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At least 523 records · Page 29Linked to original sources
PubMed1991

Antidiuretic hormone stimulation of adenylate cyclase in semicircular canal epithelium.

Basal adenosine 3',5'-cyclic monophosphate (cAMP) content and the modulation of its production were studied in the frog's semicircular canal epithelium. This epithelium secretes endolymph, a K(+)-rich, positively polarized fluid. The basal cAMP content measured by microradioimmunoassay was 244 +/- 14.2 fmol/structure per 5 min (n = 30). This content was increased about 8 times by 10(-5) M forskolin. Vasotocin, the frog antidiuretic hormone, increased the cAMP production by factors of 1.3 and 3.3 at concentrations of 10(-8) M and 10(-7) M, respectively. This stimulatory effect of vasotocin was blunted by the addition of alpha 2-adrenergic agonists, such as 10(-8) M-10(-5) M norepinephrine, in the presence of 10(-5) M propranolol, or 10(-5) M clonidine. Prostaglandin E2 at a concentration of 10(-8) M, which did not affect the cAMP production, did not modify the response to vasotocin. Glucagon (10(-6) M), calcitonin (10(-6) M), and parathyroid hormone (10 units/ml) did not affect the cAMP content. Prostaglandin E2 (10(-7) M) and the beta-adrenergic agonist isoproterenol (10(-6) M) stimulated the cAMP production by a factor of 1.6. These results indicate that the frog semicircular canal is a target of both vasotocin and catecholamines and that catecholamines through alpha 2-receptors modulate vasotocin-induced cAMP generation. Further, this interaction might be of physiological relevance in the modulation of ion transport in this structure.

Adenylyl Cyclases↗
PubMed1996

Combined effects of acute lead acetate exposure and tone exposure of the guinea pig cochlea.

Lead acetate exposure to humans can induce various disorders of the cranial nerves. Although vertigo and sensorineural deafness have been reported in lead workers, the dose effects of lead acetate on the cochlea and eighth cranial nerve are not well documented. We investigated the effects of lead acetate on the male albino Hartley guinea pig cochlea by measuring cochlear microphonics (CM), whole nerve action potential (AP), endocochlear potential (EP) and K+ ion concentration of the endolymph. Animals were given lead acetate by intraperitoneal injection as 20 mg/week for 4 consecutive weeks. A total dose < 80 mg did not induce electrophysiological changes in the cochlea. However, the AP output voltage (N1) decreased if the 80 mg lead acetate treatment was followed by an 80 dB tone exposure at 6 kHz during 24 h. A change was observed in CM and EP but not K+ ion concentration in the scala media.

Action Potentials↗
PubMed1992

Tetramethylammonium for in vivo marking of the cross-sectional area of the scala media in the guinea pig cochlea.

A physiologic technique was developed to measure endolymphatic cross-sectional area in vivo using tetramethylammonium (TMA) as a volume marker. The technique was evaluated in guinea pigs as an animal model. In the method, the cochlea was exposed surgically and TMA was injected into endolymph of the second turn at a constant rate by iontophoresis. The concentration of TMA was monitored during and after the injection using ion-selective electrodes. Cross-section estimates derived from the TMA concentration measurements were compared in normal animals and animals in which endolymphatic hydrops had been induced by ablation of the endolymphatic duct and sac 8 weeks earlier. The method demonstrated a mean increase in cross-sectional area of 258% in the hydropic group. Individually measured area values were compared with action potential threshold shifts and the magnitude of the endocochlear potential (EP). Hydropic animals typically showed an increase in threshold to 2 kHz stimuli and a decrease in EP. However, the degree of threshold shift or EP decrease did not correlate well with the degree of hydrops present.

Animals↗
PubMed1985

[Technics for postmortem removal of inner ear fluid].

Two methods for sampling inner ear fluid (a mixture of endolymph and perilymph) from corpses are described and compared. Using the classical method, a part of the petrous bone is chiselled out and, subsequently, a needle, attached to a 1-ml-syringe, is inserted through the oval foramen into the region of the utriculus. The inner ear fluid can then be removed. When the method proposed by Trela (1975) is applied, thin layers of the petrous crest are chiselled out until the common crus of the superior and posterior semi-circular becomes apparent. With a needle, attached to a 1-ml-syringe, the inner ear fluid can then be collected. The experiments show Trela's method to be simpler than the classical method. Moreover, only small amounts of inner ear fluid can be obtained by the latter technique. Trela's method is recommended for further studies on this fluid, which may be of forensic interest.

Cadaver↗
PubMed1980

Embryogenesis of the mammalian inner ear. III. Formation of the tectorial membrane of the CBA/CBA mouse in vivo and in vitro.

The development of the tectorial membrane in the basal coil of the cochlea has started already in the 15th gestational day inner ear and has reached a considerable thickness and maturation at birth. The development of the tectorial membrane occurs synchronously in in vivo labyrinths and the in vitro material cultured to an age corresponding to birth. At least during this part of the development the formation of the tectorial membrane is independent of the specific composition of endolymph. In the in vivo material a secretory maximum was reached on the 18th gestational day, whereafter the secretory activity was low, especially after birth. In the in vitro specimens, however, a rather constant secretion of material occurred also post partum, which indicates a lack of control mechanisms during in vitro conditions. A complete maturation of the tectorial membrane did not occur in vitro. When passing the point of time corresponding to birth, in the in vitro inner ear explants the gross structure of the tectorial membrane is only slightly changed. In vivo a mature configuration of the tectorial membrane is observed on the 14th DAB (day after birth).

Animals↗
PubMed1976

Pathophysiology of endolymphatic hydrops.

Endolymphatic hydrops of the nonprogressive type occurs in response to a single traumatic or toxic insult of limited duration and although it may result in permanent deficits in sensorineural function, there is total subsidence of vestibular symptoms. Endolymphatic hydrops of the progressive type, on the other hand, appears to be the result of permanent impairment of endolymph resorption and is caused principally by disorders of the endolymphatic sac. It occurs in Menière's disease, syphilitic labyrinthitis and the delayed hydrops syndrome. In addition to deafness of varying extent, it is characterized by episodic vertigo and sometimes by Hennebert's sign. Histological studies suggest that the acute vertiginous episodes are caused by potassium intoxication following ruptures of the membranous labyrinth and that Hennerbert's sign is caused by vestibular fibrosis.

Aged↗
PubMed1976

[Pathology of the endolymphatic duct and sac in inner-ear hydrops].

The morphological substrate of Menière's disease is the endolymphatic hydrops. That can be idiopathic or secondary as a sequence of a labyrinthine disease of another cause. It is possible to coordinate function loss of the sensory end-organs and pathohistological findings, but not all failures are light-microscopically explainable. The reason for the hydrops is certainly a disturbance in the endolymph physiology. For the pathogenesis are important, besides the biochemistry of the inner ear-fluids, problems of the membranes and pathological changes on ductus and saccus endolymphaticus and perimacular areals and plana semilunata. The perilymphatic space, documentated on the example of the secondary hydrops, is certainly not only passively enrolled in the procedure. All observations bring the initiation and periodicity of attacks to another point of view. A complete solution has not been possible so far, especially in the case of the etiology in idiopathic hydrops.

Ear, Inner↗
PubMed1983

Intracellular and extracellular ion content of the endolymphatic sac.

The Cl- activity in the endolymph of the endolymphatic sac and in the cochlear duct was measured with Cl- sensitive double-barreled microelectrodes. The Cl- activity in the endolymphatic sac fluid was lower than in the cochlear duct. A small, positive, DC potential was recorded in the endolymphatic sac. During anoxia, the DC potential decreased while the Cl- activity in the endolymphatic sac increased. The K/Na ratio in the epithelial cells and subepithelial tissue of endolymphatic sac was measured using the LAMMA technique. The K/Na ratio in the epithelial cells decreased after ethacrynic acid injection (60 mg/kg i.v.). These findings suggest that chloride in the endolymphatic sac is actively transported inward and outward.

Animals↗
PubMed1986

K+-induced motility and depolarization of cochlear hair cells. Direct evidence for a new pathophysiological mechanism in Ménière's disease.

In addition to an endolymphatic hydrops in various models of Ménière's disease, ruptures of the membranes lining the endolymphatic spaces or massive changes in their biochemical permeability are believed to allow large amounts of potassium-rich endolymph to deluge the normally low [K+] perilymphatic fluid. Our clinic has shown that exposure of the lateral and basal membrane parts of living isolated outer hair cells to increasing concentrations of potassium ions resulted in a sustained reversible cellular depolarization. Furthermore, potassium intoxication was accompanied by a strictly longitudinal contraction of the hair cells present. This was followed by hair cell relaxation in the presence of artificial perilymph. These findings suggest a supplementary hypothesis for the clinical manifestations of Ménière's disease: the reversible hair cell depolarization can explain the sudden tinnitus and parts of the hearing loss incurred as well as presumably the vertigo experienced; the reversible longitudinal hair cell contraction induces an abnormal change of cochlear micromechanics, resulting in concomitant attacks of deafness and also possibly contributing to the tinnitus perceived.

Action Potentials↗
PubMed1989

Maintenance of hydrostatic pressure gradients in the membranous labyrinth.

In normal guinea pig ears, hydrostatic perilymphatic pressure is equal to endolymphatic pressure. Alterations of perilymphatic pressure induced, for example, by laceration of the round window membrane are transmitted immediately to the endolymphatic compartment, probably via Reissner's membrane. In guinea pigs with experimental endolymphatic hydrops, however, pressure gradients between the endolymph and perilymph remained preserved after rupture of the round window membrane. This is considered as further evidence that after long-standing distention of Reissner's membrane the membranous labyrinth loses its ability to equalize endolymphatic and perilymphatic pressure.

Animals↗
PubMed1982

[Morphologic studies of the toxicity of ethacrynic acid in the spiral prominence].

Ultrastructural changes in the guinea pig spiral prominence were studied at various times after a single intravenous injection of ethacrynic acid (40 mg/kg body-weight). Initial swelling of endolymph-facing epithelial cells was followed by dilatation of the intercellular spaces and marked shrinkage of the stroma cells surrounding the spiral prominence vessel. While the changes in the stria vascularis and the spiral prominence progressed at about the same pace, the regression to normal ultrastructure set in earlier in the spiral prominence.

Animals↗
PubMed1987

Cytochemical localization of Ca++-ATPase activity in the lateral cochlear wall of the guinea pig.

Ca++-ATPase activity was examined cytochemically in the lateral cochlear wall of the guinea pig. The reaction products showing Ca++-ATPase activity were found along the folded plasma membrane of the strial marginal cells. In contrast, little or no reaction was seen on the apical surfaces of these cells. There were also marked reaction products on the microvilli and the endolymphatic cell surface of Reissner's membrane, and the apical and lateral plasma membranes of the spiral prominence and the external sulcus cells. These reactions completely disappeared when Ca++ or ATP was removed from the incubation medium. Our results strongly suggest that Ca++-ATPase plays an important role in Ca++ transport system for the regulation of Ca++ concentration in the cochlear endolymph.

Animals↗
PubMed1987

Cytochemical studies of Ca++-ATPase activity in the vestibular epithelia of the guinea pig.

We used ultracytochemistry to examine Ca++-ATPase activity in the vestibular epithelia of the guinea pig. Many reaction products were found along the basolateral plasma membrane of the vestibular dark cell. There were also marked reaction deposits on the apical and lateral cell membranes of the transitional cells, and the utricular and saccular wall cells. Both sensory and supporting cells showed Ca++-ATPase activity along their ciliary membrane and apical-lateral cell surfaces. Our findings indicate that the Ca++-ATPase activity found on the plasma membrane is closely related to Ca++-transport across the plasma membrane. When either Ca++ or ATP was omitted from the incubation medium, enzyme activity (as seen by the staining reaction present) was completely abolished. Our present results suggest that Ca++-ATPase located in the vestibular epithelia plays a significant role in the regulation of the Ca++-concentration in the vestibular endolymph.

Animals↗
PubMed1977

Histology of the cochlear vessels in the guinea pig.

Normal adult guinea pigs were studied in phase contrast microscopy. Perivascular spaces were clearly more common in vessels facing perilymph than in vessels facing endolymph. The so-called "avascular channels" which have been suggested to signify a degenerative phenomenon were found in some inner ear vessels in the normal animal. These sections of vessels, lacking blood cells, may constitute a normal vessel, subjected to plasma skimming. Small openings were found on some of these "avascular channels". Both perivascular spaces and "avascular channels" appear to be a part of the fluid transport system in the cochlea.

Animals↗
PubMed1997

Inhibition of experimentally induced endolymphatic hydrops by middle ear ventilation.

The tympanic membrane was perforated (n = 19) or a tube was inserted into the middle ear through the wall of the tympanic bulla (n = 6) immediately after blockage of the endolymphatic duct in guinea pigs. Total cochlear endolymph volume and volumes in each cochlear turn were determined from serial sections of the temporal bones and volume changes were analyzed statistically by comparison with hydropic controls without treatment (n = 12). Results showed that both middle ear ventilation procedures significantly reduced the subsequent development of endolymphatic hydrops. This inhibition of hydrops was presumed to be due to pressure release into the middle ear and/or improved oxygenation of the middle and inner ears. Findings suggest the possible merit of a tympanostomy as a treatment for Meniere's disease in carefully selected patients refractory to medical management.

Animals↗
PubMed1976

Atoxyl-induced damage to the sensory cells in the organ of Corti in the guinea pig cochlea.

Atoxyl-induced damage to the inner and the outer hair cells in the guinea pig cochlea starts in the apical coil and spreads successively downward toward the round window. Vesicular degeneration of both the inner and the outer hair cells and the cell organelles occurs. The degeneration is probably caused by an alteration in ionic composition of the endolymph resulting from primary changes of the stria vascularis (vesiculation and rejection of degenerated marginal and intermediate cells) as reported by Anniko and Wersäll (1975). However, a direct action of atoxyl on the sensory cells of the organ of Corti cannot be excluded.

Aniline Compounds↗
PubMed1997

[Potassium ion secretion and generation of the endocochlear potential in the stria vascularis].

Central to inner ear research are questions regarding the homeostasis of the high endolymphatic potassium concentration (approximately 150 mmol/l) and the high endocochlear potential (approximately +80 mV). Disturbances of the endocochlear potential can lead to the immediate loss of hearing which may be irreversible. The molecular mechanism leading to the generation of the endocochlear potential has not yet been discovered in spite of its clinical relevance. It is long known, however, that the stria vascularis is responsible for both the generation of the endocochlear potential as well as the secretion of potassium into endolymph. Recent investigations have clarified the mechanisms leading to the secretion of potassium and have led to the formulation of a now widely accepted model. This model explaining potassium secretion as well as the generation of the endocochlear potential is discussed in the present article.

Animals↗