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At least 235 records · Page 13Linked to original sources
PubMed1994

Transitory endolymph leakage induced hearing loss and tinnitus: depolarization, biphasic shortening and loss of electromotility of outer hair cells.

There are types of deafness and tinnitus in which ruptures or massive changes in the ionic permeability of the membranes lining the endolymphatic space [e.g., of the reticular lamina (RL)] are believed to allow potassium-rich endolymph to deluge the low [K+] perilymphatic fluid (e.g., in the small spaces of Nuel). This would result in a K+ intoxication of sensory and neural structures. Acute attacks of Ménière's disease have been suggested to be an important example for this event. The present study investigated the effects of transiently elevated [K+] due to the addition of artificial endolymph to the basolateral cell surface of outer hair cells (OHC) in replicating endolymph-induced K+ intoxication of the perilymph in the small spaces of Nuel. The influence of K+ intoxication of the basolateral OHC cell surface on the transduction was then examined. Intoxication resulted in an inhibition of the physiological repolarizing K+ efflux from hair cells. This induced unwanted depolarizations of the hair cells, interfering with mechanoelectrical transduction. A pathological longitudinal OHC shortening was also found, with subsequent compression of the organ of Corti possibly influencing the micromechanics of the mechanically active OHC. Both micromechanical and electrophysiological alterations are proposed to contribute to endolymph leakage induced attacks of deafness and possibly also to tinnitus. Moreover, repeated or long-lasting K+ intoxications of OHC resulted in a chronic and complete loss of OHC motility. This is suggested to be a pathophysiological basis in some patients with chronic hearing loss resulting from Ménière's syndrome.

Action Potentials↗
PubMed1987

Effects of carbon monoxide on cochlear electrophysiology and blood flow.

The belief that the cochlea is particularly vulnerable to a reduction in oxygen availability comes predominantly from studies reporting the disruption of electrophysiological measures, such as the compound action potential, endocochlear potential, inner hair cell intracellular potentials or afferent nerve fiber responses by asphyxiation. Because hypoxia has frequently been suggested as an underlying mechanism by which many ototoxic agents produce injury, and because such agents are not likely to completely disrupt oxygen delivery, we investigated the effects of graded hypoxia (using doses of carbon monoxide) on cochlear blood flow, the compound action potential (CAP) and the cochlear microphonic (CM). High doses of carbon monoxide injected intra-peritoneally yielded reversible loss of the CAP sensitivity for high frequency tone bursts, the extent of which was dose dependent. The loss was observed first at the highest frequency tested (50 kHz) and as carboxyhemoglobin levels increased, contiguous lower frequencies were influenced. Recovery progressed from low to high frequencies as carboxyhemoglobin levels declined. Carbon monoxide administration also produced a dose dependent elevation in the cochlear blood flow measured by a laser Doppler flow monitor. The data suggest that carbon monoxide administration disrupts cochlear function only under extremely severe exposure conditions. An elevation in cochlear blood flow may well serve as a protective mechanism which maintains cochlear function in the face of declining blood oxygen carrying capacity and delivery. While the site of action of carbon monoxide in the cochlea is uncertain, the data clearly indicate that elements involved in the generation of the CAP for high frequency tones are particularly vulnerable.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Tympanic electrocochleography for evaluation of endolymphatic hydrops.

There has been increased interest in electrocochleography for the diagnosis and intraoperative monitoring of patients with endolymphatic hydrops. Attention has been focused on the determination of the summating potential:action potential (SP:AP) ratio from alternating polarity clicks. Review of this technique at the University of Minnesota led to a reevaluation of the usual interpretation of these recordings. Separate examination of the rarefaction and condensation click recordings provides insight into abnormal response patterns. Cases are presented to illustrate a variety of normal and abnormal patterns including abnormal differences in the latency of condensation and rarefaction-click-generated action potentials, increased summating potential, uncanceled cochlear microphonic, and reduced action potential and summating potential amplitudes. These response categories may be useful in understanding the pathophysiology of Meniere's disease.

Acoustic Stimulation↗
PubMed1987

Time-related changes in cochlear potentials in guinea pigs with experimentally induced endolymphatic hydrops.

In order to examine the changes in cochlear function occurring in hydropic ears over time, endolymphatic hydrops was provoked by obliterating the endolymphatic sac in 62 albino guinea pigs. Cochlear potentials (EP, CM, SP and AP) were recorded in the 1st, 2nd, 4th and 12th postoperative weeks, respectively. A significant reduction in the level of EP was already observed in the 2nd week and the potential was further suppressed by the 4th week. There was no significant difference between the levels of the 4th and 12th weeks. The amplitudes of CM and AP decreased progressively as time elapsed after the surgery. In sharp contrast to the other potentials, the abnormality in SP was most frequently observed in the 1st week. These results are discussed in the light of the available literature.

Action Potentials↗
PubMed1980

CM tuning can be compatible with sharply tuned receptor potentials.

There is convincing evidence that cochlear microphonics (CM) arise primarily from outer hair cells and have a frequency distribution that is much broader than that measured in inner hair cells by Russel and Sellick [6,7]. The broad tuning results from the fact that CM generated at each location decays exponentially along the cochlear duct. This implies that the sources of CM (the outer hair cells) must be more sharply tuned than the CM itself. We modeled approximately the tuning of outer hairs on the assumption that it is proportional to the shear motion between the tectorial membrane and the reticular lamina. At each frequency the spatial distribution of CM is computed by convolving the shear distribution with an exponential decay function. The frequency dependence of CM at a given location can then be found by making a cut through a family of such frequency curves. The resulting CM tuning is much flatter than that of the modeled outer hair-cell receptor potentials and roughly parallels basilar-membrane tuning below the best frequency. Above the best frequency, the theoretical curves show a frequency-dependent plateau similar to that found in physiological CM measurements.

Basilar Membrane↗
PubMed1982

Corresponding effects of acoustic fatigue on the cochlear microphonic and the compound action potential.

Moderate levels of acoustic fatigue, usually induced by a 100 dB SPL pure tone at a frequency appropriate to the location of intracochlear differential electrodes, have a surprising and paradoxical influence on the cochlear microphonic and the compound action potential of the auditory nerve. While the low-level microphonic becomes smaller, the low-level action potential becomes considerably larger and exhibits a shortened latency. The high-level microphonic and the high-level action potential are left virtually unchanged at these levels of fatigue. Nonetheless, if the duration or intensity of exposure is increased, both the high-level and low-level action potentials decrease as well. Assuming that the low-level microphonics are generated by outer hair cells, these data suggest that one relationship between outer hair cell function and neural function is inhibition at low intensities. Assuming that the high-level microphonic tends to be generated by inner hair cells, the decrease in the action potential at all intensities whenever the high-level microphonic potential is impaired suggests that the functional relationship between inner hair cells and auditory nerve function is excitatory.

Acoustic Stimulation↗
PubMed1990

Salicylate, mefenamate, meclofenamate, and quinine on cochlear potentials.

The perilymphatic spaces of guinea pig cochleae were perfused with artificial perilymph, with and without drug, at a rate of 2.5 microliters/minute for 10 minutes. The compound action potential of the auditory nerve, cochlear microphonics, and the summating potential evoked by 10 kHz tone bursts of varying intensities were recorded from a wire inserted in the basal turn scala vestibuli. The endocochlear potential was recorded from the scala media. Sodium salicylate (1.25 to 10 mmol/L) reduced the magnitude of the compound action potential evoked by low-sound intensities without affecting the compound action potential evoked by high-sound intensities. Sodium salicylate also reduced cochlear microphonics and had no effect on summating potential. Cochlear perfusions of prostaglandin synthesis inhibitors, mefenamate (200 mumol/L), and meclofenamate (200 mumol/L), had no effect on the cochlear potentials. Quinine (10 to 100 mumol/L) reduced the compound action potential input-output function in a parallel fashion rather than selectively affecting the low-intensity compound action potential. Quinine (100 mumol/L) reduced cochlear microphonics and summating potential. Neither quinine (100 mumol/L) nor salicylate (5 mmol/L) affected endocochlear potential. These results suggest that salicylate-induced hearing loss is not caused by either antagonism of the hair cell transmitter or cyclooxygenase inhibition, nor is it caused by the same mechanism that causes quinine-induced hearing loss.

Acetates↗
PubMed1987

[Electrocochleographic detection of the summation potential in patients with inner ear deafness].

Pre-operative information about cochlear mechanical function is a pre-requisite for intra-cochlear implants. In more than 300 pre-operative examinations we demonstrated cochlear microphonics in many patients suffering from complete inner ear deafness; we interpret this phenomenon as evidence of mechanical function of the cochlea. A summation potential in patients with sensorineural deafness is more certain proof. We have now performed thorough electrocochleography on 43 deaf patients whose acoustic nerve was intact, i.e. whose promontory test was positive. After stimulation firstly with rarefaction tonebursts and later with condensation tonebursts and consecutive, off-line addition and subtraction we found small amplitude microphonics in 32 patients. Of these patients, 16 showed a negative potential that we interpreted as a summation potential. If these findings are verified by further investigations it will be possible to examine patients with inner ear deafness electrophysiologically. Furthermore this investigation is a very sensitive indicator of residual mechanical function of the cochlear basilar membrane.

Audiometry, Evoked Response↗
PubMed1991

Transport of HRP through Reissner's membrane in experimental endolymphatic hydrops.

Unilateral endolymphatic hydrops was produced in guinea pigs by cauterization of the endolymphatic sac. Measurements of compound action potential (CAP), cochlear microphonics (CM) and negative summating potential (-SP) confirmed endolymphatic hydrops three months after surgery. In both control and hydropic ears, reaction product of HRP was observed only on the perilymphatic surface of the epithelial cells of Reissner's membrane after 10 min perfusion, while it was observed on both the endolymphatic and perilymphatic surfaces after 30 min perfusion. Epithelial tight junctions were not stained and labelled pinocytotic vesicles were observed in the epithelial cells. These findings suggest that the transport of HRP through Reissner's membrane is unchanged in endolymphatic hydrops and that the epithelial junctions are tight regardless of the distension of Reissner's membrane.

Animals↗
PubMed1991

Cochlear efferent neurones and protection against acoustic trauma: protection of outer hair cell receptor current and interanimal variability.

We have measured the changes in neural and microphonic sensitivity in the basal turn of the guinea-pig cochlea produced by intense acoustic overstimulation (10 kHz, 115 dB SPL for 60 s and 150 s). As reported previously, the drop in neural and microphonic sensitivities observed after overstimulation were highly correlated [Patuzzi et al. (1989) Hear. Res. 39, 189-202]. Presentation of a non-traumatizing pure-tone to the contralateral ear (10 kHz, 80 dB SPL) during acoustic overstimulation reduced the amount of acoustic trauma measured using the neural response or the microphonic response. Transection of the medial olivo-cochlear system of efferent fibres at the floor of the fourth ventricle abolished this protective effect of contralateral sound and dramatically reduced the variability in the data. Since the low-frequency microphonic is a simple measure of the receptor current through the outer hair cells, and this current probably plays a part in enhancing the mechanical sensitivity of the cochlea, the protection of the microphonic we have observed suggests that the efferent system protects neural sensitivity by protecting the mechano-electrical transduction of outer hair cells. The drop in variability after sectioning the efferents also suggests that inter-animal variations in susceptibility to noise trauma may be a consequence of differing tonic activity of the efferents, and/or a variation in the sensitivity of the efferent pathway.

Action Potentials↗
PubMed1989

Changes in cochlear microphonic and neural sensitivity produced by acoustic trauma.

The low-frequency (200 Hz) microphonic potentials at the round window and in the organ of Corti of the first turn of the guinea pig cochlea have been measured before and after acoustic overstimulation. Reductions in the amplitude of this microphonic after loud sound are highly correlated with neural threshold elevation in this region. The fall in the microphonic amplitude appears due to an inactivation of mechano-electrical transduction channels at the apex of the outer hair cells into a closed state. These results are consistent with the idea that the current through the outer hair cells controls the mechanical sensitivity of the organ of Corti, and that the temporary loss of mechanical and neural sensitivity following loud sound is due to a simple inactivation of the mechano-electrical transduction channels.

Action Potentials↗
PubMedDate not supplied

Inner ear pathology in the deafness mutant mouse.

A distinctive cochlear pathology was found in deafness mutant mice. There was a delay in the formation of the fluid-filled Nuel and tunnel spaces in the organ of Corti, the hair cells were distorted and degenerate, and there was poor maintenance of synapses. No hair cells appeared normal by TEM, but SEM revealed some areas where stereocilia appeared relatively normal, suggesting that SEM of the surface of the organ of Corti is not necessarily a good indicator of hair cell pathology in hereditary hearing impairment. Mutant mice show normal development of endocochlear potential, but have no measurable cochlear microphonics or compound action potential. The data suggest that the deafness gene affects the organ of Corti and that cochlear hair cells in deafness mice are never functional.

Action Potentials↗
PubMed1980

Intracochlear sound pressure measurements in guinea pigs.

The intracochlear sound pressure in guinea pigs was measured in the scala vestibuli of the first, second and third turns as well as in the scala tympani of the first and second turns. The acoustic stimuli were pure tones delivered over the frequency range 30--20 000 Hz at sound levels ranging from 60 to 100 dB. The results achieved show the sound pressure in scala vestibuli to be practically in phase in the first three turns. In scala tympani the pressure varies within wide limits when passing from the first to the second turn, but it is equal to the pressure in scala vestibuli at frequencies in excess of the best frequency of the point considered. The difference in instantaneous pressure acting on the basilar membrane exhibits the characteristics of a traveling wave. This pressure difference corresponds to the displacement of the basilar membrane evaluated from recordings of the microphonic potential.

Basilar Membrane↗
PubMed1990

Effect of Escherichia coli endotoxin on cochlear potentials following its application to the chinchilla middle ear.

The compound action potential (CAP) of the eighth nerve and the endocochlear potential (EP) were examined in the chinchilla as an animal model when Escherichia coli endotoxin (100 micrograms) was applied to the middle ear cavity. A significant elevation of the CAP threshold at 2, 3, and 4 kHz was observed 48 h after the instillation of endotoxin, but this hearing loss was thought to be caused by a conductive component. No significant change in the CAP threshold was recognized 30 days after instillation. The EP in either period showed no significant difference. These findings indicate that the application of endotoxin at the concentration used in the present study does not cause a cochlear disturbance.

Action Potentials↗