.

Adenosine Triphosphatases↗
PubMed2000

Expression of inducible nitric oxide synthase (iNOS/NOS II) in the hydropic cochlea of guinea pigs.

Immunohistochemical investigations of the guinea pig cochlea, using a specific antibody to the inducible isoform of NO synthase (iNOS/NOS II), have been performed 3 weeks after closure of the right endolymphatic duct (n=7). Endolymphatic hydrops, the morphological substrate of Meniere's disease, became evident by distension of the Reissner's membrane. iNOS expression could be noted in endothelium, spiral ganglion cells, in nerve fibers, in supporting cells of the organ of Corti and cells of the spiral ligament. Temporal bones of non-operated controls (n=6) as well as of sham-operated animals (n=3) did not show structures positive to iNOS. These findings imply that iNOS-generated NO could be involved in the pathophysiology of cochlear dysfunction in Meniere's disease.

Animals↗
PubMedDate not supplied

Measurement of action potential thresholds in experimental endolymphatic hydrops.

Unilateral experimental endolymphatic hydrops was created by endolymphatic sac and duct obstruction in guinea pigs. Studies of action potential (AP) threshold were then performed and compared with histologic findings. Action potential thresholds were significantly increased in the hydrops ears. The close relationship between AP changes and hydrops was sufficient to allow the detection of hydrops by AP threshold measurements alone. The AP threshold changes were positively related to the degree of hydrops and postoperative interval in a manner consistent with hearing changes seen in Meniere's disease. Based upon the foregoing, experimental endolymphatic hydrops appears to be a valid and usable model for the study of the cochlear aspects of Meniere's disease.

Action Potentials↗
PubMed2004

Responses of the endolymphatic sac to perilymphatic injections and withdrawals: evidence for the presence of a one-way valve.

Although the endolymphatic sac (ES) is thought to be a primary site for endolymph volume regulation, we have limited knowledge of how it responds to volume and pressure changes. In a prior publication, we demonstrated changes of K(+), Na(+) and endolymphatic sac potential (ESP) resulting from volume injections into, and withdrawals from, scala media of the cochlea. In the present study, we compared the influence of injections into and withdrawals from scala tympani of the cochlea on the endolymphatic sac. It is assumed that similar pressure changes are induced in endolymph and perilymph of both the cochlear and vestibular compartments of the ear. Pressure changes induced by the perilymphatic injections and withdrawals did not induce similar K(+) changes in the ES. The majority of perilymph withdrawals caused K(+) and ESP reductions in the sac, but few injections caused any measurable changes in the sac. Pressure measurements from the ES demonstrated that transmission of labyrinthine pressures to the lumen was directionally sensitive, with negative pressure transmitted more effectively than positive. In other experiments, application of infrasonic stimulation to the ear canal resulted in K(+) increase in the ES. These physiological measurements suggest that the endolymphatic duct may be closed by sustained positive pressure in the vestibule but open during pressure fluctuations. Study of the anatomy where the endolymphatic duct enters the vestibule suggests that the membranous sinus of the endolymphatic duct could act as a mechanical valve, limiting the flow of endolymph from the saccule to the endolymphatic sac when pressure is applied. This structure could therefore play an important role in endolymph volume regulation.

Animals↗
PubMed1992

Tropic effects of otic epithelium on cochleo-vestibular ganglion fiber growth in vitro.

Sensory nerve fibers of the cochleo-vestibular ganglion (CVG) innervate the otic epithelium in the early chick embryo by directed growth. To see if the target tissue could exert a tropic influence, we co-cultured CVGs from chick embryos (Hamburger-Hamilton stages 16-30) in a 3D collagen matrix with their normal target epithelium or with other epithelial tissues taken from the same or different stages of development. The pattern of neurite outgrowth and the viability of the CVG after five days in vitro were assessed histologically with a silver method. On the basis of the patterns of neurite outgrowth directed toward the epithelium, the cultures were classified as having slightly, mostly, exclusively, or no directed outgrowth. Of 49 cultures containing otic epithelium, 33 had mostly or exclusively directed growth patterns. This effect did not depend on any particular stage difference between co-cultures or on their viability in vitro. Cultures of non-sensory otic epithelium (endolymphatic duct) also presented directed growth patterns. Co-cultures with ectoderm from forelimb or visceral arch had little, if any, directed growth. The directed growth could not be explained simply as a result of guidance by non-neuronal cells or of the viability of the explants. The results are consistent with the hypothesis that the otic epithelium provides a tropic factor that attracts growing CVG fibers.

Animals↗
PubMed1980

Analysis of proteins of the stria vascularis of the normal and the waltzing guinea pig.

Proteins of the stria vascularis of the normal and the genetically deaf waltzing guinea pig were analysed by one and two-dimensional acrylamide gel electrophoresis. Cochlear proteins were labeled in vivo by replacing the perilymph with a solution containing radioactive precursors. With the two-dimensional analysis, more than 200 polypeptides were resolved. Proteins that are exposed on the endolymphatic surface of the stria vascularis were identified by lactoperoxidase-catalysed iodination. Seven polypeptides were identified with this technique. No consistent changes in protein patterns of the stria vascularis from the waltzing guinea pig were detected.

Animals↗
PubMed1997

Two-phase endolymphatic hydrops: a new dynamic guinea pig model.

The classical guinea pig model for Meniere's disease, in which endolymphatic hydrops was achieved by destruction of the endolymphatic sac and obliteration of the endolymphatic duct, is a non-physiological profound model with shortcomings in relation to Meniere's disease as seen in patients. We developed a more subtle animal model; the two-phase endolymphatic hydrops. This model is based on a combination of chronic endolymphatic sac dysfunction, induced by slight destruction of the most distal part of the endolymphatic sac, and acute stress-induced endolymph production by stimulation of the Na/K-ATPase in the stria vascularis with aldosterone. Light microscopy of the fluid compartments of four groups of cochleas was used to examine them for the presence of endolymphatic hydrops: i) Normal (control) cochleas showed no hydrops; ii) some of the non-operated (no destruction) aldosterone-treated cochleas showed small degrees of hydrops mainly present in the basal turns; iii) mild dissection of the endolymphatic sac without administration of aldosterone produced a hydrops which was mainly present in the cochlear apex; iv) combination of chronic endolymphatic sac dysfunction and acute attacks of endolymph production by aldosterone administration revealed the most severe degrees of hydrops in all cochlear windings, damage to cochlear structures, and cellular disturbances of the epithelial lining of the endolymphatic sac. This new model may represent a more physiologic and dynamic approach to Meniere's disease and may explain the etiology of many symptoms in patients such as the fluctuant nature and the types of sensoneuronal hearing losses.

Aldosterone↗
PubMed2002

History of Meniere's disease and its clinical presentation.

The term Meniere's disease is used to define either the classic triad of vestibular and cochlear symptoms and aural pressure from known or unknown causes or its clinical variants, vestibular and cochlear Meniere's disease. Some variants evolve after years into typical forms, whereas others do not. Some symptoms (positional vertigo) have been long underestimated in previous reports. The more we study our patients and correlate clinical findings and the natural history with pathologic studies on temporal bones and laboratory research, the more we will understand Meniere's disease and its causes. Some causes have already been identified as most probable. Extrinsic factors (inflammation, trauma, otosclerosis, autoimmunity, endocrine disorders, and such) interact with congenital (genetic) and developmental intrinsic factors (primary or secondary, acquired) into a multifactorial inheritance that is, to date, the best explanation for the basis of Meniere's disease. Endolymphatic hydrops is widely accepted as the pathologic substrate, but not all hydrops seems to be progressive or becomes clinically manifest. Endolymphatic hydrops is the result of a dysfunction in the mechanism of production/absorption of endolymph, which is mainly due to defective absorptive activity of the endolymphatic duct and sac. Hyperproduction of endolymph cannot be excluded in some cases. Ruptures of the labyrinthine membranes do not satisfactorily substantiate the multiform duration, recurrence, and repetitiveness of attacks of Meniere's disease, nor do they explain the entire complex of symptoms. It seems reasonable to explain symptoms of Meniere's disease on the basis of mechanical factors (as observed in temporal bone studies) associated with biologic and biochemical factors.

Adult↗
PubMed1979

[The effect of sympathectomy on the cochlear oxygen pressure (pO2) under conditions of haemorrhagic hypotension (author's transl)].

Oxygen partial pressure was measured in the endolymph area of the cat cochlea under conditions of hemorrhagic hypotension. The experiments took place after unilateral upper cervical sympathectomy and under control conditions. The pO2-measurements were carried out with the aid of polarographic micro-coaxial needle electrodes according to Baumgärtl and Lübbers (1, 2, 3). In animals which had not been sympathectomized, the cochlear pO2 decreased continuously parallely to blood pressure, with the beginning of bleeding. After sympathectomy pO2-decrease in cochlea only occurred at substantially lower aortal blood pressure. This allows the following conclusions: 1. Under conditions of hemorrhagic shock the blood flow of the inner ear is not as much included in central circulation as brain and heart. 2. The blood pressure dependence of the inner ear blood flow depends on the sympathetic innervation, it can practically be abolished up to a blood pressure of 65 mm Hg by denervation. 3. It is being discussed, which therapeutic consequences can be drawn from the evident influence of the sympathetic innervation on the inner ear blood flow.

Animals↗
PubMed2006

Cochlear transducer operating point adaptation.

The operating point (OP) of outer hair cell (OHC) mechanotransduction can be defined as any shift away from the center position on the transduction function. It is a dc offset that can be described by percentage of the maximum transduction current or as an equivalent dc pressure in the ear canal. The change of OP can be determined from the changes of the second and third harmonics of the cochlear microphonic (CM) following a calibration of its initial value. We found that the initial OP was dependent on sound level and cochlear sensitivity. From CM generated by a lower sound level at 74 dB SPL to avoid saturation and suppression of basal turn cochlear amplification, the OHC OP was at constant 57% of the maximum transduction current (an ear canal pressure of -0.1 Pa). To perturb the OP, a constant force was applied to the bony shell of the cochlea at the 18 kHz best frequency location using a blunt probe. The force applied over the scala tympani induced an OP change as if the organ of Corti moved toward the scala vestibuli (SV) direction. During an application of the constant force, the second harmonic of the CM partially recovered toward the initial level, which could be described by two time constants. Removing the force induced recovery of the second harmonic to its normal level described by a single time constant. The force applied over the SV caused an opposite result. These data indicate an active mechanism for OHC transduction OP.

Acoustic Stimulation↗