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At least 685 records · Page 38Linked to original sources
PubMed1994

Strial dysfunction in a melanocyte deficient mutant rat (Ws/Ws rat).

A homozygous mutant rat at the white spotting (Ws) locus showing a deficiency of melanocytes has recently been found (4, 5). The function and morphology of the inner ear of the Ws/Ws rat were examined by auditory brainstem response (ABR), endocochlear DC potential (EP), and electron microscopy. The mean ABR threshold of the Ws/Ws rat was significantly higher than that of the control +/+ rat. Most Ws/Ws rats showed no or very little EP. In electron microscopy, the stria vascularis of the Ws/Ws rat proved to be very thin and flat with poor interdigitation of marginal cells, and absence of intermediate cells. The organ of Corti appeared to be intact in both the +/+ rat and the Ws/Ws rat. These electrophysiological and morphological findings suggest that the Ws/Ws rat suffered from severe hearing loss caused by strial dysfunction.

Acoustic Stimulation↗
PubMed1996

[Cochlear ischemia and changes in compound action potentials in the guinea pig].

To determine the degree of decrease in cochlear blood flow (CoBF) which causes compound action potentials (CAPs) to disappear, a cochlear ischemic model was created by compressing the internal auditory artery in guinea pig. CoBF was measured with a laser Doppler flowmeter, and CAPs were recorded with an electrode placed on the round window membrane. The amplitude and latency of the N1 wave of CAPs changed as CoBF decreased. When CoBF diminished to as much as 70% below the original level, N1 disappeared. In this study, we also observed the N1 recovery process following CoBF reperfusion after 20 minutes of cochlear ischemia. N1 recovery in the group with an incomplete decrease in CoBF was better than in the group with a complete decrease in CoBF. These findings suggest that both the degree of compromise of CoBF and the duration of ischemia are important factors affecting the recovery of auditory function.

Animals↗
PubMed1989

Effect of albumin-bound furosemide on the endocochlear potential of the chinchilla. Alleviation of furosemide-induced ototoxicity.

The effects of albumin-unbound furosemide and albumin-bound furosemide on the cochlear function were compared by the continuous observation of the endocochlear potential (EP) in the chinchilla using the microelectrode method. The EP depression following the intravenous injection of 50 mg/kg of furosemide was 108.5 +/- 2.7 mV, while the addition of 1.0 and 1.3 g/kg of albumin induced the EP depression to be 35.0 +/- 4.8 and 8.1 +/- 1.9 mV, respectively, and both prolonged the time to attain the minimum EP. However, there was no difference in the recovery time of the EP between the two groups. The results indicate that access to the site of furosemide action in the cochlea is dependent on the unbound fraction of furosemide and that the albumin-bound furosemide alleviates the EP depression induced by furosemide alone with the augmentation of diuresis.

Animals↗
PubMed1987

Positive endocochlear potential: mechanism of production by marginal cells of stria vascularis.

The positive endocochlear potential (EP+) and high K+ concentration of the endolymph in the scala media of the mammalian cochlea are unusual. They have long been assumed to be due to a putative K-pump in the luminal membrane of the marginal cells of the stria vascularis, which were believed to have a negative internal potential. We show that the cell potential is more positive than the EP+, and that the ion pump is conventional Na,K-ATPase, probably in the basolateral membrane. The latter was determined from experiments in which the ionic environment of the strial cells was controlled by perfusion of the perilymphatic space of the cochlea, in the absence of vascular circulation. While the usual EP+ was maintained by normal perfusate, replacement of Na+ by choline resulted in a negative EP, showing that Na,K-ATPase is necessary for the production of EP+. Elimination of K+ as well as Na+ from the perfusate did not change the value of the negative EP, showing that no K-ATPase is involved.

Animals↗
PubMed1995

Differential effects of gentamicin on the distribution of cochlear function in albino and pigmented guinea pigs.

It has been suggested that the high affinity of melanin pigment for aminoglycoside antibiotics may cause these drugs to bind preferentially to the pigmented inner ear, producing greater ototoxicity than in the amelanotic albino cochlea. However, evidence of greater ototoxicity in albinos has led to the hypothesis that melanin inhibits the toxicity of these drugs in the pigmented inner ear. On the other hand, ototoxicity in the pigmented animals may simply be delayed relative to the albinos, only to become equal or even more severe with time. The present study was conducted to determine whether a relatively low dose of gentamicin (68.5 mg/kg) would produce differential ototoxicity between albino and pigmented guinea pigs which would persist long after drug exposure had stopped. Nine pigmented and eight albino guinea pigs were given gentamicin sulfate for 14 consecutive days, and were then allowed a two-month recovery period before cochlear analysis; 11 pairs of saline-injected or untreated albino and pigmented guinea pigs served as controls. The results showed that the gentamicin-treated albinos had significantly elevated thresholds for the compound action potential from the auditory nerve (CAP), and significantly lower endocochlear potentials (EP) and cochlear microphonic (CM) input-output voltage functions when compared to their respective controls, or to either group of pigmented guinea pigs. The CAP in drug-treated pigmented animals did not differ significantly from controls, and the differences in EP and CM were marginally significant. The results indicate that the pigmented cochlea is less susceptible to gentamicin than the albino cochlea, and support the hypothesis that melanin may inhibit aminoglycoside ototoxicity in the pigmented inner ear.

Acoustic Stimulation↗
PubMed1984

Cochlear effects of locally applied inhibitors.

The round window has been used as a route for introducing ototoxic substances into the inner ear in order to bypass barriers between the systemic circulation and the inner ear. We have used this method to administer locally sodium potassium-ATPase inhibitors and chloride transport inhibitors to the inner ear of the chinchilla. Drugs dissolved in saline solution were applied on the round window membrane. Endocochlear potential (EP) was recorded from the basal turn using the round window approach. The EP was not altered following application of saline solution as a control. Following application of ouabain (1 mM), the EP steadily declined. After vanadate (27 mM), the EP initially increased, and subsequently declined. Sanguiarine did not alter the EP. The loop diuretics furosemide and piretanide caused a marked decline in the EP after local application. However, the stilbene derivative DIDS did not alter the EP after topical application. These findings raise questions about whether the loop diuretics have any effect on chloride transport in the cochlea and make appear unlikely that active chloride transport contributes to the normal EP.

Administration, Topical↗
PubMedDate not supplied

Time course of the endocochlear potential in the isolated cochlea of the guinea pig.

The temperature of Hanks' solution changed its potential (-0.48 mV/degrees C in Na(+)-Hanks' and -0.23 mV/degrees C in K(+)-Hanks' solution), but the pH had no clear effect on the potential. The time course of the endocochlear potential (EP) in the isolated cochlea of the guinea pig was measured under some different conditions. When the cochlea was moistened with Hanks' solution, negative EP increased gradually toward 0 mV at 124 min after death. When the cochlea was immersed in Hanks' solution, positive EP was obtained but it depended on the oxygen and the circulation of Hanks' solution. Moderate cooling (5 degrees C) of Hanks' solution had no significant effect on the EP of the isolated cochlea immersed in oxygen-saturated Hanks' solution circulated by oxygen bubbles. The space constant and the amplitude of the displacement responses were independent of the EP in the isolated cochlea. Thus, the positive EP might not show the physiological condition of the isolated cochlea.

Animals↗
PubMedDate not supplied

Prolonged electrode implantation in experimental studies. Critical evaluation of a technique.

Stainless steel electrodes were chronically implanted through the right facial canal of 30 guinea pigs, close to the potential generator (VIII nerve). Compound action potential (CAP) thresholds, N1 latencies and input-output curves were recorded on day of implantation and 2, 4 and 8-12 weeks later. In the same sitting, auditory evoked brain stem response (ABR) thresholds, latencies and inter-peak-latencies were measured on both sides as a control. N1 thresholds and latencies at low and high intensities were stable. N1 amplitudes, however, showed some variation. Rate of infection was low and reimplantation was successful. Preserving the facial nerve as a land mark was found advantageous, particularly on reimplantation, and did not affect the CAP recording. The technique, originally described by Hildesheimer et al., proved to be reproducible. A few technical difficulties are pointed out and the implication of some interesting findings are discussed.

Animals↗
PubMed1985

Link between functional and morphological changes in the inner ear--functional changes produced by ototoxic agents and their interactions.

Common potentials used to evaluate cochlear function are the ac cochlear potential (ACCP), N1 and the positive dc endocochlear potential (EP). The ACCP is an electrical analogue of the sound stimulus; its source is the electrical activity of the cochlear hair cells. N1 is a volume conductor recorded action potential of the auditory nerve. The EP is the positive polarization of the middle compartment of the cochlea (scala media) with respect to the other compartments (the scalae tympani and vestibuli); the stria vascularis is apparently responsible for the EP. Generally, ototoxic drugs and very intense broad-band noise affect the basal portion of the cochlea first and, because of tonotopic organization, the ACCP responses to high frequency pure tones are affected before those to the low frequencies. However, the correlation between the effect of an ototraumatic agent on the ACCP and its effect on cochlear morphology is not always reliable. The correlations between changes in N1 and EP and in cochlear morphology are even less precise. Also discussed will be the cochlear effects of noise and the ototoxic interactions between drug/drug, noise/drug, and noise/drug/otitis media.

Acetylcysteine↗
PubMed1998

Inwardly rectifying K+ currents in intermediate cells in the cochlea of gerbils: a possible contribution to the endocochlear potential.

The stria vascularis in the cochlea generates the endocochlear potential (EP) and secretes K+-rich endolymph; both are indispensable for normal sound transduction by hair cells. K+ conductance in the intermediate cell, one of the several types of cells constituting the stria vascularis, was investigated by the whole-cell patch-clamp technique. Inwardly-rectifying K+ (Kir) currents were the major currents observed. The currents were inhibited dose-dependently by Ba2+, quinine, verapamil and Cs+, but not by tetraethylammonium (20 mM), 4-aminopyridine (5 mM) or Cd2+ (1 mM). The similarity between the effect of inhibitors on Kir currents and on the EP (Takeuchi et al., Hearing Res., 101 (1996) 181-185) suggests a direct contribution of the Kir conductance to the generation of the EP.

4-Aminopyridine↗
PubMed1983

Studies on the temporary effect of noise on the auditory function in man.

ECoG and ABR recordings were performed on 22 young, normal-hearing persons, before and after exposure to fatiguing noise. Temporary Threshold Shift (TTS) of up to 35 dB at 4-6 kHz was induced by octave band noise with centre frequency at 2.8 kHz. The latency of waves I, III, V and ACAP (Auditory Compound Action Potential) and intervals between waves I-III, III-V, I-V and ACAP-V were analysed as functions of stimulus intensity in pre- and post-exposure recordings. In post-exposure recordings a threshold elevation, a significant increase of latency and unaltered intervals between the successive waves and ACAP were observed. It was concluded that the noise-induced auditory fatigue, measured as TTS, originates within the cochlea and is transferred to the auditory pathways. The great intersubject variability of the data obtained indicates that the TTS may be a useful measure of individual sensitivity to noise, but prognosis on the presumed Permanent Threshold Shifts (PTS) based on the evaluation of TTS would seem doubtful.

Auditory Fatigue↗
PubMed2005

Transient cochlear ischemia and its effects on the stria vascularis.

The effects of transient cochlear ischemia on the stria vascularis were studied. Fifteen minutes of ischemia decreased the endocochlear potential by up to 17.5 mV on day 1; it returned to normal on day 7. Immunostaining for Na+,K+-ATPase, a marker for the Na+/K+-pump, and for connexin 26, a marker for gap junctions, was inhibited on days 1 and 4, and returned to normal on day 7. Electron microscopy showed expansion of the intercellular space with abundant vacuolar formation in the stria vascularis. These morphological changes disappeared completely by day 7. The results indicate that transient ischemia causes a reversible functional disorder of the stria vascularis with fine structural changes, which may be owing to dysfunction of Na+/K+-pump or gap junctions.

Animals↗
PubMed2005

The effect of superior canal dehiscence on cochlear potential in response to air-conducted stimuli in chinchilla.

A superior semicircular canal dehiscence (SCD) is a break or hole in the bony wall of the superior semicircular canal. Patients with SCD syndrome present with a variety of symptoms: some with vestibular symptoms, others with auditory symptoms (including low-frequency conductive hearing loss) and yet others with both. We are interested in whether or not mechanically altering the superior canal by introducing a dehiscence is sufficient to cause the low-frequency conductive hearing loss associated with SCD syndrome. We evaluated the effect of a surgically introduced dehiscence on auditory responses to air-conducted (AC) stimuli in 11 chinchilla ears. Cochlear potential (CP) was recorded at the round-window before and after a dehiscence was introduced. In each ear, a decrease in CP in response to low frequency (<2 kHz) sound stimuli was observed after the introduction of the dehiscence. The dehiscence was then patched with cyanoacrylate glue leading to a reversal of the dehiscence-induced changes in CP. The reversible decrease in auditory sensitivity observed in chinchilla is consistent with the elevated AC thresholds observed in patients with SCD. According to the 'third-window' hypothesis the SCD shunts sound-induced stapes velocity away from the cochlea, resulting in decreased auditory sensitivity to AC sounds. The data collected in this study are consistent with predictions of this hypothesis.

Acoustic Stimulation↗
PubMed1992

Kinetics of gentamicin in cochlear hair cells after chronic treatment.

Presence of gentamicin (GM) in cochlear hair cells was detected by immunohistochemistry in guinea pigs (GPs) cochlea 1, 9 and 41 days after a 6-day treatment with GM at 60 mg/kg/day (s.c.). The number of GPs in each group was respectively 7, 12 and 6. Twelve other non-treated GPs served as controls. Cochlear function was measured, just before sacrifice, by VIIIth nerve compound action potential (CAP) audiograms. Functional and immunohistological evaluations were performed by two independent naïve observers respectively. Functional changes were minimal: only one out of the 25 treated GPs, from the 41-day group, showed significant threshold elevations on high frequencies. Meanwhile GM labelling was observed in most outer hair cells (OHCs) from the three rows of all the treated GPs, with radial and longitudinal gradients, and found similar in the 3 groups. These results 1) confirm that GM is significantly present in OHCs before the development of ototoxicity and 2) indicate that GM accumulates and is maintained inside the OHCs for very long periods of time, i.e. that its clearance from the hair cells, if any, would be very slow.

Animals↗
PubMed1991

Attention effects on the auditory event-related potential.

Studies on selective-attention effects on the auditory event-related brain potential (ERP) are reviewed. Brainstem components of the ERP have not been shown to be sensitive to attention. On the other hand, attention effects in the middle-latency range (12-50 ms from stimulus onset) appear to occur under some conditions but it is not clear whether these effects are exogenous or endogenous. The predominant attention effect on the auditory ERP is the processing negativity, a slow endogenous negativity which often commences well before the exogenous (supratemporal) N1 component peaks (at about 100 ms post-stimulus), therefore giving the impression that this exogenous component is attention-sensitive. It is not yet settled, however, whether even these exogenous processes under some conditions might be modulated by selective attention.

Acoustic Stimulation↗
PubMed1998

Failure of forskolin to elevate the endocochlear potential in experimental endolymphatic hydrops of the guinea pig.

The effect of forskolin (FSK) on the endocochlear potential (EP) in scala media (SM) was examined in experimental endolymphatic hydrops of the guinea pig. Two weeks after obliteration of the endolymphatic sac the EP of hydroptic ears and that of the contralateral control ears were measured by means of microelectrodes. The perfusion of scala vestibuli (SV) with FSK (200 microM) produced EP elevation in the contralateral control ears but failed to do so in the experimental hydroptic ears. Histological examination of experimental endolymphatic hydrops showed mild hydrops with intact appearance of outer and inner hair cells, and the stria vascularis. The mechanism underlying the failure of FSK to elevate the EP in experimental endolymphatic hydrops is discussed.

Animals↗
PubMed1985

Cell volume density alterations within the stria vascularis after administration of a hyperosmotic agent.

The purpose of this study was to determine the effects of an intravenous injection of a hyperosmotic agent (mannitol) on the volume density (Vv) of the primary components of the stria vascularis (SV). Chinchillas received either a 2.0 g/kg injection of mannitol or an equal volume of saline as a control. At 1, 10 and 60 min after the injection, the right cochleas were fixed with osmium tetroxide and prepared for transmission electron microscopy. At a distance of 70% from the cochlear apex, the complete radial area of the SV was photographed and stereologically analyzed. Additional animals received mannitol or bumetanide for the purpose of measuring serum osmolality and the endocochlear potential (EP). The present results showed elevation of serum osmolality after mannitol but not after bumetanide and depression of the +EP after bumetanide but not after mannitol. Vv alterations of SV components after mannitol were similar to those Vv changes observed in a previous study, after bumetanide. After treatment with either diuretic, the Vv of the marginal cells decreased and the Vv of the intermediate cells and intercellular spaces increased. We conclude that since the Vv alterations of the SV components are so similar after both diuretics, none of these alterations is a morphological correlate of a depressed +EP which was observed after bumetanide. A model of the action of mannitol on the SV is proposed.

Animals↗
PubMed1993

Effects of carbogen on decreases in endocochlear potential and cochlear microcirculation induced by ischemia of the cochlea.

Preventive effects of carbogen on decreases in endocochlear potential (EP) and cochlear microcirculation induced by ischemia of the cochlea were examined in guinea pigs with intravital microscopy. The experimental model giving a severe decline in cochlear blood flow (CBF) was established by occlusion of both common carotid arteries and one of the vertebral arteries and i.v. infusion of adenosine triphosphate (ATP). The results showed no significant difference in the magnitude and pattern of the decrease in the cochlear microcirculation induced by ATP infusion and arterial occlusion before and after carbogen inhalation. However, even with a dramatic decrease in CBF, carbogen could reduce the decline in EP. The results clearly indicate that although carbogen fails to ameliorate cochlear ischemia in the face of a large impairment of the blood supply caused by a drop of blood pressure and cardiac output, it does in fact enhance the oxygen delivery to the cochlea and thus provide a therapeutic means of treating certain inner ear diseases caused by insufficient blood supply to the cochlea.

Animals↗