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At least 217 records · Page 12Linked to original sources

PubMed1991

Course and distribution of efferent fibers in the cochlea of the mouse.

The course, distribution and termination of single efferent fibers to the cochlea has been described in only a few animals and relatively few fibers have been studied with knowledge of their ipsilateral or contralateral origin. In order to examine the efferent fibers in the mouse, the anterograde tracer Phaseolus vulgaris leucoagglutinin (PHA-L) was iontophoretically injected into one side of the brain stem near the location of known efferent nuclei. Examination of surface preparations of the cochlea revealed detailed information for both the lateral olivocochlear (LOC) and medial olivocochlear (MOC) systems. Many, but not all, fibers entered the cochlea within the intraganglionic spiral bundle (IGSB). The LOC fibers were restricted to the ipsilateral cochlea and rarely branched within the IGSB and osseous spiral lamina (OSL). In the organ of Corti, they traveled either basally or apically in the region of the inner hair cells (IHCs), spanning lengths up to 130 microns (basally) and 890 microns (apically). Terminal swellings of these fibers were ca 3.0 microns in diameter. Numerous en passant swellings were present where the fibers formed a plexus in the area of the IHCs. The MOC fibers followed a similar course in the IGSB and OSL, and within the OSL the fibers had few branches. Within the organ of Corti they traveled apically (up to 70 microns) in the nerve bundles located in the IHC area before they crossed the tunnel of Corti. In the region of the OHCs, 9% of the traceable fibers branched to innervate two to three OHCs while 91% appeared to innervate only one OHC. There was no discernible difference in the distribution of contralateral and ipsilateral MOC projections in terms of cochlear region or outer hair cell rows.

Animals↗

PubMed1992

Expression of heat shock protein, HSP72, in the guinea pig and rat cochlea after hyperthermia: immunochemical and in situ hybridization analysis.

The induction of the heat shock protein, HSP72, was studied in the cochlea of guinea pigs and rats subjected to a hyperthermic stress. Analyses were done by immunoblotting and immunocytochemistry at 6 and 12 h after heat shock, using a commercially available monoclonal antibody (Amersham), and by in situ hybridization 1 h after heat shock using an oligonucleotide probe. In guinea pig immunoblots of the cochlea, HSP72 was present in both unstressed and heat stressed animals and immunocytochemistry did not reveal any difference of staining between them. As opposed to guinea pig, HSP72 was not found in unstressed rat cochlea. Heat shock induced HSP72 expression in most inner ear tissues of the rat examined by immunoblotting. Immunocytochemistry and in situ hybridization localized HSP72 synthesis in ganglion neurons, Schwann cells, spiral limbus, spiral ligament and stria vascularis. The strongest immunoreactivity and highest density of silver grains were seen in the stria vascularis. All blood vessels were strongly immunoreactive and were outlined with silver grains. These results show that HSP72 synthesis can be induced by hyperthermia in rat cochlea and suggest that this protein could be a useful marker for assessment of the effects of specific stresses in this organ.

Animals↗

PubMed1992

Acoustic lesions in the mammalian cochlea: implications for the spatial distribution of the 'active process'.

The spatial contribution of mechanically active hair cells to tuning and sensitivity at a single point in the mammalian cochlea has been investigated in the basal turn of the guinea pig cochlea. Following the destruction of outer hair cells with acoustic overstimulation it was possible to record apparently normal tuning and sensitivity from spiral ganglion neurones innervating inner hair cells located on the apical edges of substantial lesions. The distance between the recording site, where neurones showed normal sensitivity, and areas of the cochlea showing 60-100% of the outer hair cells either damaged or missing varied between 0.2 and 1.3 mm which incorporates approximately 70 to 450 outer hair cells. In one animal neurones that demonstrated normal sensitivity were recorded within 0.2 mm of a lesion where 67% of the outer hair cells were either missing or showed severe damage to their stereocilia and within 0.5 mm of areas of the organ of Corti showing damage to 97% of the outer hair cells. This distance includes approximately 50 inner hair cells or 180 outer hair cells. The location of these neurones, whose sharp tuning presumably mirrors basilar membrane mechanics, suggests that a substantial proportion of point tuning in the cochlea may be derived over a distance of less than 0.5 mm and involve fewer than 200 active outer hair cells.

Acoustic Stimulation↗

PubMed1993

Altered malate dehydrogenase activity in nucleus magnocellularis of the chicken following cochlea removal.

The metabolism of second order auditory neurons in nucleus magnocellularis (NM) in the chick brainstem can be profoundly altered when excitatory input from the cochlea is removed. Within hours of cochlea removal, NM neurons show an increase in histochemical staining for the Kreb's cycle enzyme succinate dehydrogenase (SDH), followed in several days by decreases in SDH staining. We examined the activity of another Kreb's cycle enzyme, malate dehydrogenase (MDH) using a histochemical stain and a sensitive quantitative biochemical assay for comparison. We found changes in MDH staining similar in time course and magnitude to those of SDH; within 4 h of cochlea removal, MDH activity increases in ipsilateral NM neurons. By 9 days after cochlea removal MDH activity decreases, although not to the same degree as seen with SDH. Biochemical measurements of MDH activity also showed an early increase in activity in ipsilateral NM, followed at 9 days survival by a decrease in activity. Biochemical measurements of the activity of other enzymes in NM may be useful in further defining the metabolic consequences of deafferentation.

Animals↗

PubMed1993

Hair cell mediated responses of the auditory nerve to sinusoidal electrical stimulation of the cochlea in the cat.

Electrical stimulation of the cochlea elicits discharges of auditory nerve fibres which are mediated by the electrical or mechanical stimulation of inner hair cells (electrophonic responses). In order to isolate hair-cell mediated responses from those elicited by electrical stimulation of the nerve, the compound action potential (CAP) evoked by an acoustic probe was forward-masked by sinusoidal monopolar, or localized bipolar electrical stimulation of the base of the cochlea. The degree of masking of a given probe estimated the synaptically mediated response to the masker of the population of auditory nerve fibres innervating the cochlear location tuned to the probe. There was a peak of masking for probes close to the frequency of the electrical stimulus, suggesting a spatial tuning of the hair cell mediated response along the cochlea. This is consistent with excitation of the inner hair cells by a propagating mechanical response which is generated within the electrical field at the base of the cochlea. Furthermore, tuning curves for masking of a given probe were sharply tuned to electrical stimulation close to the probe frequency. This masking was not dependent upon the presence of functional outer hair cells close to the electrodes, suggesting an alternate transduction of electrical to mechanical energy.

Action Potentials↗

PubMed1994

Mineralocorticoid type I receptor in the rat cochlea: mRNA identification by polymerase chain reaction (PCR) and in situ hybridization.

Expression of mineralocorticoid type I receptor (MR) gene in the rat cochlea was determined using molecular biological techniques. We synthesized complementary DNA (cDNA) from rat cochlear total RNA and then amplified MR cDNA fragments by polymerase chain reaction (PCR). The amplified cDNA fragments were subcloned into an expression vector and the nucleotide sequence was analyzed to confirm the expression of mRNA encoding MR in the cochlea. We then synthesized digoxigenin-labeled riboprobes with this cloned DNA template and examined the localization of MR mRNA in the cochlea by in situ hybridization. The amino acid sequence of MR cDNA expressed in the cochlea was identical to that of the MR first cloned in the rat hippocampus. In situ hybridization showed the expression of MR mRNA in marginal cells of the stria vascularis, suggesting that aldosterone may regulate microhomeostasis of the endolymph, presumably by modulating Na, K-ATPase activity. Intense MR signal was also identified in spiral ganglion cells, the function of which remains to be determined.

Aldosterone↗

PubMed1994

Expression and localization of COL2A1 mRNA and type II collagen in human fetal cochlea.

The expression and localization of COL2A1 mRNA and protein was examined in human fetal cochlea to study the role of this gene in hearing and to begin to understand the pathogenesis of mutations in COL2A1 in hearing disorders. Northern blot analysis revealed COL2A1 expression in fetal membranous cochlea to be markedly greater than that in fetal skin, kidney, cartilage, eye and brain. In situ hybridization revealed COL2A1 expression in marrow cells, osteoblasts, fibroblasts and some osteocytes, in addition to chondrocytes in otic capsule. In the membranous cochlea, connective tissue elements (spiral ligament, spiral limbus and modiolar connective tissue), neuronal cells, secretory cells (stria vascularis) and organ of Corti cells (sensory hair cells) were found to express COL2A1. Immunohistochemistry was performed to assess distribution of type II collagen and correlation with COL2A1 mRNA in these morphologically and functionally diverse cell populations. In otic capsule, only cartilage was found to stain positively, and in membranous cochlea, only connective tissue structures including spiral ligament, spiral limbus, tectorial and basilar membranes, modiolar and spiral lamina cartilage contained type II collagen. Nonconnective tissue cells, marrow cells and osteoblasts did not contain immunohistochemically identifiable protein. Absence of type II collagen in a subset of cochlear cells may reflect potentially either inability to detect low levels of protein in these cells or posttranscriptional regulation.

Autoradiography↗

PubMed1994

Differences along the place-frequency map in the structure of supporting cells in the gerbil cochlea.

The function of supporting cells was investigated by comparing their morphologic adaptations at six different places in the gerbil cochlea. The volume of Deiters cells and tectal (cover) cells increased whereas that of Boettcher and Claudius cells decreased from base to apex. Deiters cells in the basal region tuned between 40 and 20 kHz lacked the unique rosette complex seen in regions encoding frequencies at or below 10 kHz. Deiters cells in high frequency regions differed from those at lower frequency places in several other ways: they possessed more apical microtubules, a larger basal microtubule stalk, mitochondria in the basal compartment, apical mitochondria that were unassociated with plasmalemma and more symmetric, and a less elaborately folded apicomedial plasmalemma enveloping fewer nerves. The tectal cells covering the outer tunnel appeared unlike Hensen cells in location and structure and differed further in exhibiting more variability with position in the cochlea. These covering cells in regions encoding high frequencies (20 and 40 kHz) extended a thin process medially that formed the roof of the outer tunnel and connected with the phalanx of the third Deiters cell. The tectal cells exclusively in places at 10 kHz or below projected numerous fimbriae into the outer tunnel. Hensen cells lateral to the cover cells also differed with frequency in showing abundant apical microvilli and mitochondria and basal juxtaposition to Boettcher cells only in the 40 to 20 kHz region. The observed structural differences provide evidence for functional variability along the place-frequency map. They attest to greater ion resorption from the outer tunnel by Deiters and tectal cells in low to mid frequency regions, and for greater ion exchange between endolymph and perilymph by Hensen, Boettcher and outer sulcus cells in regions of the cochlea encoding high frequencies. Amplification of the Deiters cells' microtubule system in the base of the cochlea possibly imparts increased stiffness to these cells and enhances transmission of mechanical energy at high frequency.

Acoustic Stimulation↗

PubMed1994

The effect of nimodipine on cochlear potentials and Na+/K(+)-ATPase activity in normal and hydropic cochleas of the albino guinea pig.

In experimental endolymphatic hydrops (EEH) a decrease in the endocochlear potential (EP) has been reported and is thought to be due to decreased activity of the enzyme Na+/K(+)-ATPase in the stria vascularis. By stimulating Na+/K(+)-ATPase, the EP, and thereby cochlear function as a whole, might be restored. On the other hand, stimulation of stria vascularis Na+/K(+)-ATPase might result in excessive production of endolymph and thus produce or augment hydrops. In this study we have investigated the effect of intraperitoneally applied nimodipine on cochlear potentials and on Na+/K(+)-ATPase activity in the stria vascularis, both in normal cochleas (control) and in cochleas with EEH. Nimodipine is an L-type Ca(2+)-channel blocking agent with Na+/K(+)-ATPase stimulating properties at concentrations as low as 1.5 nM. The compound action potential (CAP), evoked by 2,4 and 8 kHz tone bursts was found to be depressed in the EEH ears with and without nimodipine treatment, and in the nimodipine treated control ears. Statistical analysis (ANOVA) showed that the effects of EEH and nimodipine on the CAP were additive. The negative summating potential (SP), measured extracochlearly at the apex, in response to 4 and 8 kHz tone bursts was significantly enhanced in the EEH ears. Nimodipine treatment did not affect the SP, neither in the control, nor in the EEH ears. Cytochemically, Na+/K(+)-ATPase activity appeared to be decreased in the oedematous stria vascularis of hydropic cochleas. No effect of nimodipine on Na+/K(+)-ATPase activity could be established ultracytochemically, neither in the controls nor in the EEH ears. In the lower turns of some of the nimodipine treated control cochleas a mild hydrops was seen during light-microscopic evaluation. Although it was not possible to prove a stimulatory effect of nimodipine on the enzyme Na+/K(+)-ATPase cytochemically, the finding of mild endolymphatic hydrops in nimodipine treated control ears suggests (a history of) increased endolymph production. This hydrops might be responsible for the depression of the CAP in the nimodipine treated ears.

Animals↗

PubMed1995

Base-to-apex gradient of cell proliferation in the chick cochlea following kanamycin-induced hair cell loss.

In order to elucidate the mechanisms that drive cell proliferation in the avian cochlea, we investigated the spatio-temporal relationship between hair cell degeneration and cell proliferation after aminoglycoside ototoxicity. Neonatal chicks were given a daily intramuscular injection of kanamycin (KM) at 400 mg/kg per day for 10 consecutive days. At various times during or after KM administration, proliferating cells were labeled over a period of 2 days with bromodeoxyuridine (BrdU) and visualized with peroxidase immunohistochemistry. Changes in the location of the hair cell lesion during the KM treatment were monitored by phalloidin immunofluorescence or scanning electron microscopy. Hair cell loss began at the base of the cochlea 6 days after the start of KM injections, whereas cell proliferation was first observed in the basal region between days 6 and 8 of the KM treatment. This indicates that the latency between cell loss and cell proliferation is less than 48 h. The region of cell proliferation shifted from the base toward the apex of the cochlea over a period of 6-8 days, but cell proliferation in a specific region of the cochlea only occurred for 2-4 days. The latency as well as the total duration of cell proliferation after KM ototoxicity was virtually equivalent to that observed after acoustic trauma (Hashino and Salvi, 1993), suggesting that similar cellular events are involved in triggering cell proliferation after mechanical destruction and metabolic destruction of avian hair cells. The spatio-temporal gradient of cell proliferation followed the pattern of hair cell loss, suggesting that some aspect of hair cell degeneration provides trigger signals for cell proliferation.

Actins↗

PubMed1995

A reversible ischemia model in gerbil cochlea.

A completely reversible cochlear-ischemia animal model was developed, and an initial study of ischemia/reperfusion-induced cochlear function change is presented. The bulla of the anesthetized gerbil was opened through a ventral approach and the anterior inferior cerebellar artery and its branches were exposed. Cochlear blood flow (CBF) from the basal turn of the cochlea was monitored with a laser Doppler flowmeter. An electrically isolated microclamp was used to occlude the labyrinthine artery (LA). During LA clamping, the cubic distortion product (DP) was continuously recorded. The LA was repeatedly clamped for different durations in all animals, and CBF consistently showed full recovery after clamp release. No obvious change in vessel diameter or flow pattern was observed under a stereomicroscope. Mean blood pressure did not show significant change during clamping. Immediately upon LA clamping, CBF decreased rapidly nearly to zero. After clamp release, CBF demonstrated an immediate rapid increase, followed by a secondary gradual recovery to baseline. CBF recovery patterns were clamp duration-related. Within a few seconds of occlusion, DP decreased and reached a minimum of approximately 24% of the initial level in less that 30 s. Following reperfusion of the cochlea, DP gradually increased, decreased again, then slowly recovered. Time delay between CBF reperfusion and the first increase of DP was proportional to clamping duration, and the increased amplitudes demonstrated a negative relationship to clamp duration. We assume that the first decrease in DP during clamping was caused by ischemia in the cochlea; the second decrease, during the cochlear reperfusion, could be a form of reperfusion-induced change in cochlear function. This ischemia/reperfusion model in gerbil cochlea demonstrates excellent repeatability and reversibility. Since DP and other measurements can be used to dynamically monitor cochlear or hair cell functions, this model is useful in studies of auditory physiology and pathophysiology.

Animals↗

PubMed1996

Electrical stimulation activates two different sites within the guinea pig cochlea.

This study investigates whether auditory brainstem responses (ABRs) can be used to assess the functioning of electrically stimulated cochleas. Electrically evoked auditory brainstem responses (EABRs) were recorded in guinea pigs with normal hearing and guinea pigs deafened by amikacin, a powerful ototoxic antibiotic, combined with diuretic aminooxyacetic acid (AOAA). Two different types of EABRs were observed in normal animals, depending on the electrical pulse intensity applied to the round window: long-latency brainstem responses were evoked by low stimulation intensities, short-latency brainstem responses by high intensities. The absence of effect of strychnine applied intracochlearly ruled out the possibility of medial efferents being involved in these responses. Conversely, an intracochlear application of tetrodotoxin (TTX), an Na(+)-channel blocker, resulted in the disappearance of both types of responses, attesting that the sites activated by the electrical stimulation were located within the cochlea. In AOAA/ amikacin poisoned cochleas, in which most of the hair cells were missing with apparently normal ganglion neurons, the long-latency brainstem responses evoked by low intensities were completely lacking. These findings suggest that low currents applied to the round window of the guinea pig cochlea primarily activate the hair cells, the neurons being directly excited at higher intensities.

Acoustic Stimulation↗

PubMed2004

A novel RFP-RET transgenic mouse model with abundant eumelanin in the cochlea.

We report on the cochlea of a novel metallothionein-I (MT)/RFP-RET transgenic mouse model with severe systemic melanosis. Electron microscopy revealed that these transgenic mice possess abundant quantities of melanin in the intermediate cells of the stria vascularis. High performance liquid chromatography analysis indicated that cochleae of these transgenic mice contained about twice as much eumelanin as cochleae of control C57BL/6 mice and that the amount of pheomelanin was approximately equal in these two strains. Auditory brainstem responses at 2, 4, 8, and 16 kHz were not significantly different between transgenic and control mice. This is the first report on a mouse model of overproduction of cochlear eumelanin, and our results suggest that this transgenic mouse is an excellent model for investigating the effects of overexpression of cochlear eumelanin. In addition, we provide evidence that eumelanin overproduction in the cochlea does not affect normal hearing.

Animals↗

PubMed2006

Expression of CLC-K chloride channels in the rat cochlea.

Current models of the lateral K+ recycling pathway in the mammalian cochlea include two multicellular transport networks separated from one another by three interstitial gaps. The first gap is between outer hair cells and Deiters cells, the second is between outer sulcus cells and type II spiral ligament fibrocytes and the third is between intermediate and marginal cells in the stria vascularis. K+ taken up by cells bordering these interstitial spaces is accompanied by Cl-. Maintaining appropriate electrolyte balance and membrane potentials in these cells requires a mechanism for exit of the resorbed Cl-. One possible candidate for regulating this Cl- efflux is ClC-K, a chloride channel previously thought to be kidney specific. Here, we demonstrate the expression of both known isoforms of ClC-K in the organ of Corti, spiral ligament and stria vascularis of the rat cochlea by immunohistochemical, Western blot and RT-PCR analysis. These results indicate a role for ClC-K in mediating Cl- recycling in the cochlea. The widespread expression of both ClC-K isoforms in the cochlea may help to explain the symptoms of Bartter's syndrome Type III, a mutation in the hClC-Kb gene (human homologue of ClC-K2), which results in renal salt wasting without deafness. These data support the hypothesis that both isoforms of ClC-K are co-expressed in some cell membranes and account for the preservation of hearing in the presence of a mutation in only one channel isoform.

Animals↗

PubMed2003

Effect of acoustic stress on glucocorticoid receptor mRNA in the cochlea of the guinea pig.

As a first step toward elucidating the mechanism underlying the therapeutic effect of glucocorticoids on acute noise-induced hearing loss, we used semiquantitative reverse transcription polymerase chain reaction to study the level of glucocorticoid receptor (GR) mRNA in the cochlea of the guinea pig after acoustic overstimulation. The cochleas were dissected and divided into three portions (lateral portion, medial portion and modiolus). In the lateral portion, the glucocorticoid receptor mRNA level was significantly decreased 2 h after exposure to a 120 dB SPL sound and both 2 and 6 h after exposure to a 130 dB SPL sound. To determine where in the cochlea the changes in glucocorticoid receptor mRNA levels occur, in situ hybridization histochemistry was performed with digoxigenin-labeled sense and antisense RNA probes complementary to guinea pig glucocorticoid receptor mRNA. Glucocorticoid receptor mRNA was demonstrated in the spiral ligament, stria vascularis, spiral limbus and spiral ganglion. Moreover, the glucocorticoid receptor mRNA level was decreased in the spiral ligament, especially in the spiral prominence of the basal turn, 2 h after exposure to the 130 dB SPL sound. These results could imply that the therapeutic effect of glucocorticoids in the cochlea might be mediated in the spiral ligament, particularly in the spiral prominence.

Acoustic Stimulation↗

PubMed2005

COX-2 expression in the guinea pig cochlea is partly altered by moderate sound exposure.

The cyclooxygenase-2 isoform (COX-2) was found recently to be constitutively expressed in the guinea pig inner ear. To gain knowledge about its role in sound perception, alterations in the COX-2 level of moderate noise-stimulated cochleae were determined. Staining intensities were quantified in different regions using an immunohistochemical staining procedure and computer-assisted system. After 70 dB and 90 dB noise exposure for 1 h at 8000 Hz, COX-2 downregulation was observed in the organ of Corti, which was most prominent in Deiters' cells near Hensen cells and outer hair cells. In pillar cells, COX-2 levels were only slightly reduced after 70 dB but strongly diminished after 90 dB exposure. In Hensen cells, COX-2 was downregulated after 70 dB stimulation, revealing a decreasing COX-2 content from the third to the first turn of the cochlea and a homogeneously reduced enzyme expression in all three turns after 90 dB. The COX-2 content in inner hair cells was nearly identical to unexposed cochleae after 70 dB exposure but significantly reduced after 90 dB stimulation. In spiral ganglion cells, stria vascularis, spiral ligament and limbus, COX-2 expression was unchanged after 70 dB and 90 dB. We suggest that alterations in COX-2 expression might contribute to diminished sensitivity at the cochlea after noise exposure to reduce subsequent noise distress, termed sound conditioning.

Acoustic Stimulation↗

PubMed2004

Imaging the internal structure of the rat cochlea using optical coherence tomography at 0.827 microm and 1.3 microm.

OBJECTIVE: The purpose of this study was to use high-speed optical coherence tomography (OCT) to obtain cross-sectional images of the rat cochlea. STUDY DESIGN AND METHODS: The cochleae of Sprague- Dawley rats were imaged within 2 to 4 hours after death. Specimens were prepared by removing the bulla to expose the mesotympanum; some images were obtained in intact temporal bones removed from the cranium. The central element of an OCT imaging device is a Michelson interferometer combined with a low-coherence light source. This study used 2 OCT systems with different light sources: 1) a semiconductor optical amplifier operating and 2) a superluminescent diode with peak emissions wavelengths of 1.3 microm and 827 nm, respectively. Images (1.87 x 2.00 mm or 1.87 x 1.00 mm, 10 x 10 microm pixel resolution) were acquired at a frame rate of 1 Hz. Cross-sectional images at 100-microm increments were obtained from a medial-to-lateral direction. RESULTS: The scala vestibuli, scala media, scala tympani, modiolus, spiral ligament, and several turns of the cochlea were identified. CONCLUSION: These images reflect the ability of OCT to provide images of the internal cochlea structure with micron scale resolution and at near-real time frame rates.

Anatomy, Cross-Sectional↗

PubMed2003

Connexins 26 and 30 are co-assembled to form gap junctions in the cochlea of mice.

The importance of connexins (Cxs) in the cochlear functions has been indicated by the finding that mutations in connexin genes cause a large proportion of sensorineural deafness cases. However, functional roles of connexins in the cochlea are still unclear. In this study, we compared the relative expression levels of 16 different subtypes of mouse connexins in the cochlea. cDNA macroarray hybridizations identified four most prominently expressed connexins (listed in descending order): Cxs 26, 29, 30, and 43. Two of these connexins (Cx26 and Cx30), both belonging to the beta-group, were investigated for their molecular assemblies in the cochlea. Co-immunostaining showed expressions of Cxs 26 and 30 in the same gap junction plaques and their co-assembly was confirmed by co-immunoprecipitation of proteins extracted from the cochlear tissues. The heterologous molecular assembly of connexins is expected to produce gap junctions with biophysical characteristics appropriate for maintaining ionic homeostasis in the cochlea.

Animals↗