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Results for “Cochlear Microphonic Potentials”

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At least 325 records · Page 18Linked to original sources
PubMed2000

Acute changes in cochlear potentials due to cisplatin.

The purpose of this study was to investigate how the hair cells and stria vascularis are affected at the onset of cisplatin ototoxicity. The effects on the endocochlear potential (EP) and the cochlear microphonics (CM) were observed simultaneously in two groups of adult chinchillas receiving as follows: (1) 5 microl of cisplatin (1 mg/ml) in normal saline, and (2) 5 microl of normal saline on the round window. The EP and the CM were recorded for 12-14 h after cisplatin application, and morphological changes were assessed using scanning electron microscopy. Both the EP and the CM amplitude demonstrated a profound reduction, and a very strong correlation was observed between these two values during this time period. Although the reduction of the EP and the CM was observed by 12-14 h, only very slight degeneration of outer hair cells was seen at that time. These data suggested that a reduction of the EP which was caused by the alteration of the stria vascularis might be primarily responsible for very early changes in cochlear function after topical cisplatin application, while later changes were the direct result of hair cell damage.

Animals↗
PubMed1999

Selective loss of inner hair cells and type-I ganglion neurons in carboplatin-treated chinchillas. Mechanisms of damage and protection.

Carboplatin preferentially destroys inner hair cells (IHCs) and type-I spiral ganglion neurons while sparing outer hair cells (OHCs). Loss of IHCs and type-I ganglion cells is associated with a significant reduction of the compound action potential (CAP). However, the cochlear microphonic (CM) potential and distortion product otoacoustic emissions (DPOAEs) remain normal, indicating that the OHCs are functionally intact. In the vestibular system, carboplatin selectively destroys type-I hair cells and their afferent neurons. Damage of type-I vestibular hair cells and their afferent terminals is associated with significant depression of nystagmus induced by cold, caloric stimulation. Histochemical studies revealed a rapid decrease in succinate dehydrogenase (SDH) staining in IHCs soon after carboplatin treatment, and staining intensity remained depressed in surviving IHCs for at least 1 month after carboplatin treatment. These results suggest that carboplatin depresses the metabolic function in surviving IHCs. Several lines of evidence suggest that free radicals may contribute to carboplatin-induced sensory cell damage. Intracochlear infusion of L-buthionine-[S,R]-sulfoximine (BSO), which depletes intracellular glutathione (GSH), increases IHC and OHC loss. Previous in vitro studies have shown that neurotrophin 4/5 (NT-4/5) promotes the survival of spiral ganglion neurons from cisplatin ototoxicity. In vivo perfusion of NT-4/5 promoted the survival of spiral ganglion neurons, but did not protect the hair cells.

Action Potentials↗
PubMed1997

Ototoxic effect of erythromycin on cochlear potentials in the guinea pig.

The mechanism of hearing loss due to the administration of intravenous erythromycin was investigated in the albino guinea pig, and it was found for the first time that this drug causes cochlear dysfunction. The endocochlear potential (EP) and the cochlear microphonics (CM) recorded at the first cochlear turn transiently decreased when erythromycin was administered intravenously at dosages of 100 and 150 mg/kg. The averaged maximum decrease in EP was 16 mV (n = 5) and 33 mV (n = 5) for 100 and 150 mg/kg, respectively. The maximum decrease in the CM was about 25% when the EP reached its lowest value with the injection of 150 mg/kg. A complete recovery of the EP and CM ensured within 20 minutes after each erythromycin dose. The perilymphatic perfusion of 3 mmol/L of erythromycin decreased the EP and CM; however, in contrast to the intravenous administration, the decrease of the CM was nearly complete and both the EP and CM were irreversible. Hearing loss due to intravenously administered erythromycin could likely be attributle to the transient dysfunction of the stria vascularis, although concomitant dysfunction of the central auditory pathway cannot be excluded.

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↗
PubMed2002

Electrocochleography in auditory neuropathy.

Auditory neuropathy (AN) is a disorder characterized by the absence or the severe impairment of the auditory brainstem responses (ABRs) together with the preservation of otoacoustic emissions and/or cochlear microphonic (CM). We recorded transtympanic electrocochleography (ECohG) evoked by 0.1 ms clicks in one young adult and in four children having distortion product otoacoustic emissions and absent ABRs. In all but one patient CM and summating potential (SP) were present with normal threshold, and their amplitudes appeared comparable to or higher than the values obtained from subjects with normal hearing. The compound action potential (CAP) was absent in two patients while in one subject CM and SP were followed by a highly desynchronized neural activity. A broad CAP was found in two children and the threshold appeared clearly elevated in one of them, while it showed only a mild elevation in the other. No correlation was found between CAP and behavioral thresholds. These results suggest that ECohG can be useful in AN diagnoses since it is the only reliable tool in evaluating the auditory peripheral function in the presence of a desynchronized ABR.

Action Potentials↗
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↗
PubMed1999

Cochlear function of guinea pigs with experimental chronic renal failure.

This study aimed to evaluate electrophysiologically the cochlear function of guinea pigs that underwent a five-sixths nephrectomy and, additionally, to explore the synergistic action between chronic renal failure (CRF) and noise. Cochlear potentials were recorded at 1, 2, and 3 months postoperatively. Slight changes in compound action potential and cochlear microphonics were seen at 1 month postoperative, while moderate and profound changes were seen at 2 and 3 months. Endocochlear potential showed no significant reduction. The results indicate that CRF may be an etiologic factor for cochlear dysfunction and that the hair cells seem likely to be a main site of the lesion. One-month-postoperative animals were exposed to a broadband noise. In contrast to control animals, the test animals demonstrated no recovery from the decrease in compound action potential and cochlear microphonics that occurred immediately after noise exposure. This suggests a synergistic interaction between CRF and noise.

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↗