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PubMed1993

[The effect of calcium ion on ampullary nerve potential].

The effect of calcium ion (Ca2+) in the endolymphatic and/or perilymphatic space of the posterior semicircular canal (p.s.c.) nerve response was studied. When both endolymph and perilymph contained no Ca2+, no p.s.c. nerve response was observed. When only the endolymph contained Ca2+ and the perilymph was Ca2+ free, again no nerve response was observed. On the other hand, when only the perilymph contained Ca2+, p.s.c. nerve response was evoked. Therefore, Ca2+ in the perilymph was considered to be essential for maintaining the function of the p.s.c. as a mechanoreceptor.

Action Potentials↗
PubMed1975

Definition of fluctuant hearing loss.

In summary, fluctuant hearing loss is defined as a disorder of the inner ear characterized by fullness, roaring tinnitus, and fluctuations in hearing. It is believed to be caused by an inadequate absorption of endolymph from the endolymphatic sac, with or without one or more metabolic disorders, that interferes with the delicate balance between the production and absorption of endolymph and thus produces cochlear hydrops. This triad of fullness, roaring tinnitus, and fluctuant hearing loss resulting from cochlear hydrops is much more common than the quadrad of true turning vertigo, fullness, roaring tinnitus, and fluctuant hearing loss due to vestibular and cochlear hydrops known as Meniere's disease. Although patients with fluctuant hearing loss only may eventually develop vertigo as the chief complaint and then be said to have Meniere's disease, it is remarkable how many patients continue to suffer mainly from cochlear symptoms at all times. It would appear, because of the greater frequency of fluctuant hearing loss than in Meniere's disease, that the cochlear labyrinth is more susceptible to hydrops than the vestibular labyrinth. For the purposes of diagnosis and treatment it is very useful to separate patients into those with fluctuant hearing loss and those with Meniere's disease.

Animals↗
PubMed1994

A theoretical approach to understanding of the vestibular perception organization in microgravity condition.

This paper should be viewed as a part of our attempts to arrive at a quantitative understanding of some contradictory experimental phenomena in the vestibular perception. The most popular remains the Steinhausen's model of perception, in which the endolymph circulation, caused by the angular acceleration, is "measured" by the displacement of cupulae diaphragm. Though displacements of the cupulae top were experimentally observed, the thorough mathematical analysis shows that the applicated stop-stimuli were too much over the range of adequate stimulation conditions, so the cupulae was teared off from its normal position. The more natural mechanism of perception was proposed by McLaren & Hillman. It was experimentally demonstrated that the cupulae diaphragm remained margin attached during the normal stimulation conditions only with its bottom moved according to the value of the applicated angular acceleration. A question only arises, how will be the hair cells excited by low level stimulation, when elastic deformations of the cupulae are small and there is no visible shift of the cupulae bottom? The response is to find in the third mechanism formulated by Schmaltz, which connected the excitation of hair cells with the process of endolymph diffusion through the cupulae towards the subcupulae space.

Animals↗
PubMed2000

[Modeling of the structure and mechanics of the otolith membrane].

Behavior of otoliths of mammals against static (gravitation and changed pressure in the surrounding endolymph) and dynamic loads was surveyed using analytic and computerized (the finite difference method) models of the otolith membrane (OM). It was presumed that OM consists of gel-like and otoconial layers differing in mechanic and thickness. Comparison with available experimental data allowed to assess magnitudes of mechanic parameters of the gel-like layer responsible for OM interaction with the receptor hair cells (Yung's module for the layer is 1-10 N/m2 with the viscosity in the order of 1 poise), the characteristic times of otolith dynamics (T2 approximately 0.03 s, T1 approximately 10(-6)-10(-5) s), and the impact of changed endolymph pressure on the OM behavior. As was shown, inertial drift of mammalian OM is not so dependent on OM mass as on the relation of OM pressure on the molecular surface to Yung' module of the gel-like layer overlieing the macula.

Basilar Membrane↗
PubMed1992

[Localization of Na/K ATP-ase in the inner ear].

The perilymphatic compartment of the inner ear resembles plasma ultrafiltrate, whereas the endolymphatic compartment is characterized by a high potassium and low sodium concentration. Perilymph is considered to be the precursor of endolymph. The chemical composition of endolymph and the generation of the transepithelial potential is regulated by Na-K-activated adenosine triphosphatase. The cytochemical localization of Na/K ATP-ase is demonstrated in the guinea pig inner ear. The mechanism for cation regulation in the endolymphatic compartment is discussed.

Animals↗
PubMed1977

[The pathogenesis of the acute symptoms of Menière's disease (author's transl)].

The pathogenesis of vertigo attacks and hearing fluctuations in Menière's disease is discussed on the basis of new electronmicroscopic observations on the perilymph endolymph barrier. The zonulae occludentes (z.o.) of the epithelial cells lining the endolymphatic space are the main sealing elements which control the passive ion transport. They consist of parallel running intramembranous fibrils (cell membrane fusion lines). Recent investigations demonstrated conditions which partially destruct some of such fibrils (e.g. increased osmotic pressure, endocrine disorders). This also may be true in Menière's attacks: tight z.o. are transformed to leaky z.o. such that a high transepithelial ion exchange developes. This would result in reduced generation of the receptor potentials as well as in decreased activities of the first order afferent neurons as it was supposed earlier by other authors. This mechanism may be combined with a decompensation of active ion transport processes due to microcirculation disturbances. Finally it will be pointed out that true ruptures of the endolymphatic walls cannot be the usual mode of reversible lesions in Menières disease but a diffuse leakage of the perilymph-endolymph barrier.

Acute Disease↗
PubMed2005

Fluid-structural dynamics of ground-based and microgravity caloric tests.

Microgravity caloric tests aboard the 1983 SpaceLab1 mission produced nystagmus results with an intensity comparable to those elicited during post- and pre- flight tests, thus contradicting the basic premise of Barany's convection hypothesis for caloric stimulation. In this work, we present a dynamic fluid structural analysis of the caloric stimulation of the lateral semicircular canal based on two simultaneous driving forces for the endolymphatic flow: natural convection driven by the temperature-dependent density variation in the bulk fluid and expansive convection caused by direct volumetric displacement of the endolymph during the thermal irrigation. Direct numerical simulations indicate that on earth, the natural convection mechanism is dominant. But in the microgravity environment of orbiting spacecraft, where buoyancy effects are mitigated, expansive convection becomes the sole mechanism for producing cupular displacement. A series of transient 1 g and microgravity case studies are presented to delineate the differences between the dynamics of the 1 g and microgravity endolymphatic flows. The impact of these different flow dynamics on the endolymph-cupula fluid-structural interactions is also analyzed based on the time evolutions of cupular displacement and velocity and the transcupular pressure differences.

Algorithms↗
PubMed2005

[Effect of adriamycin on expression of mdr1 gene in guinea pig cochlea lateral wall].

OBJECTIVE: To study whether ADM affect the expression of mdr1 gene in guinea pig cochlea lateral wall. METHOD: Sixty white guinea pigs with red eyes were divided into three groups: control group, NS group and ADM group. Guinea pigs were administered an intravenous injection of 30 mg/kg ADM. Four hoars later,ten animals were then immediately sacrificed, and the bony labyrinths were removed. The remaining ten animals were sacrificed after 24 h. The effect of ADM, an ototoxicity drug, on expression of mdrl gene in guinea pigs cochlea lateral walls were observed with RT-PCR. Furthermore, the ADM concentration in endolymph were measured by high performance liquid chromatography. RESULT: For ADM group, the density ratio of mdr1 to beta-action of the 24 h was significantly greater compared to that of the 4 h or controls; In contrast, the ADM concentration of 4 h was significantly higher than that of the 24 h. CONCLUSION: mdr1 gene in normal guinea pig cochlea lateral wall is a stress gene. It can be induced by ADM; it may be not only related to reduce the accumulation of ototoxicity drug in endolymph, but also associated with the protective function of inner ear.

Animals↗
PubMed2006

New insights into the role of pendrin (SLC26A4) in inner ear fluid homeostasis.

For over 100 years after the first description of the disorder, the molecular pathology underlying the deafness and thyroid pathology in Pendred syndrome (PS) remained unknown. In 1997, early progress towards understanding the molecular basis of the disorder was made when we identified the PS gene and found it to belong to the SLC26 family of anion transporters. The realization that an anion transporter was responsible for these clinical features soon highlighted a potential role for pendrin in thyroid hormone biosynthesis. The role of pendrin in deafness, however, remained unclear. Our determination of its expression pattern in the inner ear along with the development of a mouse with a targeted disruption of the Slc26a4 gene has revealed that Slc26a4 is expressed in areas of the endolymphatic compartment known to play a role in endolymph reabsorption and that absence of this protein leads to a profound prenatal endolymphatic hydrops and destruction of many of the epithelial cells surrounding the scala media. The precise mechanisms underlying endolymph reabsorption in the inner ear are not yet known; these studies, however, provide some of the groundwork for allowing the future delineation of these processes.

Animals↗
PubMed1991

[Experimental endolymphatic hydrops. Biochemical data in the guinea pig].

The electrochemical and osmotic composition of the inner ear fluids has been studied during experimental endolymphatic hydrops in guinea pig. The data showed that the modifications of the electrochemical composition of endolymph has been detected only after more than 2 weeks after the hydrops induction. The endocochlear potential, the K and Cl concentrations, and the osmolality progressively decreased between 6 and 9 weeks of hydrops. The longitudinal gradients disappeared. After 24 weeks of hydrops, the endocochlear potential was 50% of the initial value whereas the K and Cl concentrations and the osmolality were higher than that measured at 9 weeks but remained lower than contralateral, normal values. These results suggest that the alterations of the electrochemical and osmotic composition of endolymph that were observed during the evolution of experimental endolymphatic hydrops in guinea pig are related to an alteration of the permeabilities of the Reissner's membrane induced by an increase of hydrostatic pressure.

Animals↗
PubMed1979

On pathogenesis of symptoms in Ménière's disease.

A conception of the mechanism for initiating symptoms in Ménière's disease has been forwarded. According to this conception production of endolymph may vary also in normals. The hydrops in Ménière cases is brought about by a relative insufficiency in endolymphatic draining routes and the hydrops presents itself only at peak endolymph production periods. The attacks of vertigo are brought about at the distension of the sacs as well as of the regaining of normal shape of the sacs. The mechanism causing the vertigo could be an effect of mechanical push-and-pull effect on the sensory epithelium of the cristae. The early low-tone hearing loss and the persistant normal caloric reactivity also in advanced Méière cases may be due to simple physical laws : distensions of sacs with equal walls will more easily be brought about in wider than narrow compartments.

Dilatation, Pathologic↗
PubMed1975

[Studies on the patency of the reuniting duct (author's transl)].

Using human temporal bone specimens the patency of the reuniting duct was studied. The endolymph was marked by various dyes and fluorescent substance, during the application the cochlea remained closed. It is shown that the substances in the endolymph flow from the first turn of the cochlear duct via the reuniting duct into the saccule. The patency of the reuniting duct is confirmed by histological serial sections, and the clinical significance of these findings is discussed.

Adult↗
PubMed1980

[Effects of some bivalent and trivalent ions and of EGTA on the process of activation of the ampullar receptors].

In order to define the role of Ca++ in labyrinthine receptors the endolymph in isolated canal preparations was replaced with modified solutions containing Ca-substitutes(Sr++, Ba++), Ca-antagonists(La+++, Cd++, Mg++) and Ca-chelating agents(EGTA). The response of the receptors was evaluated by recording the slow and propagated potentials from the ampullar nerve. All the tested solutions proved able to depress or cancel the mechanically evoked responses of ampullar receptors. The presence of Ca++ in the endolymph is therefore essential to grant the mechanosensitivity of the hair cells. The receptor blockade produced by Ca-withdrawal develops much earlier under continuous mechanical stimulation. This suggests that Ca++ might be bound in some structures and released during cupula deflections.

Animals↗
PubMed1993

Current view of the mechanism of benign paroxysmal positioning vertigo: cupulolithiasis or canalolithiasis?

Theoretical evidence is presented that all the typical features of BPPV (benign paroxysmal positioning vertigo) cannot be explained by cupulolithiasis in that otoconial debris become settled on the cupula of the posterior semicircular canal. A free floating clot of inorganic particles (heavier than endolymph) in the ampullofugal branch of the posterior semicircular canal is more likely to cause the syndrome. The clot always gravitates to the most dependent part of the canal as soon as the patient's head is moved in a way that alters the angle between the canal's plane and the gravity vector. As compared to a plunger (depending on the direction it moves) the clot produces push or pull forces on the cupula, thereby eliciting the BPPV attack. This clot-induced endolymph flow mechanism is compatible with all features of BPPV such as latency, limited duration, fatigability, change in direction of the induced nystagmus, and the efficacy of physical therapy in both posterior and horizontal semicircular canal BPPV. The floating clot is only activated by changes in position of the head relative to the gravitational vector (positioning vertigo) but not by prolonged static positions of the head (positional vertigo), which fits clinical experience. Therefore, canalolithiasis rather than cupulolithiasis provides a better definition of the underlying mechanism in BPPV.

Endolymph↗
PubMed1997

The origin of thermally evoked vestibular potential.

The origin of the thermally evoked ampullary nerve action potential was searched using isolated frog posterior semicircular canal (PSC). The PSC was placed in the dish with 2 chambers separating endo- and perilymphatic fluid. Cooling stimulus was given by approximating the iced bar to the ampulla, and induced action potential (CAP) was recorded. When only the endolymph contained Ca2+, no CAP was evoked, while, the perilymph contained Ca2+, CAP was observed. These findings were comparable between with and without cupula. When only the endolymph contained tobramycin (TOB), the spike count did not change. However, when TOB was added into the perilymph, the spike count decreased according to concentration of TOB. When TOB was washed out, the spike count recovered. These findings were also comparable between with and without cupula. The above results indicate that thermally evoked vestibular potentials possibly originate in the hair cell.

Action Potentials↗
PubMed1978

Pseudocaloric nystagmus.

Pseudocaloric nystagmus (PCN) is an appropriately beating nystagmus induced by cold caloric irrigation of an ear with abolished vestibular function. The nystagmus is not the result of endolymph flow but probably represents unmasking a latent nystagmus by altering the patient in this case, through tactile (caloric) stimulation. Pseudocaloric nystagmus has the following characteristics: (1) mild intensity (eyes closed-slow phase velocity usually less than 8 degrees/sec), it has not been observed with the eyes open, (2) always beats away from the diseased ear; therefore, any nystagmus induced by cold irrigation will be appropriately (contralateral) beating while that induced by warm irrigation will be inappropriately (contralateral beating; 3) the induced nystagmus will not reverse direction after inverting the ampulla. Establishing bidirectional sensitivity of the cupula by demonstrating appropriately beating nystagmus to ampullopetal and ampullofugal flow of endolymph not only assures that the lateral semicircular canal (SCC) is functionally intact to caloric stimulation but will avoid errors in electronystagmorgraphic (ENG) interpretation.

Caloric Tests↗
PubMed1981

Mannitol-induced stria vascularis edema.

After administration of mannitol, an osmotic diuretic, edema of the stria vascularis occurs, which is morphologically indistinguishable from the stria edema observed after administration of loop-inhibiting diuretics. Similar edema also was observed after glycerin administration. Both mannitol and glycerin may act osmotically to draw fluid from the endolymph into the stria. Temporary improvement in the hearing level and discrimination from the glycerin test in endolymphatic hydrops could be explained by this potential mechanism of endolymph volume reduction.

Animals↗
PubMed1999

Gap junctions and connexin expression in the inner ear.

Several different recessive mutations in the connexin26 (Cx26; beta 2) gene have been associated with non-syndromic hereditary deafness. This suggests gap junctions are important to cochlear function. Numerous large gap junctions are present between adjacent supporting cells in both the vestibular and auditory sensory epithelia of the mature inner ear. In vestibular organs, Cx26 is highly expressed, but antibodies of Cx32 (beta 1) also label the supporting cells. In the organ of Corti of the cochlea, Cx26 is the predominant connexin isoform; neither Cx32 nor Cx43 (alpha 1) can be detected by immunohistochemistry. One role for gap junctions between supporting cells may be to provide a pathway for the rapid removal of ions away from the region of the sensory cells during transduction in order to maintain sensitivity. In the cochlea gap junctions are also associated with the basal cells of the stria vascularis, an ion-transporting epithelium that maintains a positive electrical potential in the potassium-rich endolymph fluid which bathes the apical surfaces of the sensory 'hair' cells and which is crucial for auditory transduction. Gap junctions are present between fibrocytes in the spiral ligament that underlies the stria vascularis, and between these fibrocytes and strial basal cells. During cochlear development, the initial formation and subsequent increase in size and number of gap junctions in the stria vascularis coincides with the initial generation and rise of the endocochlear potential. This and other evidence suggests that one role of gap junctions in the cochlea is to provide a pathway for passage of ions to maintain endolymph and, thus, auditory acuity. Mutations to Cx26 could, therefore, disrupt this ion circulation, resulting in deafness.

Amino Acid Sequence↗