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PubMed2005

Vitamin D upregulates expression of ECaC1 mRNA in semicircular canal.

The low luminal Ca2+ concentration of mammalian endolymph in the vestibular labyrinth is required for normal balance. We found transcripts in primary cultures of semicircular canal duct (SCCD) epithelial cells from neonatal rats representing a complete transport system for transepithelial absorption of Ca2+ that is comprised of the epithelial Ca2+ channels ECaC1 (CaT2, TRPV5) and ECaC2 (CaT1, TRPV6), calbindin (calbindin-D9k, calbindin-D28k), Na+/Ca2+ exchanger (NCX1, NCX2, and NCX3), and plasma membrane Ca2+-ATPase (PMCA1, PMCA3, and PMCA4) by RT-PCR. Further, vitamin D receptor was also expressed in SCCD and it was found by quantitative RT-PCR that incubation for 24 h with 1,25-dihydroxyvitamin D3 upregulated the expression of ECaC1, calbindin-D9k, and calbindin-D28k. These observations provide evidence for the first time of an ECaC-based Ca2+ transport system in SCCD that could maintain the low Ca2+ concentration in vestibular endolymph.

Animals↗
PubMed2004

Localization of TREK-1, a two-pore-domain K+ channel in the peripheral vestibular system of mouse and rat.

The distribution of two-pore-domain (2P-domain) K(+) channels of the TREK subfamily was studied using immunocytochemistry in the peripheral vestibular system of mouse and rat. Using RT-PCR, the mRNA for TREK-1, but not for TREK-2 or TRAAK, were detected in mouse vestibular endorgans and ganglia. The TREK-1 channel protein was immunodetected in both nerve fibers and nerve cell bodies in the vestibular ganglion, both afferent fibers and nerve calyces innervating type I hair cells in the utricle and cristae. The post-synaptic localization in afferent calyces may suggest a neuroprotective role in glutamatergic excitotoxicity during ischemic conditions. In non-neuronal cells, TREK-1 was immunodetected in the apical membrane of dark cells and transitional cells, both of which are involved in endolymph K(+) secretion and recycling. TREK-1 may subserve some neuroprotective function in afferent nerve fibers as well as play a role in endolymph potassium homeostasis.

Animals↗
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↗
PubMed1997

Plasmalemmal ATPase calcium pump localizes to inner and outer hair bundles.

Recent studies demonstrate calcium ion influx at the tips of hair cell stereocilia during mechano-transduction. These ions must be either pumped from the cytosol into the extracellular space or endoplasmic envelope, or else sequestered by binding to specific proteins. A plasma membrane calcium pump (ATPase-type) was analysed in whole-mounts of rat organ of Corti using a monoclonal antibody to a large cytoplasmic loop of this protein. The reactivity was particularly high on the tips of longer stereocilia and was found along the shafts. Inner hair cell stereocilia had much less reactivity than outer hair cells. The reactivity lined the plasma membrane of inner hair cell bodies while a higher reactivity appeared in the cytoplasm of outer hair cells. Supporting cells were unreactive. Ultrastructural examination confirmed the plasma membrane calcium pump location on stereocilia and along the endolymph surface of receptor cells. Reaction product lined the plasma membrane of stereocilia as intense puncta. More reactive puncta occurred near the distal ends of stereocilia and the number decreased toward the ciliary base. The endolymph plasma membrane over the cuticular notch was especially reactive. The finding of more intense pump reactivity at the tips of stereocilia than the base is consistent with the hypothesis that during transduction, calcium ions enter stereocilia, distally, and the ATPase plasma membrane calcium pump rapidly extrudes these ions to the extracellular space.

Adenosine Triphosphatases↗
PubMed2002

K+ cycling and the endocochlear potential.

Sensory transduction in the cochlea and the vestibular labyrinth depends on the cycling of K+. In the cochlea, endolymphatic K+ flows into the sensory hair cells via the apical transduction channel and is released from the hair cells into perilymph via basolateral K+ channels including KCNQ4. K+ may be taken up by fibrocytes in the spiral ligament and transported from cell to cell via gap junctions into strial intermediate cells. Gap junctions may include GJB2, GJB3 and GJB6. K+ is released from the intermediate cells into the intrastrial space via the KCNJ10 K+ channel that generates the endocochlear potential. From the intrastrial space, K+ is taken up across the basolateral membrane of strial marginal cells via the Na+/2Cl-/K+ cotransporter SLC12A2 and the Na+/K+-ATPase ATP1A1/ATP1B2. Strial marginal cells secrete K+ across the apical membrane into endolymph via the K+ channel KCNQ1/KCNE1, which concludes the cochlear cycle. A similar K+ cycle exists in the vestibular labyrinth. Endolymphatic K+ flows into the sensory hair cells via the apical transduction channel and is released from the hair cells via basolateral K+ channels including KCNQ4. Fibrocytes connected by gap junctions including GJB2 may be involved in delivering K+ to vestibular dark cells. Extracellular K+ is taken up into vestibular dark cells via SLC12A2 and ATP1A1/ATP1B2 and released into endolymph via KCNQ1/KCNE1, which concludes the vestibular cycle. The importance of K+ cycling is underscored by the fact that mutations of KCNQ1, KCNE1, KCNQ4, GJB2, GJB3 and GJB6 lead to deafness in humans and that null mutations of KCNQ1, KCNE1, KCNJ10 and SLC12A2 lead to deafness in mouse models.

Animals↗
PubMed2004

Increased antisecretory factor reduces vertigo in patients with Ménière's disease: a pilot study.

It has been hypothesized that the symptoms of vertigo in patients with Ménière's disease somehow are related to impaired production and/or transport of endolymph. Antisecretory factor (AF) is a protein known to affect transport processes in the intestine and it has been shown that intake of specially processed cereals (SPC) can increase endogenous AF synthesis. In a prospective open pilot study, 24 patients with severe Ménière's disease (functional level scale 5-6 according to the criteria of AAO-HNS) received SPC for 14-30 days. AF levels in plasma increased by 83% in 20 of the 24 patients studied. The attacks of rotatory vertigo were reduced, to final AAO-HNS functional level scale 1-3, in 12 patients and in three of these hearing was normalized. Twelve patients had no or minor effects of the treatment. The correlation between AF activity after treatment and the final AAO-HNS functional level scale was -0.65, P<0.001. Studies in rats using immunohistochemistry methods showed that AF was localized to the cochlea and the vestibule of the inner ear. The present results suggest that AF might be a new regulator of the endolymph.

Adult↗
PubMed1997

Changes in the volume of marginal cells induced by isotonic 'Cl- depletion/restoration': involvement of the Cl- channel and Na+-K+-Cl- cotransporter.

Marginal cells constitute the endolymph-facing epithelium responsible for the secretion of endolymph by the stria vascularis in the inner ear. We have studied the possible involvement of Cl- conductance and Na+-K+-Cl- cotransport in the mechanism of changes in cell volume upon isotonic Cl- depletion/restoration. Changes in cell volume were estimated from video-microscopic images with the aid of an image processor. Marginal cells shrank to approximately 80% of their original volume in 30 s and to 65-70% in 90 s upon total replacement of [Cl]o (approximately 150 mM) by gluconate-, and the original volume of the shrunken cells was restored within 2 min after restoration of Cl-. The order of potency of anions to induce isotonic shrinkage was gluconate > I- > F- > Br-. The cell shrinkage caused by Cl- depletion was partially inhibited by 5-Nitro-2-(3-phenyl-propylamino)-benzoic acid (NPPB, 0.2 mM), but not by either 4-acetamido-4'-isothiocyanato-stilbene-2,2'-disulfonic acid (SITS, 0.5 mM), bumetanide (10 microM) or ouabain (1 mM). The cell shrinkage caused by a reduction of [Cl]o from approximately 150 mM to 7.5 mM was not affected by [K]o in the range of 3.6 mM to 72 mM. These results suggest that the main efflux pathway(s) responsible for the 'Cl removal'-induced shrinkage depends on volume-correlated Cl- conductance (Takeuchi and Irimajiri, J. Membrane Biol. 150, 47-62, 1996) and that this pathway(s) is essentially independent of the Na+-K+-Cl- cotransporter, the Na+,K+-ATPase, and the K+-Cl- cotransporter. With regard to volume recovery after isotonic shrinkage, its critical dependence on the simultaneous presence of Na+, K+ and Cl- in the bath and its substantial inhibition by bumetanide (10 microM) both indicate a major role for Na+-K+-Cl- cotransport. The strong influence on cell volume of solute fluxes working through the Cl- channel and the Na+-K+-Cl- cotransporter implies an essential role for these pathways in the ion transport mechanism(s) of the marginal cell.

Animals↗
PubMed1998

Development of the endolymphatic sac and duct in the Japanese red-bellied newt, Cynops pyrrhogaster.

The development and maturation of the endolymphatic sac (ES) and duct (ED) were studied in the newt Cynops pyrrhogaster. The ES first appears as an oval capsule at the dorsal-medial tip of the otic vesicle at stage 39, about 11 days after oviposition. The ES consists of polymorphous epithelial cells with a minimum of cytoplasm. The intercellular space (IS) between the epithelial cells is narrow and has a smooth surface. At stage 44, the size of the ES increases as many vacuoles in the IS become filled. At stage 46, 18 days after oviposition, the ES elongates markedly and a slit-like lumen is found in the ES. The epithelium contains a few cell organelles which are scattered in the cytoplasm. The vacuoles in the IS are fused, which expands the IS. Two days later (stage 48), floccular material (endolymph) is present in the expanded lumen. The IS dilates and has a wide and irregular appearance. At stage 50, approximately 26 days after oviposition, the ES extends and expands significantly and crystals (otoconia) can now be seen in the widened lumen of the ES. The cytoplasm of the cuboidal epithelial cells contains an abundance of vesicles surrounded by ribosomes and Golgi complexes. Intercellular digitations are formed in the expanded IS. At stage 54, the ES forms a large bellow-like pouch. Numerous otoconia accumulate in the lumen. Free floating cells and cell debris can be seen in the lumen at this stage. The epithelial cells contain numerous cytoplasmic organelles which are evenly distributed in the cytoplasm. Granules are found in the apical and lateral cytoplasm. The IS is loose and displays a labyrinthine appearance. The primitive ED first appears as a connection between the ES and the saccule but no lumen is present inside at stage 39. At stage 46, a narrow lumen is formed in the ED, which corresponds to the formation of the ES lumen. At stage 50, as the ED extends, floccular material is seen in the lumen. At stage 54, the ED bears numerous microvilli on its luminal surface. Otoconia and endolymph are present in the ED. Tight junctions between the epithelial cells are formed at stage 46. A fully developed intercellular junctional complex is produced at stage 54. Based on the development of the ES and ED, the maturation of function of the ES and ED are discussed.

Animals↗
PubMed2000

Embryonic and postnatal accumulation of homogeneous substance in the endolymphatic sac in the guinea pig.

OBJECTIVE: The endolymphatic sac (ES) of vertebrates contains varying amounts of a homogeneous substance (HS) that stains deeply with basic aniline dyes. Histochemically, HS is characterized as a carbohydrate-protein complex, being both neutral and acidic in nature. In the present study, deposition of HS in the ES was studied in the guinea pig from the 3rd week of gestation to 104 weeks postnatally in order to find out if HS accumulates with age, at which point during embryonic development this substance appears, if its presence is correlated to the sense of hearing and if the amount of substance in the left versus right ear of one and the same animal is correlated to any degree. METHODS: Sixty-nine endolymphatic sacs were evaluated in 38 guinea pigs. The ES specimens were sectioned for light and transmission electron microscopy and the amount of HS filling was categorized in four groups: none, low, medium and a high level of substance. RESULTS: The substance was not discerned until after 7 weeks of gestation, when it filled only a minor part of the distal ES lumen. At 9 weeks gestation the nature of the substance altered, becoming homogeneous, as visualized by osmium-toluidine blue staining and approximately filling the distal half of the luminal space. In the postnatal period, 65% of ES specimens were filled with HS to the intermediate or proximal ES, whereas only 6.5% of the ES specimens were devoid of the substance. The extent of filling of the ES in the prenatal temporal bones was significantly less than postnatally (P < 0.0001, chi2-test). The extent of postnatal filling was not correlated with age. Left and right ears were closely correlated in one and the same animal. Phagocytic cells were often found at the border between clear endolymph and stainable substance. CONCLUSION: The appearance of HS seemed to coincide temporally with the onset of hearing during the prenatal period indicating that it could play a part in normal inner ear functioning in the guinea pig. The close correlation regarding the level of the HS in the left and right ear, both pre- and postnatally could reflect a general symmetry in endolymph pressure-volume conditions within the inner ear fluid systems, as well as in the environmental hydrostatic pressure in the posterior cranial fossa.

Animals↗
PubMed1988

Ruthenium red staining of the endolymphatic sac in the guinea pig.

The ultrastructure of the guinea pig endolymphatic sac was studied, using the ruthenium red staining technique. The dye stained the apical cell surface coat and the homogeneous substance in the luminal space of the endolymphatic sac, when introduced from the luminal side of the epithelium. It is suggested that the surface coat and homogeneous substance may play an important part in the endolymph regulatory mechanism in the endolymphatic sac. When ruthenium red was introduced from the subepithelial side, the basolateral surface of the epithelial cells usually became brightly stained in the absence of staining of the apical cell surface, due to the presence of the tight junctions. In some instances, however, the dye penetrated beyond the level of the tight junctions. Pinocytotic vesicles and larger vacuoles in the epithelial cells were also sometimes stained, both apically and near the lateral cell surface. These findings suggest that endolymph efflux mechanisms in the endolymphatic sac may involve the combined actions of a paracellular and transepithelial flow as well as a transcellular, vacuolar bulk flow.

Animals↗
PubMed1984

Pathology as it relates to ear surgery. IV. Surgery of Menière's disease.

Conservative shunting procedures, i.e. ESS, ultrasonic irradiation and cryosurgery, are based on the assumption that there is increased volume and/or pressure of endolymph in Menière's disease. Since there is no reliable clinical test to detect endolymphatic hydrops, shunting procedures on cases without hydrops are doomed to failure. Surgery on the endolymphatic sac was not associated with fibrosis or obliteration of its lumen. Silastic shunt tubes were well tolerated by the body, and the shunt between the sac and the subarachnoid space seemed to remain open. The results of experimental surgery on the endolymphatic sac and its applicability to humans should be revised. Temporary improvement of Menière's symptom-complex may be expected from any surgical procedure on the membranous labyrinth, even in cases without endolymphatic hydrops. Post-operative serous labyrinthitis with associated biochemical changes is the cause of this improvement. The success of shunting procedures cannot be judged histologically by the position of Reissner's membrane. This membrane acts like varicose veins: once dilated, always dilated. Ultrasonic irradiation and cryosurgery of the labyrinth result in limited degenerative changes close to the site of probe application. Degenerated intact membranous walls may act as an internal otic-perotic shunt and may result in symptomatic improvement in Menière's disease. The idea of selective vestibular neurectomy and internal shunting procedures, i.e. without drainage of endolymph to the outside (mastoid) or to the inside (CSF), should be developed further. Recurrence of symptoms following shunting procedures may be due to failure of the shunt, or to the presence of endolymphatic hydrops in the non-operated ear. MF vestibular neurectomy results in complete denervation of the vestibular end-organs, without effect on the cochlea or facial nerve. Excision of Scarpa's ganglion causes retrograde degeneration in the proximal stump of the vestibular nerve, most probably to the level of the brain-stem. Recurrence of dizziness following TC labyrinthectomy is most commonly due to inadequate removal of the vestibular end-organs. The high regenerative capacity of the vestibular nerve is evidenced by the formation of traumatic neuromas in the vestibule following TC labyrinthectomy. Whether these neuromas produce symptoms is unknown. Persistent cochlear hydrops occurs following TC labyrinthectomy and TL vestibular neurectomy owing to obstruction in the hook region of the cochlea and in the ductus reuniens. This may result in persistent tinnitus and feeling of pressure in the ear.

Aged↗
PubMed1998

Effect of serotonin on ouabain-sensitive, K+-dependent, p-nitrophenylphosphatase activity in strial marginal cells of normal and reserpinized guinea pigs.

Na+,K+-ATPase activity is abundant on the basolateral infoldings of the strial marginal cells and contributes to the maintenance of the characteristic electrolyte composition of the endolymph. However, the stria vascularis of the cochlea is known not to be innervated. In order to clarify its humoral regulation by serotonin, the K+-p-nitrophenylphosphatase activity of strial marginal cells was investigated with a cerium-based method in normal guinea pigs and in guinea pigs treated with reserpine, 5-hydroxytryptamine or reserpine plus 5-hydroxytryptamine. K+-p-nitrophenylphosphatase activity was almost completely depressed 3-20 days after reserpine administration. Ten days after reserpinization, followed by repeated 5-hydroxytryptamine treatment, the enzyme activity was detectable. These results suggest that 5-hydroxytryptamine increases the phosphatase activity. Thus, the function of the stria vascularis in producing cochlear endolymph may be regulated by 5-hydroxytryptamine.

4-Nitrophenylphosphatase↗
PubMed1983

Origin of the receptor potential in inner hair cells of the mammalian cochlea--evidence for Davis' theory.

The primary sensory hair cells of the mammalian cochlea are located in the organ of Corti, a sensory epithelium which separates fluids of widely differing chemical composition. The apical, sensory surfaces of the hair cells are exposed to the potassium-rich endolymph of the scala media and their lateral and ventral surfaces are exposed to the perilymph of the scala tympani whose chemical composition resembles that of other extracellular fluids. The high potassium concentration of the endolymph (150 mM) is believed to result from the activity of electrogenic potassium pumps located in the stria vascularis which lines the lateral walls of the cochlea. These pumps are also the source of the positive endocochlear potential of about +80 mV which can be recorded from the scala media. When the ear is stimulated with sound, receptor potentials may be recorded extracellularly from the fluid-filled spaces of the cochlea, and intracellularly from the rows of inner and outer hair cells. According to the 'resistance microphone' theory of Davis, these receptor potentials are derived from the pre-existing polarization of the hair cells by a change in the ohmic resistance of the mechanosensitive portion of the cell membrane (Fig. 1). This procedure potential changes in the scala tympani and scala media of opposite phase, thus giving rise to the cochlear microphonic (CM). Evidence is presented here to support this theory. When sufficient depolarizing current is injected into inner hair cells to cancel the polarizing voltage, the receptor potentials disappear, and their phase is reversed when the polarizing voltage across the apical membranes of the hair cells is reversed.

Acoustic Stimulation↗
PubMed1999

Mutations in the gene encoding B1 subunit of H+-ATPase cause renal tubular acidosis with sensorineural deafness.

H+-ATPases are ubiquitous in nature; V-ATPases pump protons against an electrochemical gradient, whereas F-ATPases reverse the process, synthesizing ATP. We demonstrate here that mutations in ATP6B1, encoding the B-subunit of the apical proton pump mediating distal nephron acid secretion, cause distal renal tubular acidosis, a condition characterized by impaired renal acid secretion resulting in metabolic acidosis. Patients with ATP6B1 mutations also have sensorineural hearing loss; consistent with this finding, we demonstrate expression of ATP6B1 in cochlea and endolymphatic sac. Our data, together with the known requirement for active proton secretion to maintain proper endolymph pH, implicate ATP6B1 in endolymph pH homeostasis and in normal auditory function. ATP6B1 is the first member of the H+-ATPase gene family in which mutations are shown to cause human disease.

Acidosis, Renal Tubular↗
PubMed1999

Mice lacking the basolateral Na-K-2Cl cotransporter have impaired epithelial chloride secretion and are profoundly deaf.

In chloride-secretory epithelia, the basolateral Na-K-2Cl cotransporter (NKCC1) is thought to play a major role in transepithelial Cl(-) and fluid transport. Similarly, in marginal cells of the inner ear, NKCC1 has been proposed as a component of the entry pathway for K(+) that is secreted into the endolymph, thus playing a critical role in hearing. To test these hypotheses, we generated and analyzed an NKCC1-deficient mouse. Homozygous mutant (Nkcc1(-/-)) mice exhibited growth retardation, a 28% incidence of death around the time of weaning, and mild difficulties in maintaining their balance. Mean arterial blood pressure was significantly reduced in both heterozygous and homozygous mutants, indicating an important function for NKCC1 in the maintenance of blood pressure. cAMP-induced short circuit currents, which are dependent on the CFTR Cl(-) channel, were reduced in jejunum, cecum, and trachea of Nkcc1(-/-) mice, indicating that NKCC1 contributes to cAMP-induced Cl(-) secretion. In contrast, secretion of gastric acid in adult Nkcc1(-/-) stomachs and enterotoxin-stimulated fluid secretion in the intestine of suckling Nkcc1(-/-) mice were normal. Finally, homozygous mutants were deaf, and histological analysis of the inner ear revealed a collapse of the membranous labyrinth, consistent with a critical role for NKCC1 in transepithelial K(+) movements involved in generation of the K(+)-rich endolymph and the endocochlear potential.

Animals↗
PubMed2004

Expression of connexin 26 in the lateral wall of the rat cochlea after acoustic trauma.

OBJECTIVE: Although the mutation in the Gap Junction Beta 2-encoding gap junction protein connexin 26 (Cx26) has been related to hereditary non-syndromic deafness and maturation of cochlear development, the physiological role of Cx26 in the cochlear lateral wall remains unclear. It has been suggested to be responsible for the recycling of K+ in the endolymph and for maintenance of the endocochlear potential (EP). In noise-induced hearing loss, alterations in the EP and the K+ concentration in endolymph have been observed. Thus Cx26, which is widely expressed in the cochlear lateral wall, may play a role in the mechanism of acoustic trauma. MATERIAL AND METHODS: We used a rat model of noise-induced hearing impairment to detect changes in Cx26 expression in the cochlear lateral wall. By means of immunofluorescent staining and Western blotting, we investigated whether Cx26 was involved in the pathophysiological mechanism of acoustic trauma. RESULTS: The results indicated that abundant Cx26 protein was found on fibrocytes of the spiral ligament in the cochlear lateral wall. Protein extract of cochlear lateral wall expressed Cx26 with a molecular weight of approximately 21 kDa. After noise exposure, with an increasing threshold of the auditory brainstem response (ABR) of approximately 54.2 +/- 21.8 dB SPL, the expression of Cx26 protein increased significantly (p < 0.05) as revealed by semi-quantitative analysis from Western blotting. CONCLUSION: Cx26 protein was present in the cochlear lateral wall of rats and was upregulated when the ABR threshold shifted after intense noise exposure. Cx26 protein was involved in the pathogenesis of acoustic trauma.

Animals↗
PubMed2004

Aquaporin-2 in the human endolymphatic sac.

OBJECTIVE: To detect and localize aquaporin-2 (AQP-2), a water channel regulated by the antidiuretic hormone, in human endolymphatic sac. MATERIAL AND METHODS: Human endolymphatic sacs were sampled during removal of vestibular schwannomas via a translabyrinthine approach. Samples were immediately fixed in 10% formalin (24 h) and embedded in paraffin; in situ hybridization and immunohistochemistry were performed with an AQP-2-specific probe and a polyclonal antibody. RESULTS: Both AQP-2 mRNA and protein were detected in the epithelium of the endolymphatic sac. AQP-2 immunostaining was mainly cytoplasmic, suggesting that most AQP-2 was located in intracellular pools. CONCLUSIONS: In the endolymphatic sac, AQP-2 probably participates in the homeostasis of endolymph; the possibility of reducing the volume of endolymph by inhibiting its expression and membranous insertion using an antidiuretic hormone inhibitor represents a new therapeutic approach for the treatment of Ménière's disease.

Aquaporin 2↗
PubMed1998

Experimental study on the effects of gentamicin injection on the guinea-pig: electrophysiological studies.

The inner ear distortion induced by gentamicin (GM), a type of aminoglycoside antibiotic, was examined in guinea-pigs. Previous studies which investigated the function of the eighth cranial nerve and organ of Corti using cochlear microphonics (CM) and compound action potential (CAP) reported ototoxicity following experimental exposure to GM. In this report, the effects of GM on the cochlea and the eighth cranial nerve were investigated systematically by measuring CM, CAP, summating potentials induced by 90 dB (SPL) tone burst, endocochlear potential (EP) and K+ ion concentration of the endolymph. Guinea-pigs were treated with a daily intramuscular injection of GM (60 mg in 1.5 cc) at a dose of 60 mg/kg during different treatment periods. The maximum output voltage of AP was decreased by injection of GM (60 mg/kg x 24). A decrease in the CM maximum output voltage and the elevation of CM pseudothreshold were typically seen after GM injection at a test frequency of 8 kHz and a decrease in CAP was also observed. Changes in EP during 3 min anoxia were observed, in particular a decrease in the absolute value of the negative potential. The endolymph K+ ion concentration remained unchanged. These findings indicate that the diffusion potentials decreased at the same time as reduction of maximum output voltage in CM induced by GM injection.

Action Potentials↗