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Results for “Cochlear Microphonic Potentials”

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At least 1,117 records · Page 62Linked to original sources
PubMed1978

Normative data on the cochlear microphonic in rat using differential electrodes.

Isopotential (1-muV) cochleograms were obrained from 19 anesthetized rats from electrodes inserted into scala vestibuli and scala tympani of the first turn. The differential electrode technique is suitable for frequencies above 1-2 kc/s in the rat. CM sensitivity in rats as measured with intracochlear electrodes (26 micrometer in diameter) was considerably poorer than in guinea pigs at frequencies below 2 kc/s, but was within 10-14 db at 2 kc/s and above. The shape of the CM input-output functions were similar to those in the guinea pig and chinchilla, except that the intensity level where the CM becomes non-linear is higher in the rat.

Animals↗
PubMed1994

[Enlarged and prolongated cochlear microphonics and its clinical significance].

Bilateral cochlear microphonics (CM) were evoked by tone burst simultaneously. A speaker was put in head-foot axis 2m from the mid-point of a given line connecting the bilateral external meatus. Seven normal persons and 106 cases of unilateral sensory hearing loss and recruitment were examined. When recruitment was present, CM at corresponding frequencies were enlarged and prolongated. In 62 cases CM delayed slowly, while other 27 cases quickly. In addition to 2 cases of bilateral Ménière disease with sensory hearing loss and recruitment, CM were enlarged and prolongated at some frequencies in left ears and at other frequencies in right ears in accordance with predominant recruitment. Meanwhile CM of the opposite normal ear decreased obviously. CM could not be evoked from profound and totally deaf ears.

Acoustic Stimulation↗
PubMed1995

Comparison of tympanic membrane-recorded electrocochleography and the auditory brainstem response in threshold determination.

The purpose of this study was to evaluate the usefulness of electrocochleography (ECoG) recorded with a tympanic membrane electrode as an adjunctive measure to auditory brainstem response (ABR) in frequency-specific threshold estimation. In a group of 10 normally hearing and 10 sensorineural hearing-impaired subjects, ABR and ECoG were simultaneously recorded in response to tone-burst stimuli centered at 500, 1000, 2000, and 4000 Hz. At each frequency, stimulus intensity was reduced in 12-dB decrements from an initial level of 110 dB SPL until no replicable response could be discerned. Electrocochleography and ABR thresholds were determined at each frequency, and correlation to behavioral audiometric threshold was determined. Input/output functions were also computed. At 2000 and 4000 Hz, both ABR and ECoG thresholds correlated with behavioral audiometric threshold. At 1000 Hz, ABR threshold correlated with behavioral audiometric threshold; ECoG did not. At 500 Hz, neither ABR nor ECoG threshold correlated with behavioral audiometric threshold. Input/output functions were steeper for ECoG than for ABR at all frequencies tested in the normally hearing group.

Auditory Threshold↗
PubMed1996

Additional findings on heritability and prenatal masculinization of cochlear mechanisms: click-evoked otoacoustic emissions.

A previous demonstration of a substantial genetic contribution to the expression of spontaneous otoacoustic emissions (SOAEs) is here extended to an aspect of click-evoked otoacoustic emissions (CEOAEs). CEOAEs were measured in the same twins and non-twins used for the SOAE heritability study. The stimuli were 100-microsecond clicks presented a nominal rate of 2/s; the emitted waveforms from 50 clicks were summed, and a 20-ms sample of that averaged waveform (beginning 6 ms after click presentation) was subjected to spectral analysis. The total power in the spectrum from 1 to 5 kHz in this temporal segment of the CEOAE waveform was used as the primary dependent variable. This overall power was significantly greater in female and right ears than in male and left ears, but the difference between dark- and light-eyed subjects was not significant. The overall power in the two left, and two right, ears of monozygotic co-twins was more highly correlated than in dizygotic co-twins, and structural modeling indicated that about 65-85% of the individual variation in the expression of CEOAE power could be attributed to genes-essentially the same heritability estimate as obtained previously from the SOAE data. Within-subject correlations between CEOAE power and number of SOAEs ranged from about 0.3 to 0.7, suggesting that these two forms of otoacoustic emission may depend upon somewhat different aspects of the same underlying mechanism and, thus, that heritability estimates based on one measure are not completely redundant to those from the other. While the average spectral power of the CEOAEs in opposite-sex dizygotic (OSDZ) females was smaller than that in same-sex dizygotic (SSDZ) females- and thus approached the value for males-the difference did not achieve statistical significance. Thus, the evidence for a prenatal masculinizing effect was less definitive in these CEOAE data than in the SOAE data obtained from the same subjects. An interpretation that accounts for both the CEOAE and SOAE results is that the strength of the so-called cochlear amplifiers is under genetic control that is to some extent mediated and/or modified through prenatal exposure to androgens. The indicated direction of effect is that weak cochlear amplifiers result when prenatal androgen levels are high. Under this view, then, androgen level contribute both to the sex differences observed in otoacoustic emissions and the prenatal masculinizing effects observed in opposite-sex twins, and they may be a factor in individual differences in OAE expression as well. Additionally it is shown that, although the powers of the CEOAE waveforms were reasonably highly correlated for the two ears of subjects in all groups, and across MZ co-twins, cross-correlations on the fine structures of those same pairs of CEOAE waveforms were essentially zero-presumably owing largely to the synchronizing of (different) SOAE frequencies in the ears being compared.

Acoustic Stimulation↗
PubMed1998

Increased otoacoustic-emission amplitude secondary to cochlear lesions.

OBJECTIVE: The measurements of transient evoked otoacoustic emissions and distortion-product otoacoustic emissions are being used increasingly, both as an objective hearing test clinically, and as a research tool to investigate the micromechanical aspects of cochlear function. We hypothesized that localized damage in the apical or middle cochlear turns may have an influence on the micromechanics and the function of adjacent, apparently normal cochlea. For that purpose, we used an animal model of localized apical and middle-turn cochlear lesions. METHOD: Extent of damage was assessed by scanning electron microscopy and the function of the damaged cochlea by change in the otoacoustic emission (OAE) levels. RESULTS: We found that localized damage to the apical or middle turn may be accompanied by an increase in OAE measured from adjacent apparently normal cochlea. CONCLUSION: Explanations to this phenomenon are suggested, and possible clinical associations such as to Meniere's disease and to sudden hearing loss are reviewed.

Animals↗
PubMed1983

Cochlear inner hair cells: effects of transient asphyxia on intracellular potentials.

Intracellular potentials were recorded from inner hair cells in the guinea pig cochlea. Transient asphyxia was induced by interrupting respiration for brief periods. Asphyxia caused a hyperpolarization of the resting membrane potential (resting Em). The hyperpolarization averaged 2.9 mV for 30 s asphyxias and 5.7 mV for 45 s asphyxias. The membrane potential recovered quickly after normal ventilation was resumed. Asphyxia also induced a rapid and profound decrease of the d.c. receptor potential in response to moderate intensity tone bursts at the characteristic frequency of the inner hair cell. At maximal depression, the receptor potential was reduced about 60% for a 30 s asphyxia and 100% for a 45 s asphyxia. The receptor potential recovered slowly after normal ventilation was resumed. A similar percent reduction and time course of recovery were observed for the a.c. receptor potential. In recordings from the same animals, the round window compound action potential (CAP) was as severely depressed by asphyxia as the hair cell receptor potentials. The time course of recovery for the CAP was similar to the slow recovery of the d.c. receptor potential. In contrast, the round window cochlear microphonics (CM) and the endolymphatic potential (EP) were affected less by asphyxia and recovered quickly after ventilation was resumed. Frequency tuning curves (FTCs) for the d.c. receptor potential were measured during the period of maximal receptor potential depression. These FTCs showed decreased tip sensitivity and a decrease in sharpness of tuning, as measured by the Q10. These changes were fully reversible. Low frequency (tail) segments of the FTCs were much less affected by asphyxia. The inner hair cell FTC changes during asphyxia were compared with neural FTC changes reported by other investigators. The similarities lead us to the conclusion that the inner hair cell and the auditory neural response to sound are equally sensitive to asphyxia.

Animals↗
PubMed1996

Combined effects of acute lead acetate exposure and tone exposure of the guinea pig cochlea.

Lead acetate exposure to humans can induce various disorders of the cranial nerves. Although vertigo and sensorineural deafness have been reported in lead workers, the dose effects of lead acetate on the cochlea and eighth cranial nerve are not well documented. We investigated the effects of lead acetate on the male albino Hartley guinea pig cochlea by measuring cochlear microphonics (CM), whole nerve action potential (AP), endocochlear potential (EP) and K+ ion concentration of the endolymph. Animals were given lead acetate by intraperitoneal injection as 20 mg/week for 4 consecutive weeks. A total dose < 80 mg did not induce electrophysiological changes in the cochlea. However, the AP output voltage (N1) decreased if the 80 mg lead acetate treatment was followed by an 80 dB tone exposure at 6 kHz during 24 h. A change was observed in CM and EP but not K+ ion concentration in the scala media.

Action Potentials↗
PubMed1996

[Effects of adenosine on cochlear function in guinea pigs].

As a neuromodulator, adenosine is able to decrease the release of most neurotransmitters and plays a role of negative feedback regulation. In the present experiment, the effects of adenosine, and its uptake inhibitor dipyridamole and antagonist theophylline on cochlear potentials were investigated by means of perilymphatic perfusion. 0.01 mmol/L adenosine and dipyridamole was shown to suppress compound action potentials (CAP) and cochlear microphonics (CM). The amplitudes of CAP and CM were decreased under high sound intensity stimulation. The I/O function curve was shifted toward the right and the N1 peak latency of CAP was prolonged. 1 mmol/L theophylline showed opposite effects. All these changes are reversible after washing out of the artificial perilymphy. Normal endocochlear potentials (EP) and anoxia induced negative EP (N-EP) were not changed significantly, while the rapid response of EP to noise exposure, i.e. a rapid fall with onset of noise (EP-on) and a rapid increase with offset (EP-off), could be suppressed by adenosine. These results suggest that adenosine is an inhibitory neuromodulator subserving a negative feedback role in the regulation of cochlear function.

Adenosine↗