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PubMed1997

[In vivo cochleoscopy through the round window].

The overall aim of the present investigation was to develop a technique for endoscopic investigation of the cochlea. In the experiments reported here, the possible effect of the endoscope-called the "cochleoscope"-on the electrophysiology of the cochlea was investigated by recording the cochlear action potential (CAP) threshold tuning curve from (0.1-34 kHz). The dorsolateral bulla of anesthesized guinea pigs (with ketamine 60 mg/kg and Rompun 12 mg/kg) was opened, after which the cochleoscope was introduced under micromanipulator control through the round window membrane. Three cochleoscopes were used and had diameters of 0.29 mm, 0.7 mm and 0.89 mm, respectively, containing 2000, 3000 and 3000 fibers each. Experiments in 7 animals showed that the cochleoscope did not influence CAP thresholds. Although the present resolution of the endoscopes is limited, the basilar membrane can be clearly distinguished from the osseous spiral lamina. It is anticipated that improved resolution will allow the cochleoscope to be used for diagnostic purposes in cases of sensorineural hearing loss.

Animals↗
PubMed1990

The influence of acute venous congestion on the guinea pig cochlea.

The effects of sudden occlusion of the vein of the cochlear aqueduct (VCAQ) on the cochlear blood flow, endocochlear potential (EP), endolymphatic and perilymphatic fluid pressures (PE and PP) were studied in the guinea pig. Cochlear blood flow showed a sudden decrease, and EP began to drop within 90 s, ranging from 50 to 70 mV in 5 of 11 animals studied, recovering to normal levels when the animals were placed on a continuous inhalation of carbogen. The PE and PP increased simultaneously (max. PE = 3.4 +/- 1.4 mm Hg; max. PP = 2.5 +/- 1.0 mm Hg) and returned to their initial values after 5 min. The EP was sustained within the normal range, even when there was an apparent decrease in cochlear blood flow (61.4 +/- 8.4%). We believe that variations in EP following VCAQ occlusion were due to anatomical differences in collateral venous communications among the animals studied. Carbogen inhalation produced uniform recovery patterns, indicating that individual collateral vessel responses were eliminated.

Animals↗
PubMed1982

[What effect does ligation of the large neck arteries have on cochlear potentials?].

In guinea-pigs the course of summating potentials (SP) is observed. After the potentials have been identified by their typical form, their sensitivity to a reduction of oxygen, damage by streptomycin and adaptation to excessive noise, the quantity of the SP after ligature of the main neck arteries is recorded. After ligature of the external carotid arteries, the internal carotid arteries and the vertebral arteries on both sides, the SP remain active. This is presumably caused by anastomoses between the external carotid and subclavian arteries, the subclavian and spinal arteries, the external carotid and basilar arteries, and the double origin of the vertebral arteries on both sides. The subclavian arteries and the common carotid arteries can be ligated on both sides in random order. The SP remain almost unchanged as long as one vessel is open.

Animals↗
PubMed1993

Inner ear injury caused by air intrusion to the scala vestibuli of the cochlea.

In a previous communication, we demonstrated that the introduction of air into the scala tympani of the cochlea causes a decrease of cochlear potentials; however, the change in endocochlear dc potential (EP) was mild and the decreased cochlear microphonics (CM) and compound action potentials (CAP) were, at least partially, reversible. In contrast, we have now found that air perfusion (3-60 microliters/min) in the scala vestibuli decreased cochlear potentials more drastically than that in the scala tympani. The change in the EP after air perfusion in the scala vestibuli was characterized by a decrease of the negative EP in response to anoxia. The CM drastically decreased upon the initiation of air perfusion and no recovery was observed after refilling of the perilymph. Histological examination showed collapse of Reissner's membrane in 12 out of 17 cochleas examined. The extent and frequency of the collapse increased with an increase in the amount of air perfused in the scala vestibuli. As the minimal amount of air needed to cause inner ear damage by air perfusion in the scala vestibuli is as small as 3 microliters, it is possible that the prognosis is worse in cases with fistula of the oval window compared to that of the round window area, if the pneumolabyrinth is involved in the pathophysiology of perilymphatic fistula. It is also indicated that air inflation of the middle ear is dangerous in cases with fistula in the oval window.

Air↗
PubMed1986

An experimental study using sodium salicylate to reduce cochlear changes induced by furosemide.

Furosemide is a loop diuretic which has been found to be ototoxic in humans and experimental animals. The ototoxic effects seem to be directed primarily towards the stria vascularis, since its shrinkage and extracellular edema have been observed in correlation with electrophysiologic changes. The present study was designed to examine the interaction of sodium salicylate and furosemide on the cochlear microstructures. Chinchillas weighing 400-600 g were used in all tests performed. The endocochlear potential (EP) was monitored continuously through a microelectrode inserted through the basilar membrane. A control group of animals was injected with 0.5 ml saline intravenously (IV) 30 min before 25 mg/kg furosemide was given. The experimental group of animals was injected with 50 mg/kg sodium salicylate IV 30 min before 25 mg/kg furosemide. The control animals were found to have a mean decrease in EP of 61.1 +/- 7.0 mV. In contrast, the experimental group had very little alteration of the EP following furosemide injection (18.7 +/- 3.9 mV). These findings suggest that sodium salicylate markedly reduces the ototoxic effect of furosemide. This effect may be mediated by an alteration of local or systemic prostaglandin metabolism, or may be due to inhibition of organic acid uptake in the cochlea.

Animals↗
PubMed1985

Ontogenic changes in cochlear characteristic frequency at a basal turn location as reflected in the summating potential.

In these experiments the development of summating potential (SP) responses in gerbils from neonates to adults was followed. Special recording techniques were used to eliminate maturational effects associated with the middle ear so that developmental changes in cochlear physiology were isolated for study. Results indicate that as development proceeds the frequency that maximally excites the basilar membrane (BM) of the gerbil at a specific mid-basal turn electrode location progresses from low to high, demonstrating a 1.5 octave shift from the onset of the generation of electrical activity until adult-like response are obtained. These findings support the theory proposed by E.W. Rubel (in: Handbook of Sensory Physiology, Vol. IX: Development of Sensory Systems, pp. 135-237. Editor: M. Jacobsen. Springer-Verlag, New York) which explains the observed development of physiological responses measured in the cochlea and higher centers in terms of changing micromechanical transduction properties of the BM.

Aging↗
PubMed1981

Origin of the guinea pig cochlear action potential produced by a click.

1. The sound pressure level required to produce a detectable gross action potential (N1) in the guinea pig was measured for a range of frequencies. The resulting electrocochleogram was compared with the click level require to produce a detectable N1. 2. Over most of the auditory range (1-30 kHz) the required click level was 5 dB higher than the level of the most sensitive part of the electrocochleogram. 3. The click evoked N1 therefore reflects the condition of neither the whole cochlea nor any fixed part of it, instead it is a measure of the most sensitive region of any particular cochlea. 4. A click which produces a threshold N1 fails to produce a single-unit change which is detectable by the usual criteria. At threshold, the click-evoked N1 is a result of partial synchrony of single units.

Acoustic Stimulation↗
PubMedDate not supplied

Ionic changes in cochlear endolymph of the guinea pig induced by acoustic injury.

The effects of acoustic overstimulation on the endocochlear potential (EP) and on concentrations of ions (K+, Na+, Cl-, H+, HCO3-, and Ca2+) in endolymph were investigated using ion-selective microelectrodes. A slight but significant elevation of the EP and alkalinization of the endolymph were induced by acoustic overstimulation, whereas there was little change in the K+, Na+, Cl-, and HCO3- concentrations. The changes in H+ and HCO3- concentrations implied a depression of PCO2, suggesting an increase in blood flow to the cochlea. On the other hand, the Ca2+ concentration increased abruptly to 48 times the pre-exposure value. In contrast, no significant change in the Ca2+ concentration was observed in cochleae with damaged hair cells. We discuss the mechanism of the tone-induced Ca2+ elevation in endolymph and its effect on hearing acuity.

Animals↗
PubMed1998

Interaction of methylprednisolone and transient asphyxia on the inner ear of the adrenalectomized rat.

Methylprednisolone has been shown clinically to have beneficial effects on certain types of hearing loss. In the current study, compound action potential (CAP) thresholds, endocochlear potentials (EPs), and potassium concentration (CK+) values in the endolymph were determined under conditions of transient asphyxia (45 seconds) and methylprednisolone treatment (24 hours) in bilateral adrenalectomized rats. Treatment with methylprednisolone significantly reduced the effect of transient asphyxia on CAP thresholds as compared with nontreated animals. Methylprednisolone did not alter the dramatic short-term reduction in the EPs produced by anoxia. Potassium concentrations in treated adrenalectomized rats were significantly lower before transient asphyxia than in nontreated adrenalectomized rats. In the nontreated rats, transient asphyxia induced a reduction in CK+ levels that was not seen in the methylprednisolone-treated animals. The data support the clinical application of methylprednisolone for certain forms of hearing loss and for potassium imbalance in the endolymph.

Adrenalectomy↗
PubMed1989

[Correlation of changes in compound action potential (CAP) tuning curves and cochlear lesion in guinea pigs after explosion].

The purpose of the present study was to investigate the sensitivity of compound action potential (CAP) tuning curves to changes of the cochlear status in guinea pigs after explosion and their ability to reflect specific histological variations. The results were as follows: 1. The CAP tuning curves were abnormally broad and the Q 10 dB values were reduced by a factor of 1 after explosion, indicating wider tuning. 2. The degree of broadening of the CAP tuning curves seemed to increase as the hair cell loss increased. 3. After explosion, the tip of the tuning curve shifted to frequencies significantly higher or lower than that of the signal, it might be related to the location of hair cell loss in the cochlea. 4. In animals for which damage was restricted to only three rows of outer hair cells, changes of the CAP tuning curves were observed. It provides further evidence that the tuning properties of cochlear nerve fibers are dependent upon the integrity of the outer hair cells even though the great majority of fibers innervate inner hair cells only.

Animals↗
PubMedDate not supplied

Effects of carbon dioxide in the middle ear cavity upon the cochlear potentials and cochlear pH.

To elucidate the effects of CO2 in the middle ear upon the cochlea, measurements were made of the cochlear potentials (compound action potential and endocochlear potential) and of the pH of the inner ear fluids and the organ of Corti. Gas containing CO2 did not affect the AP threshold, except for a slight decrease in AP threshold elicited by an 8 kHz tone burst with 10% CO2 flow. The EP did not vary with CO2 gas. The CO2 gas mixture reduced the pH in perilymph significantly, by 0.11 +/- 0.05 with 5% CO2 and by 0.17 +/- 0.04 with 10% CO2, in comparison with 100% N2. The CO2 gas slightly but significantly decreased the endolymph pH, by 0.05 +/- 0.04 with 5% CO2 and by 0.09 +/- 0.06 with 10% CO2. The removal of perilymph led to a greater acidification of endolymph with CO2 gas. Acidification of the organ of Corti was also noted with the CO2 gas flush. These findings indicate that CO2 in the middle ear influences the acid-base regulation of inner ear fluids and the cochlear function.

Animals↗
PubMed1997

Steady state EP is not responsible for hearing loss in adult chickens following acoustic trauma.

The steady state DC endocochlear potential (EP) in young chicks shows a large decrease after acoustic overstimulation followed by a rapid recovery that parallels the recovery of threshold (Poje et al., Hear. Res. 82 (1995) 197-204). These results raise a question as to whether or not the EP could account for the hearing loss and make a significant contribution to the recovery of the threshold. In contrast to results in young chicks, we show that acoustic overstimulation, which causes extensive hair cell damage, does not cause a decrease in the steady state EP in adult chickens. However, there is a significant reduction in the negative EP seen during anoxia which persists even after 4 weeks of recovery. Thus, our results indicate that the steady state EP cannot account for the hearing loss observed in adult chickens.

Acoustic Stimulation↗
PubMed1995

Effect of hypoxemia and ethacrynic acid on ABR and distortion product emission thresholds.

Various studies have shown that induction of hypoxemia in animals such that arterial blood oxygen tensions reach 20-30 mm Hg is accompanied by reversible threshold elevations of the auditory nerve-brain-stem evoked response (ABR). In this state, the endocochlear potential (EP) is depressed, causing a smaller potential difference across the hair cells and/or reduced activity of the cochlear amplifier of the outer hair cells. In order to test these possibilities, ABR threshold (an expression of the overall sensitivity of the cochlea) and changes in threshold of the cubic (2f1-f2) distortion product emissions (DPE) (an expression of activity of the cochlear amplifier) were measured in the same cats while the EP was depressed by hypoxemia or by ethacrynic acid. During the episodes of hypoxemia, DPE thresholds were elevated by 10 dB while ABR thresholds were elevated by 22.8 dB. Therefore, it seems that a normal EP is necessary both for normal cochlear transduction (inner hair cells) and for normal cochlear amplification (outer hair cells). The human fetus in utero is relatively hypoxic and there is evidence that its auditory threshold is also similarly elevated. Therefore the threshold elevation in the fetus in utero, estimated to be about 20 dB, is a consequence of both reduced transduction current through the inner hair cells (about 10 dB) and an additional 10 dB reduction in the activity of the cochlear amplifier of the outer hair cells.

Animals↗
PubMed1984

Hypothermia protects the cochlea from noise damage.

Thresholds of the cochlear action potential were obtained from rodents at euthermic (38 degrees C) and hypothermic (30 degrees and 25 degrees C) rectal temperatures. In the gerbil, low and middle frequency (1-8 kHz) thresholds increased an average of 2.3 dB per degrees C decrease of body temperature; at 16 kHz, 3.5 dB/degrees C; and at 32 kHz, an increase of 4.4 dB/degrees C. In the mouse, these values were: 2-16 kHz, 1.4 dB increase per degrees C decrease; 32 kHz, 2.7 dB/degrees C; 64 kHz, 3.8 dB/degrees C. When subjects maximally susceptible to permanent threshold shift (PTS) at low and middle frequencies (anesthetized, immature mice) were exposed to 115 dB noise, hypothermia reduced PTS at these most susceptible frequencies (2-16 kHz). When awake adult mice were exposed to this noise, hypothermia protected them from PTS at their most vulnerable frequency (32 kHz).

Animals↗
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↗
PubMedDate not supplied

Reduction of acoustically induced auditory impairment by inhalation of carbogen gas. II. Temporary pure-tone induced depression of cochlear action potentials.

Guinea pigs were exposed to a 4.5 kHz pure-tone at 104 dB for 10 min during artificial ventilation with either carbogen gas (95% O2/5% CO2) or normal air. Mean N1 response amplitudes to tone bursts at 32 test frequencies extending from 2.1 kHz through 30 kHz were measured at standardized intervals before and after the acoustic overstimulation. All animals received normal air during recovery. Significant reduction of N1 response amplitude depression within a 3/8 to 1 octave frequency domain above the exposure frequency was found in the group which received the carbogen gas. Those frequencies found to be maximally depressed and the relative rate of recovery from the acoustic overstimulation were not affected by carbogen inhalation. The invariance of the "half-octave shift" following pure-tone acoustic overload was confirmed. Arterial blood gas analysis of guinea pigs respiring carbogen revealed a marked rise in PO2 and PCO2. Carbon dioxide is a potent stimulator of cerebral and cochlear vasodilatation. Sound-induced vasoconstrictive ischemia has been implicated in noise-induced cochlear pathology. The beneficial effects of elevated arterial PCO2 are suggested to have been mediated by reduction of acoustically induced vascular insufficiency within the inner ear.

Animals↗
PubMed1990

The clinical utility of distortion-product otoacoustic emissions.

Otoacoustic emissions permit, for the first time, an unbiased means of examining the preneural elements of the peripheral auditory pathway that make the initial contribution to the perception of acoustic stimuli. Distortion-product otoacoustic emissions (DPOAEs) represent one type of evoked emission that has significant potential for becoming an important test in the audiometric evaluation of hearing capacity. In the present review, selected examples of several forms of sensorineural hearing loss demonstrate that DPOAEs have the ability to act as objective indicators of the frequency/level configuration of the conventional audiogram in cases in which hearing impairment results primarily from damage to the outer hair cells. In contrast, normal DPOAE functioning, in the presence of a significant hearing loss, indicates a locus of damage central to the region of the outer hair cells. Like the other emitted responses, DPOAEs can be measured noninvasively, are highly repeatable, under test-retest conditions, and are simple and rapid to detect using microcomputer-based instrumentation. Further, DPOAEs test both the "threshold" and suprathreshold levels of outer hair-cell activity in the form of response/growth functions, over a 30- to 40-dB stimulus range. In combination, these attributes indicate that DPOAEs can provide an objective and comprehensive assessment of the cochlear reserve of a given ear.

Audiometry, Evoked Response↗
PubMed1999

Strial dysfunction in the MRL-Fas mouse.

The MRL-Fas(lpr) mouse, a model of multisystemic autoimmune disease, has been proposed as a potential model of autoimmune inner ear disease. Cochlear pathology, consisting of hydropic degeneration of the stria vascularis, has been documented to occur coincident with the establishment of systemic disease in this animal. Because the cochlear pathology is restricted to the stria, this study was designed to evaluate whether the endocochlear potential (EP) would be diminished in these animals because of a loss in strial Na, K-ATPase. Experimental (MRL-Fas(lpr)) mice, with established systemic disease, had auditory brain stem response thresholds and EPs recorded. MRL-+/+ mice served as controls. Animals were then euthanized, and their cochleas were processed for immunohistologic assay for the alpha1 and beta2 subunits of Na,K-ATPase. Density of staining was evaluated by use of quantitative means with densitometry image analysis of digitized images. MRL-Fas(lpr) mice revealed significant elevations in auditory brain stem response thresholds and reductions in EPs but no reductions in Na,K-ATPase levels, as evidenced by immunohistochemical assay. The reduction of EP likely occurs as a result of cellular degeneration within the stria vascularis and likely results from an abrogation of the strial perilymph/endolymph barrier and not from a reduction in strial Na, K-ATPase levels.

Animals↗