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PubMed2004

Immunohistochemical localization of cyclooxygenase isoforms in the organ of Corti and the spiral ganglion cells of guinea pig cochlea.

Prostaglandins have been used in experimental models and clinical studies for the therapy of sudden hearing loss and tinnitus with conflicting results. However, little is known about the rate-limiting enzymes of prostaglandin synthesis in the inner ear, the generally constitutively expressed cyclooxygenase 1 (COX-1) and the distress-inducible cyclooxygenase 2 (COX-2). To extend our knowledge concerning the physiological expression and localization of these two enzymes, immunohistochemical stainings of the guinea pig cochlea were performed. Light microscopical analysis revealed a homogenous distribution of COX-1 within nearly all cell types of the organ of Corti, but no COX-1 expression in the cuticular plates of pillar cells. COX-2 was found to be expressed in all cell types, with much stronger expression in Hensen cells, neighboring Deiters cells and cuticular plates of outer hair cells. Both COX-1 and COX-2 immunoreactions were also found in the spiral ganglion. We conclude that both COX subtypes are expressed in the guinea pig cochlea under physiological conditions. The prominent expression of the distress-inducible COX-2 isoform in cell types under mechanical stress during noise reception might support the hypothesis of a cytoprotective function of COX products in hearing and in cellular stress situations like intense noise exposure.

Animals↗
PubMed2007

Loss of Fgfr3 leads to excess hair cell development in the mouse organ of Corti.

Previous studies have demonstrated the importance of FGF signaling at several stages in the development of the cochlea. At early stages of embryogenesis, Fgfr1, Fgfr2, and several FGFs are critical for both the induction of the otic vesicle and the initial development of the sensory epithelium. At late stages of cochlear development, Fgfr3 is necessary for the development of the tunnel of Corti. To determine the stage of development when Fgfr3 is required, we examined the expression of Fgfr3 and Fgf8 at various developmental stages. We also re-examined the Fgfr3 -/- mouse with additional markers for developing supporting cells. We confirmed the previous analysis of the Fgfr3 -/- mice, indicating that there are deficiencies in support cell differentiation. Specifically, we find that the inner pillar cell never develops, while the outer pillar cell is stalled in its differentiation. In addition, we found an extra row of outer hair cells, and accompanying Deiters' cells, in the apical two thirds of the organ of Corti in the Fgfr3 mutant. Thus, in addition to controlling the fate decision between pillar cells and Deiters' cells, we find that Fgfr3 also regulates the width of the sensory epithelium.

Animals↗
PubMed1998

Ultrastructural localisation of spectrin in sensory and supporting cells of guinea-pig organ of Corti.

Spectrin is a cytoskeletal protein found in the cortex of many cell types. It is known to occur in cochlear outer hair cells (OHCs) with previous immunoelectron microscopical studies showing that it is located in the cuticular plate and the cortical lattice. The latter is a network of filaments associated with the lateral plasma membrane that is thought to play a role in OHC motility. Spectrin has also been found in inner hair cells (IHCs) and supporting cells using immunofluorescent techniques, but its ultrastructural distribution in these cells has not yet been described. This has, therefore, been investigated using a monoclonal antibody to alpha-spectrin in conjunction with pre- and post-embedding immunogold labelling for transmission electron microscopy. Labelling was found in a meshwork of filaments beneath the plasma membranes of both IHCs and supporting cells and, in pillar cells, close to microtubule/microfilament arrays. It was also found in association with the stereocilia of OHCs and IHCs and, as expected, in the cortical lattice and cuticular plate of OHCs. Thus, spectrin is a general component of cytoskeletal structures involved in maintaining the specialised cell shapes in the organ of Corti and may contribute to the mechanical properties of all the cell types examined.

Animals↗
PubMed1997

Alteration of loosely bound calcium in the guinea pig organ of Corti after treatment with diltiazem as calcium channel blocker.

After oral administration of the organic calcium channel blocker diltiazem to guinea pigs for 7 days, calcium ions were precipitated with potassium antimonate in the cochleae. The spatial distribution of the precipitates was studied by energy-filtering transmission electron microscopy and the amount of the ultrastructural reaction products formed was determined semiquantitatively by an image processing system. Compared with untreated control ears, the number of the formed precipitates was reduced drastically in the inner hair cells after diltiazem treatment. In addition, electron microscopic analysis revealed that the number of calcium precipitates attached at the basolateral membrane of the outer hair cells was clearly reduced when compared with untreated control specimens. A large number of histochemical reaction products could be identified in the basilar membrane and were also observed in the untreated control specimens. The spatial distribution of the calcium precipitates in the lamina reticularis was not affected by diltiazem treatment and calcium precipitates could be identified within different cell membranes. The techniques used was considered to be helpful for identifying calcium channels ultrastructurally in intact undissected tissues and to support light microscopic analyses and patch-clamp electrophysiological measurements.

Administration, Oral↗
PubMed1981

Specificity of action of vanadate to the organ of corti.

Although vanadate strongly inhibits Na/K-ATPase activity of the stria vascularis in vitro, it initially causes no depression of the ouabain-sensitive endocochlear potential (EP) when perfused perilymphatically or via the vasculature. However, when the perilymph of scala tympani is replaced with artificial media containing 0.1 to 1 mM vanadate, there is a large (about 17 mV) increase in the EP of the second cochlear turn. Further experiments showed that the cochlear microphonics declined during the time in which the EP increased, and that the response of these two potentials to vanadate is greater in the second turn than in the first. Injection of 50 n1 of 1 mM vanadate (in artificial endolymph) into the endolymphatic space of the second turn caused no increase in the EP. These results support the notion that the early effects of vanadate are on the contra-luminal membranes of cells of the organ of Corti rather than on the stria vascularis. By superimposing anoxia or furosemide (i.v.) upon vanadate intoxication, we determined that the initial increase of the compound EP due to vanadate alone was due to a reduction in magnitude of the negative component of the EP. It is argued that of the three prevalent theories concerning the generation of the negative EP, the data tend to support the hypothesis that the intracellular potential of the hair cells gives rise to the negative EP.

Adenosine Triphosphatases↗
PubMed2003

Transient cochlear ischemia causes delayed cell death in the organ of Corti: an experimental study in gerbils.

To elucidate whether ischemia-reperfusion can cause delayed cell death in the cochlea, the effects of transient cochlear ischemia on hearing and on neuronal structures in the cochlea were studied in Mongolian gerbils. Ischemia was induced by bilaterally occluding the vertebral arteries for 5 minutes in gerbils, which lack posterior cerebral communicating arteries. In gerbils, the labyrinthine arteries are fed solely by the vertebral arteries. Occlusion of the vertebral arteries caused a remarkable increase in the threshold of compound action potentials (CAPs), which recovered over the following day. However, 7 days after the onset of reperfusion, the threshold began to increase again. Morphologic changes in the hair cell stereocilia were revealed by electron microscopy. The number of nuclear collapses was counted in cells stained for DNA and F-actin to evaluate the degree of cell death in the organ of Corti. Changes in spiral ganglion cell (SGC) neuron number were detected, whether or not progressive neuronal death occurred in the SGC. These studies showed that sporadic fusion of hair cells and the disappearance of hair cell stereocilia did not begin until 4 days after ischemia. On subsequent days, the loss of hair cells, especially inner hair cells (IHCs), and the degeneration of SGC neurons became apparent. Ten days after ischemia, the mean percentage cell loss of IHCs was 6.4% in the basal turn, 6.4% in the second turn, and 0.8% in the apical turn, respectively, and the number of SGC neurons had decreased to 89% of preischemic status. These results indicate that transient ischemia causes delayed hearing loss and cell death in the cochlea by day 7 after ischemia.

Action Potentials↗
PubMed1981

Spiral ganglion neuron loss following organ of Corti loss: a quantitative study.

The packing density of spiral ganglion neurons was measured in 2.5- and 13-15-month-old guinea pigs, in guinea pigs at various times after drug-deafening or acoustic trauma, and in Waltzing guinea pigs of various ages. Analysis of variance and Duncan's new multiple range tests were used to determine significant differences between treatment/survival groups. Spiral ganglion neurons in young and old normal ears did not have significantly different packing densities. Drug-deaf guinea pigs showed a significant loss of neurons by 2 weeks following treatment, a further significant loss by 2 months, and a marginally significant loss between 4 and 8 months. The neuronal population was then stable through 15 months, at about 13% of normal. Acoustic trauma ears showed the first significant loss isn the lower second turn at 1 month. Long-term (12-14 months post-exposure) trauma ears were highly variable. Waltzers lost about 50% of their normal neuronal population between 4 and 8 months; they showed an unexpected greater-than-normal density at 2 months, possible explanations of which are discussed. Thus, loss of the organ of Corti from various causes results in a slow but progressive loss of spiral ganglion neurons, the time course of which varies with the type of cochlear insult.

Animals↗
PubMed1997

Electron microscopic localization of nitric oxide I synthase in the organ of Corti of the guinea pig.

Nitric oxide synthase (NOS) activity has been detected previously in the mammalian cochlea at a light microscopic level. Here we present results of electron microscopic analysis for post-embedding immunoreactivity of neural-type NOS I in the cochlea of the guinea pig. Strong enzyme immunoreactivity was identified in the cytoplasm of inner and outer hair cells. Gold-labeled NOS I antibodies were mainly located in electron-dense areas of the cytoplasm, whereas electron-lucent regions of the receptor cells were nearly free from any immunoreactivity. In both types of hair cells anti-NOS I antibodies were also visible in the cuticular plates, hair bundles and nuclei. Further ultrastructural analysis revealed that the submembranous cisternae of the outer hair cells were nearly free from any reaction product, demonstrating that the whole cytoplasm of this hair cell was not immunoreactive. Other NOS I immunoreactivity was identified in the cuticular plates of the inner and outer pillar cells and in the cytoskeletal elements located in the apical parts of Deiter cells, forming the lamina reticularis or in cytoskeletal-containing regions in basal Deiter cells. Anti-NOS antibodies were visible in the nuclei of various cell types. Our findings suggest that nitric oxide produced by NO I synthase in the organ of Corti may act as a modulator of hair cell physiology during the processes of signal transduction with frequency selectivity.

Animals↗
PubMed1991

Furosemide alters organ of corti mechanics: evidence for feedback of outer hair cells upon the basilar membrane.

A widely held hypothesis of mammalian cochlear function is that the mechanical responses to sound of the basilar membrane depend on transduction by the outer hair cells. We have tested this hypothesis by studying the effect upon basilar membrane vibrations (measured by means of either the Mössbauer technique or Doppler-shift laser velocimetry) of systemic injection of furosemide, a loop diuretic that decreases transduction currents in hair cells. Furosemide reversibly altered the responses to tones and clicks of the chinchilla basilar membrane, causing response-magnitude reductions that were largest (up to 61 dB, averaging 25-30 dB) at low stimulus intensities at the characteristic frequency (CF) and small or nonexistent at high intensities and at frequencies far removed from CF. Furosemide also induced response-phase lags that were largest at low stimulus intensities (averaging 77 degrees) and were confined to frequencies close to CF. These results constitute the most definitive demonstration to date that mechanical responses of the basilar membrane are dependent on the normal function of the organ of Corti and strongly implicate the outer hair cells as being responsible for the high sensitivity and frequency selectivity of basilar membrane responses. A corollary of these findings is that sensorineural hearing deficits in humans due to outer hair cell loss reflect pathologically diminished vibrations of the basilar membrane.

Acoustic Stimulation↗
PubMed2002

Differentiation of spinous synapses in the mouse organ of corti.

The inner hair cells, the primary auditory receptors, are perceived only as a means for transfer of sound signals via the auditory nerve to the central nervous system. During initial synaptogenesis, they receive relatively few and mainly somatic synapses. However, around the onset of hearing (10-14 postnatal days in the mouse), a complex network of local spinous synapses differentiates, involving inner hair cells, their afferent dendrites, and lateral olivocochlear terminals. Inner hair cell spines participate in triadic synapses between olivocochlear terminals and afferent dendrites. Triadic synapses have not yet been confirmed in the adult. Synaptic spines of afferent dendrites form axodendritic synapses with olivocochlear terminals and somatodendritic synapses with inner hair cells. The latter are of two types: ribbon-dendritic spines and stout dendritic spines surrounded only by a crown of synaptic vesicles. Formation of spinous afferent synapses results from sprouting of dendritic filopodia that intussuscept inner hair cell cytoplasm. This process continues in the adult, indicating ongoing synaptogenesis. Spinous processes of olivocochlear synaptic terminals contact adjacent afferent dendrites, thus integrating their connectivity. They develop about 14 postnatal days, but their presence in the adult has yet to be confirmed. Differentiation of spinous synapses in the organ of Corti results in a total increase of synaptic contacts and in a complexity of synaptic arrangements and connectivity. We propose that spinous synapses provide the morphological substrate for local processing of initial auditory signals within the cochlea.

Animals↗
PubMed1996

Tectorial membrane-organ of Corti relationship during cochlear development.

The development of stereociliary attachment to the tectorial membrane was investigated in the mouse cochlea using transmission and scanning electron microscopy. At the 18th gestational day, only the major tectorial membrane can be identified covering the greater epithelial ridge and the inner hair cells in all turns. At the 19th gestational day, the minor tectorial membrane was first seen in the basal turn, over the outer hair cells. During early stages of development, the stereocilia of hair cells were surrounded by a loose fibrillar material underneath the tectorial membrane. After the 10th postnatal day, the outer hair cells' stereocilia were attached to Kimura's (or Hardesty's) membrane, while inner hair cells' stereociliary bundles were attached to the undersurface of the tectorial membrane near the Hensen's stripe. Between the 10th and the 14th postnatal days, the space between the inner hair cells and the first row of outer hair cells widened by virtue of the growth of the heads of pillar cells, and the inner hair cells' stereocilia were displaced towards the Hensen's stripe. After the 14th postnatal day, the inner hair cells' stereociliary bundles detached from the tectorial membrane, while the outer hair cells' stereocilia remained attached to it. The tip-link system, which connects the tips of the stereocilia to the next tallest stereocilia, is present at birth in the outer hair cells. The marginal pillar, that anchored the tectorial membrane to the underlying organ of Corti during development, first appeared on the 6th postnatal day and disappeared on the 14th-15th postnatal day. The present data together with other reports support the idea that although some structures, such as hair cells' stereocilia and innervation, are already formed early during development, the cochlear microarchitecture is not fully developed morphologically and ready to function normally until the end of the second postnatal week in the mouse.

Animals↗
PubMed1986

Comparative oto-vestibular effects in the pigmented guinea pig after dibekacin and netilmicin treatment.

We treated groups of pigmented guinea pigs with either intramuscular netilmicin or dibekacin at 100 and 150 mg/kg per day for 3 weeks. Saline was used as the control solution. All animals were tested weekly for both vestibular and auditory functions. The vestibular function was evaluated by the duration of post-rotatory nystagmus (PRN) elicited by interrupting the rotation of the animal around the vertical axis; auditory function was evaluated by the threshold response for the Preyer's pinna reflex (PPR). All animals were then sacrificed and either their labyrinths or Corti organs were processed for further investigations using the scanning electron microscope (SEM). The duration of PRN decreased over the treatment period in all of the groups as a result of adaptation. However, 150 mg/kg dibekacin produced a significant decrease of the PRN responses as compared to the control and other groups. This effect also continued during the recovery period. Likewise, the PPR threshold of the animals receiving 150 mg/kg dibekacin showed a significant increase at the end of the treatments and during the recovery period, while the other dibekacin group had no significant auditory impairment. Netilmicin at both doses did not significantly affect responses following either vestibular or auditory stimulations. SEM observations demonstrated that the sensory epithelia of the labyrinths and Corti organs affected by 150 mg/kg dibekacin had great losses of stereocilia, while comparable doses of netilmicin (150 mg/kg) had only very moderate losses of stereocilia in the labyrinths but not in the Corti organs.

Animals↗