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Results for “Cochlear Microphonic Potentials”

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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↗

PubMed2001

Quinine-induced alterations of electrically evoked otoacoustic emissions and cochlear potentials in guinea pigs.

Quinine is a well-known ototoxic drug which may affect portions of the auditory system with different biochemical effects, causing reversible hearing loss and tinnitus. Recent investigations indicate that quinine at high concentrations can act directly on cochlear outer hair cells to affect their motility and the mechanical response of the basilar membrane. This study aimed to investigate the effect of quinine on the electromotility of outer hair cells in vivo by means of measuring the electrically evoked otoacoustic emissions (EEOAEs), and the relationship between EEOAE and hearing sensitivity alterations in guinea pigs. Quinine was infused into the scala tympani with concentrations between 0.05 and 5 mM. An alternating current (35 microA RMS) swept from 400 Hz to 40 kHz was applied to the round window to evoke the EEOAE. The compound action potential (CAP), cochlear microphonic (CM) and summating potential (SP) were also measured. Results show that quinine affects the EEOAE in a dose-dependent manner and that its effects are reversible. Two aspects of the EEOAE were affected by quinine, depending on concentration: (1) the 'fine structure' only for concentrations below 0.1 mM and (2) the overall amplitude and the 'fine structure' for concentrations above 0.1 mM. At 5 mM the fine structure was completely absent and the mean amplitude of the EEOAE greatly decreased. Multiple component analysis shows the short delay component of the EEOAE is related to the mean value of the amplitude spectrum while the long delay component is related to the fine structure. The alterations of the EEOAE are roughly comparable to that of the cochlear potentials. A 'threshold concentration' for quinine's effects was found at 25 microM. CAP was significantly affected at 25 microM while EEOAE, CM and SP were not. Enhancement of the EEOAE amplitude was noticed in five out of 20 animals in the current study. The enhancement appears only related to the EEOAE mean level or short delay component. The results suggest that quinine can affect in vivo electromotility of outer hair cells at low concentration and therefore change the cochlear amplifier performance via an effect on electro-mechanical transduction. Its effects on the cochlear spiral ganglion neurons and/or their presynaptic process are also suggested, and these are speculated to be the primary sites for quinine's effects on the auditory system.

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↗

PubMed1998

Cisplatin ototoxicity. An electrophysiological dose-effect study in albino guinea pigs.

Recently, the effect of the ACTH(4-9) analog, ORG2766, on cisplatin ototoxicity was studied by Hamers et al. (1994). This study showed that the ACTH(4-9) analog partially prevents the ototoxicity of cisplatin. The authors suggested that the daily dose of 2.0 mg/kg/day for 8 days might have been too high to obtain full protection. Knowledge about dose-effect relations for cisplatin ototoxicity is rather meager. Therefore, we conducted a basic dose-effect study for cisplatin without any concomitant additives. A follow-up of the Hamers et al. (1994) study, based on dose-effect data from this paper, is presented in a companion paper. The effects of cisplatin on the compound action potential (CAP), cochlear microphonics (CM) and summating potential (SP) were determined in acute experiments, in different groups of albino guinea pigs, each group injected with a different dose of cisplatin. Daily doses ranged from 0.7 to 2.0 mg/kg/day cisplatin (i.p.) for 8 consecutive days. Electrocochleography was performed at day 10. The measurements were performed over a broad range of frequencies (0.5-16 kHz). The results showed clustering of the data in two groups, the first group concerning the treatments of 1.5 and 2.0 mg/kg/day with large frequency-dependent losses in the three cochlear potentials, the second group concerning the treatments with lower doses of cisplatin (0.7, 1.0 and 1.25 mg/kg/day) where almost no losses in the three cochlear potentials were found. The threshold curves regarding the lower doses (0.7-1.25 mg/kg/day) were almost indistinguishable from the control threshold curve except at the higher frequencies (12 and 16 kHz). Thus, a marked transition from almost no ototoxic effect to a large effect seems to occur between cisplatin doses of 1.25 and 1.5 mg/kg/day for 8 days. The small difference between the effects found for 1.5 mg/kg/day and 2 mg/kg/day suggests that a smaller dose than the one of 2 mg/kg/day for 8 days used previously (Hamers et al., 1994) might better suit research into protection against cisplatin ototoxicity.

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↗

PubMed2002

Ethacrynic acid rapidly and selectively abolishes blood flow in vessels supplying the lateral wall of the cochlea.

The mechanisms underlying the ototoxicity of ethacrynic acid (EA) are not fully understood. Previous studies have focused on morphologic and enzymatic changes in the stria vascularis. The current experiment shows that one of the earliest effects of EA is ischemia, resulting from impaired blood flow in vessels supplying the lateral wall of the cochlea. Inner ear microcirculation, endocochlear potentials, compound action potentials (CAP), cochlear microphonics (CM) and summating potentials (SP) were monitored over time in chinchillas following a single injection of EA (40 mg/kg i.v.). At all times after EA injection, blood vessels supplying the spiral lamina, modiolus, and vestibular end organs appeared normal. In contrast, lateral wall (spiral ligament and stria vascularis) vessels were poorly stained with eosin 2 min after EA injection, and devoid of red blood cells at 30 min post EA. Decline, but not recovery, of CAP, CM and SP followed the microcirculation changes in the lateral wall. Reperfusion was delayed in stria vascularis arterioles relative to other lateral wall vessels. The ischemia-reperfusion caused by EA would be expected to generate large quantities of free radicals, which may trigger or contribute to the cellular, enzymatic, and functional pathologies that have been described in detail previously.

Action Potentials↗

PubMed1992

Fine structure of the intracochlear potential field. II. Tone-evoked waveforms and cochlear microphonics.

1. Extracellular evoked potentials to low-frequency pure-tone stimuli were recorded in the second cochlear turn of the anesthetized guinea pig. Spatial variations of the field potentials were characterized by advancing and withdrawing micropipettes along radial tracks in scala tympani (ST) and scala vestibuli (SV). Compound action potentials (CAPs) and cochlear microphonics (CM) are the major components of the evoked responses to 50- to 1,600- Hz stimuli. The relative contribution of CM and CAP to the evoked potentials varies with cochlear scala and location within the scala as well as with stimulus frequency and intensity. 2. In the 50- to 800-Hz frequency range, the largest CM in the second turn was recorded from scala media (SM). Below 500 Hz the CM in SV is larger than in ST, whereas above 500 Hz a larger CM is present in ST. The CM in SV is nearly in phase with the CM in SM, although it is smaller by a factor of two to four. The CM diminishes by another factor of two over a 100-microns depth range as an electrode is withdrawn out of SV through the spiral ligament. While the electrode is in SV or in the fluid outside the spiral ligament, the CM magnitude does not change by greater than 10%. The shape of the radial CM magnitude profile along tracks in SV shows little or no dependence on intensity in the 65- to 105-dB SPL range or on frequency in the 50- to 800-Hz range. 3. Unlike the CM profiles in SV, the shape of the CM magnitude and phase profiles in ST are a complex function of frequency and intensity. Below 500 Hz, the CM goes through a 140-180 degree radial phase shift over a 100-microns distance near the spiral ligament bordering ST. Concomitant with the large radial phase shift is a local minimum of the CM magnitude. The location of this "virtual ground point" can shift radially by as much as 100 microns over a 30-dB intensity range. The CM magnitude deep in ST is always larger than the CM outside the spiral ligament bordering ST. However, the ratio of the CM magnitudes at these two locations can vary from 0.1 to 0.8, the ratio tending to increase with intensity in the 200- to 800-Hz range.(ABSTRACT TRUNCATED AT 400 WORDS)

Acoustic Stimulation↗

PubMed1983

Chronological changes of electrocochleogram in experimental endolymphatic hydrops. Special reference with AP output potential and hair cell cilia.

Chronological changes of the whole nerve action potential (AP), cochlear microphonics (CM) and summating potential (SP) in experimental endolymphatic hydrops in guinea pigs were studied during a period from 1 week to 13 months after the endolymphatic sac obliteration. Endolymphatic hydrops became extensive in month 3 and persisted thereafter. The threshold of AP increased with the lapse of time but good AP output potential was obtained, being maximum in month 3. The threshold of CM increased with the lapse of time. The CM output potential was the highest around week 3 when endolymphatic hydrops was slightly formed, and it decreased thereafter. SP responses at the frequencies of 8, 4, 1 and 0.5 kHz showed the reversed polarity of -SP in month 3 and changed towards potential 0 thereafter. In animals showing super-normal AP output potential, the cilia in the third row of outer hair cells were disarranged. This seems to be involved in recruitment.

Action Potentials↗

PubMed1984

Single unit responses in the cochlear nucleus of the deaf quivering mouse.

Mice homozygous for the autosomal recessive gene quivering do not have a classical Preyer reflex and appear to be deaf. Round window recordings including both cochlear microphonics and compound action potentials failed to reveal any abnormality. However, auditory-evoked potentials recorded from the inferior colliculus (IC) are small with long latencies, and the thresholds are at least 50 dB higher than those recorded in controls. This suggests that the auditory deficit arises in the auditory pathway between the cochlear nerve and IC and underlines the need for a description of the functioning of the cochlear nucleus (CN). Single units were recorded extracellularly from the CN in 9 mutants (qv/qv) and 11 control animals (+/qv, or +/+) in the age range 60-120 days. The spike response pattern in mutant animals was broadly similar to that in the controls: a sustained response with monotonic rate-intensity functions. In addition the mean Q10dB for units in the mutants was similar to that of the controls. However, in mutants the group mean threshold at the characteristic frequency was higher and the latency to the first evoked spike at 20 dB above threshold was longer than in controls. Some unit responses in the mutants were similar to those of the controls. Nevertheless, in the quivering mouse, evidence now exists of single unit dysfunction in the cochlear nucleus.

Acoustic Stimulation↗

PubMed2000

Effects on cochlear responses of activation of descending pathways from the inferior colliculus.

The inferior colliculus (IC) has been shown anatomically to make direct descending connections with medial olivocochlear (MOC) neurones in the auditory brainstem. The MOC neurones project to the outer hair cells in the cochlea and inhibit cochlear neural output. This study investigated the effect of IC stimulation on cochlear output in both guinea pigs and rats in order to determine the functional significance of the IC-to-olivocochlear system projection. Stimulation of the central nucleus and the external cortex of the IC in paralysed guinea pigs, both contra- and ipsilaterally to the test cochlea, resulted in a small increase of the cochlear microphonic amplitude and a small decrease of the compound action potential (CAP) amplitude, the latter equivalent to a 3-6 dB change in acoustic input. Effects on the CAP were maximal in the frequency range 6-10 kHz. These effects were consistent with partial activation of the MOC system. In unparalysed rats, stimulation of the inferior colliculus evoked a large, prolonged suppression ranging from 5-12 dB in the amplitude of distortion product otoacoustic emissions (2f(1)-f(2); DPOAE), as reported previously by Scates et al. (1999). However, this suppression was decreased to only 0-3 dB when the animals were paralysed, suggesting that the larger suppression in the unparalysed state was the consequence of either a general masking effect caused by animal movement, or activation of middle ear muscles by the inferior colliculus stimulation. The results indicate a small but significant excitatory effect of the inferior colliculus on the medial olivocochlear system under conditions of anaesthesia and paralysis.

Action Potentials↗

PubMed1994

Application of a neuroprotective ACTH(4-9) analog to affect cisplatin ototoxicity: an electrocochleographic study in guinea pigs.

Ototoxicity and neurotoxicity are among the most serious side-effects of cisplatin therapy. Previous experiments have shown that neurotoxicity can be delayed or prevented by treatment with the melanocortin-derived peptide ORG 2766, and ACTH4-9 analog. A remedy against ototoxicity is not available. In this study we describe cisplatin-induced abnormalities in cochlear potentials in guinea pigs. These included changes in compound action potential (CAP), cochlear microphonics (CM) and summating potential (SP) at frequencies from 500 Hz to 16 kHz. Cisplatin (2 mg/kg for 8 days) reduced CAP amplitude with the effect becoming more pronounced at higher frequencies. Cisplatin also reduced CM and SP. Concurrent treatment with ORG 2766 prevented cisplatin ototoxicity partially or completely in four out of ten animals. In the other six animals the effects were comparable to those seen in control animals not treated with the peptide. The protective effects found with this neurotrophic peptide warrant further experimentation.

Acoustic Stimulation↗

PubMed2001

The effects of histamine and its antagonists on the cochlear microphonic and the compound action potential of the guinea pig.

OBJECT: we studied the effects of histamine, the H1 receptor antagonist pyrilamine, and the H2 receptor antagonist cimetidine on the cochlear potential of guinea pigs (cochlear microphonic, CM; compound action potential, CAP). METHODS: histamine was applied into the cochlear perilymph at three different dosages (10 microM, 50 microM or 10 mM). Pyrilamine and cimetidine were applied at 50 microM each. RESULTS: histamine increased the CAP at 10 and 50 microM without any significant effects on the CM. The effects of histamine at 50 microM were suppressed by the 50-microM of pyrilamine and cimetidine. At 10 mM of histamine, CAP and CM amplitudes were significantly decreased. CONCLUSION: in low concentrations, histamine may act as an extracellular signal on inner hair cells (IHCs) or it may stimulate the afferent nerve by binding to their H1 and H2 receptors. A possible explanation for the inhibitory effects of histamine at 10-mM dosage was apparently found in that the effects of the high concentration may be supraphysiological; and furthermore, there is a difference in the mechanism by which histamine exerts its effects mediated by the histamine receptors on the cochlea.

Administration, Topical↗

PubMed1982

Cochlear potentials in the Bronx waltzer mutant mouse.

The Bronx waltzer mutant mouse has a unique cochlear abnormality in which the outer hair cells appear normal but the inner hair cells are absent. Potentials recorded from the round window indicate that the gross cochlear nerve action potential is very small or absent and cochlear microphonics are present but of small amplitude. Positive and negative summating potentials can both be recorded, indicating that mammalian outer hair cells are capable of producing both positive and negative DC potentials.

Animals↗

PubMed1983

Effect of xipamide and furosemide on guinea pig cochlear recorded potentials.

The effects of furosemide and xipamide on guinea pig cochlear potentials were studied under acute conditions. Auditory nerve action potentials (AP) and cochlear microphonics (CM) were depressed by both diuretics in a dose-related manner. Furosemide was more effective on AP than on CM. In contrast, the xipamide-induced reductions of AP and CM were similar. Our results suggest that the depressive effects of furosemide or xipamide may be related to a direct action on cochlear mechanisms.

Action Potentials↗

PubMed1993

[Functional and morphological changes of the cochlea in guinea pigs during anoxia].

The influence to endocochlear potential (EP), cochlear microphonics (CM) and summating potential (SP), the ultrastructural changes of the cochlea and the survival time of hair cells in guinea pigs during anoxia and suffocation were investigated. We found that: 1) The stria vascularis was much more sensitive to anoxia than hair cells. 2) 85% CM was highly sensitive to anoxia, and 15% kept stable until the destruction of outer hair cells. 3) -SP turned into +SP after anoxia. 4) EP was related to the destruction of outer hair cells and the disappearance of CM.

Animals↗

PubMed1986

Electrocochleographic study of low-tone hearing loss without vertigo.

Auditory nerve action potential (AP), cochlear microphonics (CM) and summating potential (SP) were recorded from 6 patients with low-tone hearing loss without vertigo. All these cases showed high AP and -SP amplitude and satisfactory CM response. These findings resembled the electrocochleographic findings of type 1, which is an early stage of Ménière's disease. Hearing returned to normal range in half of the cases but remained hardly changed in the other half. The difference between these two groups could not be clarified electrocochleographically. On the other hand, low-tone hearing loss due to retrolabyrinthine lesion and due to familial sensorineural deafness was shown to have a low AP amplitude.

Adolescent↗