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Results for “Cochlear Microphonic Potentials”

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At least 217 records · Page 12Linked to original sources
PubMed1975

[Evoked response audiometry of the guinea pig before and after drop in hearing induced by furosemid (author's transl)].

Using particular surface electrodes evoked response audiometry (ERA) can be applied to small laboratory animals without any sedation or anaesthesia. In addition to other methods we have studied in this way the influence of extreme doses of Furosemid on the guinea pig inner ear. 6-20 mg Furosemid per 100 g of bodyweight (about 100 times the human therapy dose) were applicated i.v. within 5 min resulting in a drop of hearing immediately. For the anaesthesized animal the cochlear microphonic potentials (CM) decrease simultaneously, indicating Furosemid to act at the inner ear itself. By both methods recovery of inner ear function is seen to start about 10 min later according to the little biological half life of Furosemid. As being restricted in respect of time for the CM-measurements we are sure about reversibility only by the ERA-method.

Animals↗
PubMed1989

[Frequency-dependent cochlear microphonics in inner ear hearing loss with various pitch thresholds].

Promontory recordings of the cochlear microphonics (CM) after stimulation with 0.5, 1 and 2 kHz tone bursts at 120 dB SPL were performed on normal subjects and patients with various, levels of sensory hearing loss. A significant correlation was found between frequency-related CM amplitudes and the configuration of the pure-tone audiogram. Such recordings provide objective information on hearing abilities at low and middle frequencies and are thus a relevant tool in clinical audiometry.

Auditory Threshold↗
PubMed1986

[The promontory test and electrocochleography in deafness caused by mumps].

Contradictory histological findings in patients with deafness following mumps led us to conduct electrophysiological investigations. Promontory testing (PT) and measurement of cochlear microphonics (CM) enabled us to distinguish between neural and sensory deafness. On the basis of a careful history and serological tests in 19 cases of unilateral deafness we found that the hearing loss was probably caused by mumps. In all patients except one auditory sensations could be obtained by electric stimulation of the acoustic nerve whereas no CM were detectable even with strong stimuli of 100 dB tonepips. In view of the electrophysiological findings, doubt is cast on the neural genesis of deafness following mumps as assumed by Lehnhardt (1962).

Audiometry, Evoked Response↗
PubMed1994

Influence of calcitonin-gene related peptide on cochlear blood flow and electrophysiology.

Intra-arterially infused calcitonin gene-related peptide (CGRP) induced dose-dependent decreases in both systemic blood pressure and cochlear blood flow (CBF). However, when subjects were pretreated systemically or locally with the specific receptor antagonist CGRP(8-37), CBF increased, despite decreases in systemic blood pressure in response to CGRP infusions. Micro-infusions of CGRP directly into the supplying arterial network of the cochlea induced dose-dependent increases in CBF that were blocked by CGRP(8-37) pretreatment. Cochlear electrophysiology, as assessed by cochlear action potential and cochlear microphonics, remained unchanged following each condition tested. These results indicate that CGRP is involved in systemic regulation of blood pressure and contributes to the regulation of CBF.

Animals↗
PubMed1992

Study of the effect of 350-Hz tone exposure on electrophysiological function of the inner ear of guinea pigs.

The effects of noise exposure were studied in fifty-nine 4- to 5-week-old albino Hartley guinea pigs with normal hearing (body weight 250-300 g). The following experiments and results were carried out: exposure to 350 Hz pure tones at 115 dB for 40 h and exposure to 350 Hz tones at 120 dB for 64 h. In order to investigate the effects of low-frequency tone exposures on the hearing of the guinea pigs, cochlear microphonics (CM), whole nerve action potentials (AP) and endocochlear potentials (EP) were measured. With a high-sound pressure, a decrease was observed in the CM maximum output voltage in the test frequencies of 2, 4 and 6 kHz while the CM threshold (pseudothreshold) of 6 kHz was elevated. Output voltage of the N1 potential of the AP using a 7-kHz tone burst decreased while the threshold of the N1 potential was elevated. An extension of latency and a decrease in the absolute value of the negative potential in EP were also observed.

Acoustics↗
PubMed1996

A comparative study on the effect of pure-tone exposure of the guinea pig cochlea.

Electrophysiological methods were applied to 160 healthy adult male guinea pigs in order to investigate the effects of pure-tone exposure for 24 h on the inner ear. A reduction in cochlear microphonics (CM), action potential (AP) and endocochlear potential was observed following exposure to 110 dB at 100 Hz, 100 dB at 200 and 600 Hz and 95 dB at 2 kHz. The observed K+ endolymphatic concentration during 40 min anoxia remained unchanged. In contrast K+ decreased in control animals and following exposure to pure tones varying from 110 dB at 60 Hz to 85 dB at 2 kHz. These findings indicate that high frequency tones have a greater effect on inner ear functions than those of lower frequency, decreasing the maximum output voltage of CM and AP but not changing K+ endolymphatic concentration.

Acoustic Stimulation↗
PubMed1989

Correlative changes of auditory nerve and microphonic potentials throughout sleep.

Gross cochlear potentials in response to alternating clicks and pure tone bursts were recorded in guinea-pigs with chronically implanted electrodes in the round window during sleep and the awake state. A significant increase in both averaged potentials, the compound auditory nerve action potential (cAP) and cochlear microphonics (CM) occurred in slow wave sleep (SWS) with a subsequent diminution in paradoxical sleep (PS) periods. The cAP, CM, amplitude and area averages were similar during quiet wakefulness and in PS. Moreover, as an episode of PS progressed, the recorded potentials continued to decrease. On the other hand, increased averaged values were again observed during a subsequent episode of SWS. An involvement of the efferent olivo-cochlear bundle is postulated, first, because it is the only known pathway connecting the CNS and the auditory periphery and, second, because several key pre-receptor variables (middle ear muscles and ossicles and sound-source ear relation) were either abolished or altered dramatically.

Acoustic Stimulation↗
PubMed1981

Electrocochleographic study of patients with cerebral vascular lesions.

Electrocochleographies were performed on three patients with deafness resulting from cerebral vascular lesions. Recording was made by the transtympanic needle electrode technique. In a patient who had anterior-inferior cerebellar artery aneurysm that showed fluctuating hearing loss, auditory nerve action potential (AP), cochlear microphonics (CM), and summating potential fluctuate in amplitude in concert with episodes of ischemic hearing loss. This indicates the pathophysiology of reversible impairment of the cochlear nerve and of sensory epithelium of the inner ear caused by disturbance of blood flow into the inner ear. It was also conjectured that the cochlea is hardly impaired in the case with normal AP and CM responses despite the increased threshold in pure-tone audiometry and that the cochlea undergoes irreversible organic changes in the patient who has no AP or CM response in tests after a long period.

Action Potentials↗
PubMed1986

Differential effects of benzodiazepines on cochlear and auditory nerve responses.

The influence exerted by chlordiazepoxide or midazolam upon auditory nerve compound action potential (cAP) and cochlear microphonic (CM) has been analyzed in chronic as well as in acutely prepared guinea pigs. Pre-receptorial variables were carefully controlled. The benzodiazepines dissociated the cochlear recorded potentials, increasing the cAP amplitude, in response to clicks, and decreasing the CM area, produced by a coherent pure tone pip. Both responses were dose related. A direct effect upon the cochlea was eliminated by local infusion of the drugs. It was also demonstrated to be a specific benzodiazepinic action because the use of an antagonist, Ro 15-1788, abolished the effect. Benzodiazepines could have increased the GABAergic activity at the pontine origins of the olivo-cochlear bundle or in the reticulo-cochlear fibers. These are the only central pathways that could be responsible for the effects obtained at the cochlea or auditory nerve levels. We suggest that this is the cause of the withdrawal of inhibitory tonus from the primary afferent fibers mediated by the efferent system (lateral superior olive), as may occur during dishabituation. It may also be the cause of the CM decrement, but the effect in this case would be exerted mainly through another set of efferent fibers (trapezoid body nucleus).

Action Potentials↗
PubMed1992

The effects of moderate cooling on gross cochlear potentials in the gerbil: basal and apical differences.

Changes in the threshold of the compound action potential (CAP) response in the gerbil to low- and high-frequency tonebursts were monitored during uniform cooling of the cochlea by 7-8 degrees C below normal body temperature. Recordings of the endocochlear potential (EP), cochlear microphonic (CM), and summating potentials (SP) were also obtained from the base and apex of the cochlea under the same conditions. Cooling-related changes in the CAP, as well as the CM and SP response obtained near the best frequency of the recording location, were greater in the base than in the apex. In contrast, reductions in the EP appeared uniform throughout the cochlea. Thus the greater vulnerability of CAP thresholds in the base does not result from a greater vulnerability of the stria vascularis in this region. Our results suggest that the enhanced susceptibility to cooling of the CAP in the cochlear base reflects changes in hair cell mechanisms.

Acoustic Stimulation↗
PubMed1997

Cisplatin-induced ototoxicity; electrophysiological evidence of spontaneous recovery in the albino guinea pig.

For 8 days albino guinea pigs (n = 48) were treated with cisplatin (cis-diamminedichloroplatinum(II), 1.5 mg/kg body weight/day). Compound action potentials (CAP), cochlear microphonics (CM) and summating potentials (SP) were recorded from the apical surface of the cochlea in response to tone bursts ranging in frequency from 0.5 to 16 kHz. The recordings were collected in different groups of animals, 1 day, 1 week, 2, 4, 8 and 16 weeks after cisplatin treatment, respectively. One day after the 8-day treatment we found frequency-dependent loss in the amplitudes of the three cochlear potentials, with the larger losses occurring at the higher frequencies. In terms of threshold shift the losses were larger for the CAP than for the hair cell-related potentials SP and CM. A salient improvement in both CAP and CM amplitude occurred over the next 8 weeks. Also, the SP showed improvement. These results indicate that guinea pig cochlear transduction recovers spontaneously after cisplatin injury. Recovery of the hair cell-related potentials suggests that recovery occurs already at the hair cell level. The question whether this recovery originates with the formation of new hair cells or with repair of damaged hair cells should be answered on the basis of subsequent morphological investigations.

Acoustic Stimulation↗