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At least 757 records · Page 42Linked to original sources
PubMed1995

Effect of focal cochlear vascular lesion on endocochlear potential in guinea pigs.

The alteration endocochlear potential (EP) in response to total cochlear ischemia induced by various experimental manipulations has been studied. However, the effect of restricted areal damage to the microvessels (restricted to small area in the lateral wall of a cochlear turn) on the EP value is still unknown. In the current investigation we adopted a photochemical method to produce a focal (i.e., restricted area) microvessel injury in the lateral wall of the guinea pig cochlea and examined the effect of these insults on EP recorded in the same region. The small area of the microvessel lesion (small fenestra: approximately 0.2 x 0.4 mm2) induced by photoactivation did not yield significant EP changes, suggesting that damage to such a small area of microcirculation in the lateral wall of the cochlea has no statistically significant effects on EP values. In subjects with a large area of the microvessel lesion (large fenestra: approximately 0.2 x 0.8 mm2), a decrease in the EP value (mean +/- SEM 7.9 +/- 0.8 mV) was noted. However, the control group animals with a large fenestra but without microvessel lesion also displayed a decrease (8.6 +/- 0.8 mV) in EP. In the current study we were unable to differentiate whether the EP changes in animals with the large fenestra microvessel lesions were caused by the cochlear blood flow decrease or by the surgical preparation. However, the results of this study indicated if the EP value was affected by the large area of the microvessel lesion, the level of decrease would not be large. That is, the EP decrease was less than the EP change in the control group (mean: 8.6 mV). Considering the dependence of EP on blood flow, the data of this study suggest that compensatory mechanisms in the cochlea may maintain the EP following a focal lesion in the lateral wall of the cochlea. This study also indicates that the photochemical method provides a reliable approach to produce the animal model with the focal microvessel lesion in the lateral wall of the cochlea.

Animals↗
PubMed1999

Comparative study of effects of impact tone and steady state tone exposure: EP and concentration of K+ ion and Na+ ion.

To test the adequacy of equal energy principle (EEP), guinea pigs were exposed to impact tone. The changes in electrophysiological data, namely endocochlear potential (EP) and the change in K+ ion and Na+ ion concentrations in the endolymph were investigated. The frequency of impact tone was 1 pulse/second or 1 pulse/3 seconds. The steady state tone had Leq24h = 100, 95, 90 or 85 dB, and impact tone had Leq24h = 95, 90 or 85 dB. The results are the following. Both steady state and impact tone exposure cause changes of electrophysiological data. The effects on the absolute value of negative EP induced by impact tone exposures were smaller than that of steady state tone of the same Leq. The rate of pulses was also an important factor for impact tone exposure. Impact tone exposure of 1 pulse/second caused smaller absolute value of negative EP than that of 1 pulse/3 seconds. The K+ ion concentration time course in the endolymph remained similar to the control (Exp. 1) only in Exp. 8 (85 dB; the lowest steady state noise exposure in our experiments), but no decrease in the K+ ion concentration was detected in the other experiments, suggesting an alteration in the K+ ion flow. The Na+ ion concentration time course was also influenced showing no increase in Na+ ion concentration compared to the control (Exp. 1c) and the lowest steady-state exposure experiment (Exp. 8c). Our experimental results suggest that both the K+ ion and Na+ ion movement are altered by tone exposure. We found also that the different types of noise exposure with the same Leq value does not exhibit the same changes. Leq24h is not an accurate damage risk criteria.

Acoustic Stimulation↗
PubMed2005

Endolymphatic perfusion with EGTA-acetoxymethyl ester inhibits asphyxia- and furosemide-induced decrease in endocochlear potential in guinea pigs.

We examined the effect of the Ca(2+) concentration in the endolymph ([Ca](e)) or in the endolymphatic surface cells ([Ca](i)) on the endocochlear potential (EP) by using an endolymphatic or perilymphatic perfusion technique, respectively. (i) A large increase in [Ca](e) up to approximately 10(-3) M with a fall in the EP was induced by transient asphyxia ( approximately 2 min) or by the intravenous administration of furosemide (60 mg/kg), and a significant correlation was obtained between the EP and p[Ca](e) (= -log [Ca](e), r = 0.998). (ii) Perfusion of the endolymph with 10 mM EGTA for 5 min neither produced any significant change in the EP nor altered the asphyxia-induced change in EP (DeltaEP(asp)), suggesting that neither [Ca](e) nor the Ca(2+) concentration gradient across the stria vascularis contributed directly to the generation of the EP in the condition of low [Ca](e). In contrast, endolymphatic perfusion with high Ca(2+) (more than 10 mM) produced a decrease in EP and a significant correlation was obtained between the EP and the Ca(2+) concentration of perfusion solution (r = 0.982), suggesting that Ca(2+) permeability may exist across the stria vascularis. (iii) The administration of a Ca(2+) chelator, EGTA-acetoxymethyl ester (AM, 0.3 mM), to the endolymph, which produced a gradual increase in EP, suppressed significantly, by 60-80%, DeltaEP(asp) or furosemide-induced changes in EP. In contrast, perilymphatic administration of 0.5 mM EGTA-AM caused no significant suppression of the DeltaEP(asp). These findings suggest that [Ca](i) plays an important role in generating/maintaining a large positive EP.

Animals↗
PubMed2000

Electrocochleography and gentamicin therapy for Ménière's disease: a preliminary report.

OBJECTIVE: It is widely held that an enlarged summating potential (SP) relative to the eighth nerve action potential (AP) is a reflection of endolymphatic hydrops. Aminoglycosides are an accepted treatment for incapacitating Ménière's disease and are known to affect both sensory and secretory cells of the inner ear. The intent of this study was to determine whether this effect on secretory cells could be objectively confirmed by virtue of changes in the electrocochleogram (ECoG) of patients receiving gentamicin therapy for Ménière's disease. STUDY DESIGN: This was a prospective longitudinal study of repeated ECoG measures in three groups of subjects. Ménière's patients undergoing gentamicin treatment were compared with two control groups: individuals with stable Ménière's disease and normal-hearing control subjects. SETTING: The study was conducted at a tertiary referral center. PATIENTS: The sample included 21 normal-hearing subjects, 15 patients with stable unilateral Ménière's disease, and 12 with disabling unilateral Ménière's disease. INTERVENTIONS: For patients with disabling Ménière's disease, gentamicin was administered transtympanically. Audiograms, impedance tests, and ECoG were performed twice for all subjects. MAIN OUTCOME MEASURES: The SP and AP amplitudes, AP latency, and SP/AP ratio of the EcoG were measured. RESULTS: A statistically significant reduction in the SP/AP ratio was observed after gentamicin administration (analysis of variance interaction effect: F2 = 5.64; p = 0.0065). CONCLUSIONS: The significant reduction in the SP/AP ratio in the gentamicin-treated Ménière's group supports the hypothesis that gentamicin improves the electrophysiologic function of the cochlea, possibly by reducing the severity of the associated endolymphatic hydrops.

Acoustic Impedance Tests↗
PubMed2002

Reduction in the endocochlear potential caused by Cs(+) in the perilymph can be explained by the five-compartment model of the stria vascularis.

In an earlier publication (Takeuchi et al., Biophys. J. 79 (2000) 2572-2582), we proposed that K(+) channels in intermediate cells within the stria vascularis may play an essential role in the generation of the endocochlear potential (EP), and we presented an extended version of the five-compartment model of the stria vascularis. In search of further evidence supporting the five-compartment model, we studied the effects of Cs(+) added to the perilymph on guinea pig EP. Cs(+) is known as a competitive K(+) channel blocker. Both the scala tympani and the scala vestibuli of four cochlear turns were perfused at a flow rate of 10 microl/min, and the EP was recorded from the second cochlear turn. Cs(+) at 30 mM caused a biphasic change in the EP; the EP increased transiently from a control level of 89.6 mV to 94.8 mV within 10 min, and then decreased to a steady level of 24.5 mV within the next 40 min. We propose that the initial transient increase in the EP results from Cs(+)-mediated blockade of K(+) conductance in the basolateral membrane of hair cells, and that the subsequent EP decrease is due to effects of Cs(+) on the stria vascularis. We believe that Cs(+) in the perilymph is able to access the stria vascularis by being taken up by fibrocytes in the spiral ligament and then being transported to intermediate cells because it is known that Cs(+) is taken up via Na(+),K(+)-ATPase and that gap junctions connect fibrocytes in the spiral ligament to basal cells and basal cells to intermediate cells. To clarify the effect of intracellular Cs(+) on the electrophysiological properties of intermediate cells, these cells were dissociated from guinea pigs and studied by the whole-cell patch-clamp method. Intracellular Cs(+) depolarized intermediate cells in a dose-dependent manner. In addition, efflux of Cs(+) from the intermediate cell was much less than the efflux of K(+). Thus, Cs(+) may accumulate in the intermediate cell, which depolarizes the cell, which in turn decreases the EP. We conclude that the five-compartment model of the stria vascularis can explain the EP decrease caused by Cs(+) in the perilymph.

Animals↗
PubMed2000

Sensitivity of the endocochlear potential level to cochlear blood flow during hypoventilation.

To study the relationship between endocochlear DC potential (EP) and cochlear blood flow (CoBF) under hypoxic conditions, we recorded the EP and CoBF from the basal turn of the cochlea in 21 guinea pigs. Hypoventilation for 10 minutes was induced by reducing the respiratory rate and volume. During hypoventilation, the EP declined in most of the cases to an intermediate level of the positive range in a few minutes. At the midpoint of the 10-minute hypoventilation, angiotensin II (5 microg/kg or 1 mL/kg) was infused for 60 seconds to raise the systemic blood pressure. In this experimental manipulation of systemic blood pressure, the CoBF and EP generally rose transiently. We determined the sensitivity of the EP to a CoBF change (delta) by calculating the deltaEP/deltaCoBF. More specifically, we analyzed the relationship between the deltaEP/deltaCoBF and the EPi (EP level just before angiotensin II infusion). The deltaEP was equal to the maximum EP level after angiotensin II infusion minus the EPi. The deltaCoBF was equal to the maximum CoBF value after angiotensin II infusion minus the CoBF value just before infusion. The deltaEP/deltaCoBF increased most in the range near 70% of the EPi. That is, the deltaEP/deltaCoBF was greater and the EPi was lower in the range above 70% of the EPi. To elucidate this linear correlation in the range above 70% of the EPi, we must consider several factors. In the supplementary experiments for blood gas analysis using 11 guinea pigs, most of the data of the EPi in the range above 70% were found to be obtained under conditions of a PaO2 of more than 12 mm Hg. As to the sensitivity increase of the EP to the deltaCoBF above mentioned, we propose that among several factors in the stria vascularis during hypoxemia, the activation of glycolysis in aerobic metabolism may be involved. As another possible factor, we postulate the increase in the reactive rate of the enzymatic activities that are linked with EP production and respond to the elevated cyclic adenosine monophosphate activity induced by the sympathicotonic state due to hypercapnia.

Angiotensin II↗
PubMed1998

[Summating potential evoked by long-tone burst stimuli in Menière's disease].

It is now well documented that in cases of Menière's disease/endolymphatic hydrops, the electrocochleography (ECochG) evoked by a broad-band click is often characterized by an enlarged summating potential (enlarged-SP) and a large negative summating potential to action potential ratio (large -SP/AP) but these mechanism have not been clarified. The aim of this study was to find clues to the mechanism of enhanced -SP and large -SP/AP in Menière's disease, by using long-tone burst stimuli. We also sought to determine the significance of SP measurement for evaluating the cochlear function in Menière's disease/endolymphatic hydrops. ECochG was performed on 29 ears of patients with Menière's disease and 12 ears of adults with normal hearing as a control group. Extratympanic ECochG was carried out using an HN-7 electrode. The sound intensity used for measuring the SP and SP/AP was 90dBnHL. Both SP and AP were elicited by clicks and long-tone bursts of 50 ms duration with a 1-ms rise-fall time. The clicks and long-tone bursts with frequencies of 0.5, 1, 2, and 4 kHz were delivered by the tubal transducer (NC-3). In most of the patients with Menière's disease, SP evoked by the long tone burst stimuli showed negative polarity (-SP) at each frequency. Analysis of variance (X2test) indicated a significant difference in -SP at 0.5 and 1 kHz between Menière's disease and the control group (0.5 kHz: p < 0.001, 1 kHz: p < 0.02). When setting the normal upper limit of the -SP/AP to 0.4, we found that the number of cases over 0.4 which showed -SP at 0.5 and 1 kHz was much larger than those below 0.4 in the 29 ears of patients with Menière's disease. There was no difference between the types of Menière's disease or glycerol test and SP polarity elicited by long-tone burst stimuli. The enhanced -SP and large -SP/AP obtained by the broad band clicks seem to reflect a component of negative SP polarity in the low and middle frequency ranges. It was assumed that the reverse phenomena of SP polarity in the low and middle frequency ranges were related to changes in hydrodynamic characteristics in the upper cochlear turns due to abnormal endolymphatic pressure. Our findings suggest that SP recording by long-tone burst stimuli is useful in detecting changes in cochlear partition due to abnormal intracochlear pressure, most likely in the early phase of Menière's disease based on the wide frequency information of SP.

Acoustic Stimulation↗
PubMed1997

Nitrosoglutathione suppresses cochlear potentials and DPOAEs but not outer hair cell currents or voltage-dependent capacitance.

Biochemical and pharmacological evidence support a role for nitric oxide (NO) and glutathione (GSH) in the cochlea. GSH combines with NO in tissue to form nitrosoglutathione (GSNO) that can act as a storage form for GSH and NO. Therefore, we tested GSNO on sound-evoked responses of the cochlea (cochlear microphonic, CM; summating potential, SP; compound action potential, CAP; cubic distortion product otoacoustic emission, DPOAE), on the endocochlear potential (EP), on isolated outer hair cell (OHC) currents and voltage-dependent capacitance, and on Deiters' cell currents. In vivo application of GSNO in increasing concentrations reversibly reduced low-intensity sound-evoked CAP, SP and DPOAEs starting at about 1 mM (CAP) and 3.3 mM (SP, DPOAE). However, even at 10 mM, GSNO had little effect on the EP. In vitro, salicylate (10 mM) but not GSNO (3 and 10 mM) suppressed the early capacitative transients of OHCs. GSNO (3 and 10 mM) had no effect on the whole cell currents of OHCs or Deiters' cells. Results show that GSNO suppresses cochlear function. This suppression may be due to an effect of GSNO on the cochlear amplifier. The actions of GSNO were different from those of other NO donors; therefore, the effects of GSNO may not be mediated by NO. The mechanisms underlying GSNO effects seem to be different from those of salicylate.

Action Potentials↗
PubMed1991

Effects of 250 and 500 Hz tone exposure on the inner ear of guinea pigs as determined by electrophysiological techniques.

The electrophysiological study of cochlear microphonics (CM), whole nerve action potential (AP) and endocochlear potential (EP) were examined. (1) With the extension of the exposure time of 500 Hz tone, a decrease of CM maximum output voltage in test frequency from 2 to 6 kHz was observed. (2) N1 potential of AP decreased very significantly by 500 Hz tone exposure. (3) A very pronounced decrease of the absolute value of the negative potential of the EP in 500 Hz exposure was seen.

Action Potentials↗
PubMed1980

A comparative study of the ototoxicity of gentamicin and gentamicin C1.

Dose-response experiments comparing the ototoxic liability of the aminoglycoside antibiotics gentamicin sulfate and gentamicin C1 sulfate were conducted on guinea pigs. Measures of cochlear electrophysiology, histology, and the pharmacokinetic disposition of the drugs in the plasma and perilymph were made. Electrophysiological and histological measures indicated that gentamicin is more ototoxic than is gentamicin C1.

Animals↗
PubMed1994

Excitatory amino acid antagonists protect cochlear auditory neurons from excitotoxicity.

Since ischemic damage in the brain is linked to glutamate excitotoxicity, the effects of an acute exposure to glutamate, alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid (AMPA) or N-methyl-D aspartate (NMDA) on the radial dendrites were compared with those occurring after a severe cochlear ischemia. Glutamate and AMPA, but not NMDA, produced a drastic swelling restricted to the radial dendrites below the inner hair cells (IHCs). At a concentration of 20 microM AMPA, a full electrophysiological recovery could be observed in some cochleas after washing the drug out. A prior perfusion of 6-7-dinitroquinoxaline-2,3-dione (DNQX, 50 microM) prevented the 25 microM AMPA-induced dendritic swelling. No protective effect of D-2-amino-5-phosphonopentanoate (D-AP5) could be observed. In the same way, ischemia (5-40 minutes) resulted in a clear swelling of the radial dendrites. While D-AP5 had no protective effects, 50 microM DNQX protected most of the radial dendrites from the ischemia-induced swelling, excepting those contacting the modiolar side of the IHCs. Finally, 50 microM DNQX + 50 microM D-AP5 resulted in a nearly complete protection of all the radial dendrites. Altogether, these results suggest that the acute swelling of radial dendrites primarily occurs via AMPA/kainate receptors. However, in radial dendrites contacting the inner hair cells on their modiolar side, NMDA receptors may be also involved.

2-Amino-5-phosphonovalerate↗
PubMed1991

Transmission of cerebrospinal fluid pressure changes to the inner ear and its effect on cochlear microphonics.

Alterations in inner ear fluid pressure and cochlear microphonics (CM) associated with increased cerebrospinal fluid (CSF) pressure were studied in the guinea pig. Hydrostatic pressure in the endolymph and perilymph of the cochlea were measured by use of a servo-controlled micropipet system. Endolymphatic and perilymphatic pressure increased in a linear manner with little or no time lag following pressure increases of 0-50 mm Hg. There was no pressure gradient between the endolymph and perilymph. CM in response to 500 Hz and 4000 Hz tone bursts was recorded before, during and after CSF pressurization. The input-output function of CM showed suppression of 2-8 dB in both maximum output and sensitivity unless the increase in CSF pressure exceeded a level which reduced the cochlear blood flow.

Animals↗
PubMed1994

A method for calculating the spectral response of a hair cell to a pure tone.

Using Corey and Hudspeth's hair cell transducer function and that of Assad and Corey as models, the output of the haircell is calculated for an input of a single tone. These results are then compared with experimental data obtained by Hubbard et al. (1979) from guinea pig cochlear. The theoretical and experimental data are found to be similar for low to moderate sound pressure levels.

Acoustic Stimulation↗
PubMed1985

Preliminary electrophysiological data after the obliteration of cochlear blood vessels by the action of a magnetic field on circulating iron particles.

In order to develop an experimental model for studying local disturbances of the inner ear microcirculation we conducted a series of experiments using small iron particles. Suspensions of iron were infused into the carotid artery of a tracheotomized guinea pig, after which a magnetic force was applied to the basal part of the cochlea. The cochlear microphonics were measured every 10 min over a frequency range from 200 Hz to 10 000 Hz. The amplitude of the cochlear microphonic decreased with this decrease dependent on the time after the application of the magnet. We then found that this amplitude was up to 30 dB less after 110 min. We were able to demonstrate histologically that the thrombosis induced by the iron particles blocks the circulation of the inner ear and results in a loss of its function.

Acoustic Stimulation↗
PubMed1987

The effect of round window membrane rupture on endolymphatic and perilymphatic pressures.

We used a guinea pig model to investigate the effect of round window membrane rupture on endolymphatic and perilymphatic pressures under conditions known to increase these pressures: anoxia, hypercapnia, increased intracranial pressure, and occlusion of the vein of the cochlear aqueduct. When the round window membrane was not ruptured, increases in endolymphatic pressure paralleled the perilymphatic pressure following exposure to each of the experimental conditions. After the round window membrane had been ruptured, however, no increases in perilymphatic pressure or endolymphatic pressure were seen. These results suggest that endolymphatic pressure is dependent on perilymphatic pressure, even when the round window membrane is ruptured.

Animals↗
PubMed1981

The frequency selectivity of the normal and pathological human cochlea.

Human AP tuning curves (tone on tone simultaneous and forward masking curves) were measured during transtympanic electrocochleography. For subjects with near normal thresholds, average Q10 dB values (simultaneous masking) were 2.3 at 2 kHz, 3.6 at 4 kHz, and 4.7 at 8 kHz. Patients with threshold elevations of more than 40 dB, resulting from sensorineural hearing loss of cochlear origin, had tuning curves less sharply tuned by a factor of 2-3, with Q10 dB values of 1-2 at 2 kHz and at 4 kHz, and 1-2.3 at 8 kHz. AP tuning curves and single fibre tuning curves (frequency threshold curves) were measured in normal guinea pigs; cochlear fibre tuning is sharper than AP tuning (simultaneous masking) by a factor of 1.8 (2-20 kHz). Assuming that this factor can be applied to the human cochlea, estimates of normal human cochlear fibre Q10 dB values are 4.2 at 2 kHz, 6.5 at 4 kHz, and 8.5 at 8 kHz.

Animals↗