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PubMed2003

Effect of current stimulus on in vivo cochlear mechanics.

In this paper, the influence of direct current stimulation on the acoustic impulse response of the basilar membrane (BM) is studied. A positive current applied in the scala vestibuli relative to a ground electrode in the scala tympani is found to enhance gain and increase the best frequency at a given location on the BM. An opposite effect is found for a negative current. Also, the amplitude of low-frequency cochlear microphonic at high sound levels is found to change with the concurrent application of direct current stimulus. BM vibrations in response to pure tone acoustic excitation are found to possess harmonics whose levels relative to the fundamental increase with the application of positive current and decrease with the application of negative current. A model for outer hair cell activity that couples changes in length and stiffness to transmembrane potential is used to interpret the results of these experiments and others in the literature. The importance of the in vivo mechanical and electrical loading is emphasized. Simulation results show the somewhat paradoxical finding that for outer hair cells under tension, hyperpolarization causes shortening of the cell length due to the dominance of voltage dependent stiffness changes.

Acoustic Stimulation↗
PubMed1969

Cochlear distortion: effect of direct-current polarization.

Intermodulation components (combination tones) appearing in microphonic potentials were measured from guinea pig cochleas with and without polarizing direct currents passing through the cochlear partition. At moderate intensities of stimulus the polarization had a qualitatively different effect on the distortion components than on their eliciting primaries or on pure tones simulating the distortion products. At high intensities, the primaries and the combination tones were similarly influenced by the polarizing current. It is concluded that cochlear distortion is a two-stage process, mechano-electrical at low levels and mechano-hydraulic at high levels.

Animals↗
PubMed1976

[Temporal cochlear changes evoked by prolonged exposure to low intensity noise. Electrophysiological study in guinea pigs].

Behavioral temporal threshold shifts (TTS) have been shown in the chinchilla, to be correlated with cochlear microphonic (CM) and whole-nerve action potential (AP) losses in the sensitivity as well as in maximum voltage. The Guinea-pig's ear differs significantly both anatomically and physiologically from the chinchilla's; as a result, it does not seem to be as susceptible to TTS at non-injurious noise levels, except at those frequency bands were middle-ear impedance and other factors are more favorable. At times varying from 2 hrs to 48 hrs after termination of noise exposures of 48 hrs duration to an octave-band of noise (7-14 KHz) with a sound-pressure level of 95 dB, the CM from the first three cochlear turns as well as the whole-nerve AP were measured in Guinea pigs. Losses in sensitivity as well as in maximum voltage were found in the CM recorded from the first turn. CM recovered gradually with time, reaching normal levels at about 40 hrs after termination of noise exposures. The AP +showed similar losses. Microscopic examination of the organ of Corti showed no loss of hair cells.

Acoustic Stimulation↗
PubMedDate not supplied

Cochlear microphonics in the jaundiced Gunn rat.

INTRODUCTION: Bilirubin toxicity causes brain damage and deafness. Brainstem auditory areas are damaged, but the effects of bilirubin toxicity on the peripheral auditory system are less well defined. As a first step in the study of cochlear physiology, we performed studies of scalp-derived cochlear microphonic (CM) responses in the jaundiced (jj) Gunn rat model of acute bilirubin toxicity. MATERIALS AND METHODS: CMs were obtained from scalp needle electrodes in response to acoustically delayed 500-, 1,000-, 2,000-, 4,000-, 6,000-, and 8,000-Hz tonebursts delivered by overhead speakers, and brainstem auditory-evoked potentials (BAEPs) were obtained to clicks. At 18 days of age, one nonjaundiced (Nj) and two jj Gunn rats in each of four litters were anesthetized. CMs and BAEPs were performed before and 4 hours after either (1) sulfonamide was injected into jj rats to produce acute bilirubin toxicity, (2) jj controls were injected with saline, or (3) Nj controls were given sulfonamide. In a second experiment, 16-day-old jj-sulfa and Nj-saline littermates were studied with insert speakers at 60 and 75 dB hearing level (HL) at baseline and 6 hours later, and CM amplitude was analyzed with a fast fourier transformation. RESULTS: No statistically significant differences were found by repeated measures analysis of variance in the CMs in either experiment between groups or after sulfonamide, despite BAEP changes of decreased amplitude of waves II and III and increased latency of I-II and I-III interwave intervals in jjs given sulfa. CONCLUSION: Alterations of CM after acute bilirubin toxicity did not occur at a time when there was electrophysiologic evidence of brainstem dysfunction. Although more subtle effects might be detected with a larger sample studied at longer intervals after the insult, CM seems insensitive or less sensitive to acute bilirubin toxicity than brainstem auditory function. These results suggest that retrocochlear tests of central auditory function may be more sensitive to the effects of hyperbilirubinemia than tests of peripheral auditory function in humans.

Acoustic Stimulation↗
PubMed1980

Relations between cochlear fatigue and the asymmetrical nonlinearity of the cochlear microphonics.

It is generally assumed that noises have a detrimental effect when the cochlear receptor is overloaded and, more specifically, when the cochlear microphonic (CM) fails to increase linearly with intensity. In order to investigate further the relations between the nonlinearity of CM and damage to the cochlea, a series of experiments was carried out on guinea pigs to relate the short-term CM depression following the presentation of noises or tones with the nonlinearity and the assymmetry. The asymmetrical non-linearity of CM was measured in tracing the input-out functions and also the wave-forms. Two other important tests of the asymmetrical nonlinearity were used: the measure of interference and of summating potential (SP DIF). The results show that the fatigability is greater when there is a large negative asymmetry or a large negative SP. Variations in asymmetry and in SP were observed among individuals. Other changes of symmetry were provoked by asphyxia or by introducing solutions of KCl in the perilymph. These changes were well correlated with the fatigability. These results are interpreted in a model of the cochlear transducer derived from the model of Davis. The assymetry of a flux of potassium ions between endolymph and the hair cells is assumed to be responsible for the alterations associated with cochlear fatigue and trauma.

Acoustic Stimulation↗
PubMed2000

Effects of industrial noise exposure on distortion product otoacoustic emissions (DPOAEs) and hair cell loss of the cochlea--long term experiments in awake guinea pigs.

Distortion product otoacoustic emissions (DPOAEs), a sensitive detector of outer hair cell (OHC) function, cochlear microphonics (CM), and hair cell loss have been monitored in 12 awake guinea pigs before and after 2 h exposure to specific, played-back industrial noise (105 dB SPL maximal intensity). All animals had stable DPOAE levels before noise exposure. In the first hours after noise exposure DPOAE levels were reduced significantly. In about 70% a partial recovery of the DPOAEs was found within 4 months after noise exposure. In 16% of the investigated ears no recovery of DPOAEs was observed. However, in a few ears increased DPOAEs were observed after noise exposure. Exposure to industrial noise caused both morphological changes in the middle turns of the cochlea and electrophysiological changes in the middle frequency range. A close correlation existed between reduced DPOAE levels, loss in CM potentials, and area of damaged or lost OHCs, but not with the numbers of damaged or lost OHCs in the cochlea. It can be concluded that continuous industrial noise causes a damage to OHCs which differs form the damage caused by impulse noise.

Animals↗
PubMed1984

Use of intraoperative auditory evoked potentials to preserve hearing in unilateral acoustic neuroma removal.

Twenty-two patients with unilateral acoustic neuromas and preoperative speech discrimination scores of 35% or more had intraoperative monitoring of the electrocochleogram (ECoG) using a transtympanic electrode, and of the brain-stem auditory evoked potentials (BAEP's) using scalp electrodes. Rapid feedback was provided about the status of the cochlear microphonics from the hair cells of the inner ear (CM of the ECoG), the compound action potential of the auditory nerve (N-1 of the ECoG or Wave I of the BAEP's) and the potentials from the lower brain stem (Wave V of the BAEP's). All patients had total removal of the tumor. In 21, the cochlear nerve was anatomically preserved, and 20 had good postoperative facial nerve function. Correlation of tumor size with postoperative hearing was as follows: discrimination scores of more than 35% in three of four patients with 1-cm tumors, two of eight with 1.5-cm tumors, two of six with 2- to 2.5-cm tumors, and one of four with tumors of 3 cm or more. Two other patients with 1.5-cm tumors had discrimination scores of less than 35%, and one patient with a 2-cm tumor had only sound perception. In two patients, the discrimination scores improved. At the end of the operation, all patients with hearing had a detectable N-1, and, when recorded, CM. All but one patient with no hearing had lost N-1, and CM was absent or reduced. Unless Wave V was unchanged, it was a poor predictor of postoperative hearing, and its absence did not preclude preservation of good hearing. The electrophysiological changes during each stage of the operation were analyzed and correlated with events during surgery. Areas in which there was an increased risk of loss of the potentials were determined. In some patients monitoring was unnecessary, because either there were no significant changes or the changes were abrupt and no recovery occurred. However, in other patients, monitoring alerted the surgeon to a possible problem and the method of dissection was altered. Possible mechanisms of hearing loss were suggested from the changes in the recordings.

Adult↗
PubMed1989

Measurement of low-frequency receptor potentials in inner hair cells: a theoretical analysis.

The measurement of the low-frequency responses of inner hair cells is complicated by the fact that extracellular cochlear microphonic may be larger than the intracellular inner hair cell potential. A subtraction technique is proposed in which the extracellular and intracellular potentials are recorded sequentially and then subtracted to give an estimate of the true membrane potential. A theoretical analysis is presented which predicts that this calculated inner hair cell membrane potential is a more accurate measure of inner hair cell receptor current than the membrane potential measured with respect to a remote indifferent electrode.

Acoustic Stimulation↗
PubMed1991

Acute ototoxicity of trialkyltins in the guinea pig.

Two trialkyltin compounds, trimethyltin chloride (TMT) and triethyltin bromide (TET) were evaluated for their acute effects on cochlear function in pigmented guinea pigs. Compound action potential (CAP) thresholds and 1 microV RMS cochlear microphonic (CM) isopotential curves were generated for 25 subjects following ip injection of TMT (2 mg/kg), TET (12 or 24 mg/kg) or inert vehicle (0.9% saline or 15% ethanol). The CAP is generated by the release of neurotransmitters from the inner hair cells and the subsequent depolarization of spiral ganglion cells. However, the sensitivity of the CAP is influenced by other cochlear structures including the outer hair cells which are thought to influence sensitivity of the inner hair cells. By contrast, CM reflects electromechanical function of the outer hair cells. CAP function was severely disrupted by organotin exposure while CM was unaffected by these agents. TMT administration impaired CAP thresholds at all frequencies within 30 min of administration. Thresholds deteriorated slightly more between 30 and 60 min. TET also reduced the sensitivity of the CAP to all frequencies. At the lower dose moderate impairments of function were observed at 30 min which became more noticeable at 60 min. Following 24 mg/kg TET injection, CAP sensitivity was markedly impaired even at 30 min. The CM isopotential values were not significantly altered 30 min or 60 min after either TMT or TET treatment at any of the 11 frequencies tested. These data document far more rapid toxic effects of TMT and TET than have been seen in most intact neuronal systems. They indicate that both organotins initially disrupt the functional integrity of either inner hair cells or spiral ganglion cells within the cochlea such that depolarization occurs only following a significant increase in stimulus intensity.

Action Potentials↗
PubMed1986

Cochlear microphonics and the initiation of spikes in the auditory nerve: correlation of single-unit data with neural and receptor potentials recorded from the round window.

On the basis of comparisons of responses of guinea pig ganglion cells and inner hair cells to intense low-frequency tones, Sellick et al. [Hear. Res. 7, 199-221 (1982)] have proposed that basal inner hair cells can be depolarized (and thus, VIII-N. spikes generated) by the extracellular microphonic generated during hyperpolarization of outer hair cells. VIII-N. data for the chinchilla have been presented that, to a first approximation, support such a hypothesis [Ruggero and Rich, J. Acoust. Soc. Am. 73, 2096-2108 (1983)]. However, an apparent discrepancy exists in our results, vis à vis Sellick et al.'s hypothesis, in that basal fiber near-threshold responses precede maximal negativity of the round window microphonic (i.e., maximal hyperpolarization of outer hair cells) by up to 90 degrees (but generally less than 45 degrees), depending on frequency. It is shown here that the discrepancy is resolved if certain nonlinear phase changes and overall distortion of the microphonic waveshapes, both of which occur at intense stimulus levels, are taken into account. It is also shown that compound action potentials (AP's), superimposed on the round window microphonics, can be identified at multiple times within each stimulus cycle, closely matching the near-threshold response phases of single-unit excitation. AP1 is nearly synchronous with the negative-to-positive transition of round window microphonics and with the excitation of fibers innervating apical-to-middle cochlear regions. AP2 is synchronous with the positive-to-negative transition of the microphonics and with the excitation of basal fibers. One or two other AP's probably reflect "peak splitting" in the responses of both basal and apical fibers.

Acoustic Stimulation↗
PubMedDate not supplied

Electrophysiological studies of the auditory system.

Electrophysiological measures of cochlear function can be obtained using the techniques of transtympanic electrode and surface electrocochleography. These provide measures of the basic parameters of the cochlear microphonic, cochlear nerve and auditory brainstem nuclei action potentials, which enable the functional mechanisms of the cochlea and auditory pathway to be defined for normally hearing subjects and, by comparison, give diagnostic information about the pathologies involved in auditory disorders. Data are presented on the values and variability of the responses obtained from normally hearing subjects. The comparative values of each technique in estimating auditory threshold, cochlear function and in evaluating neurological conditions are discussed using data from clinical patients.

Acoustic Stimulation↗
PubMed1993

[Mechanism of hearing. I. Efferent system of innervation of the organ of Corti].

The authors present some morphological, physiological and pathophysiological aspects of efferent system of innervation (i.e. olivocochlear system) of the organ of Corti. The cochlea is innervated by two different systems: 1) the medial efferent system which originates in the medial nucleus of the trapezoid body and synapses on outer hair cells, 2) the lateral efferent system which originates in the superior olivary nucleus and synapses on the dendrites of the auditory nerve under inner hair cells. An electrical stimulation as well as an acoustic stimulation of efferent fibers results in: a) suppression of the auditory nerve response (N1 amplitude reduction), b) increase in amplitude of cochlear microphonics and c) reduction of the endolymphatic potential. Due to presence of the crossed olivocochlear bundle, an ipsilateral stimulation of efferent fibers results in both ipsi- and contralateral response. Efferent fibers response is a feedback response to afferent fibers stimulation. There are some evidence that efferent system of innervation protects the cochlea against the effects of intense sound exposure.

Auditory Pathways↗
PubMed2006

Effects of nimodipine, an L-type calcium channel antagonist, on the chicken's cochlear potentials.

At most synapses in the brain, neurotransmitter release depends on N-type or P/Q-type calcium channels. However, available in vitro experimental data suggest that there exist almost exclusively L-type calcium channels in sensory hair cells of most species. To test whether chicken hair cells depend on L-type calcium channels for neurotransmitter release, we examined the effects of nimodipine, a selective L-type calcium channel antagonist, on acoustically evoked cochlear potentials in 10-15 week old chickens in vivo. Diffusion of nimodipine into scala tympani significantly elevated threshold, dramatically decreased the amplitude and increased the latency of the compound action potential within 20 min of drug application. The summating potential was also significantly reduced in amplitude, but the cochlear microphonic was relatively less affected. All the effects were reversible after nimodipine was washed out with artificial perilymph except that the cochlear microphonic amplitude remained decreased. Application of omega-conotoxin GVIA, an N-type calcium channel antagonist and agatoxin Tk, a P-type calcium channel antagonist had no observable effects on the cochlear potentials. These results suggest that L-type calcium channels control neurotransmitter release from avian hair cells.

Action Potentials↗
PubMed1979

Comparison of the spectra of the cochlear microphonic and of the sound-elicited electrical impedance changes measured in scala media of the guinea pig.

The harmonic structure of the cochlear microphonic (CM) and that of a sound-elicited signal which we have considered as an (apparent) changing resistance (CR) were simultaneously determined in scala media of the first turn of the guinea pig cochlea. We analyzed our data in the context of the Davis variable resistance hair-cell model (1965), which predicts CM and CR to be proportional to each other. But, plotted as functions of the sound-pressure level, CM and CR were found to have qualitatively similar but quantitatively disproportionate spectra. The preparations with the highest endolymphatic potential showed the least correspondence between the spectra of the two measured quantities. The phase angles of the fundamental components in CM and CR were equal within approximately 10 degrees, but the phase of the even harmonics of the two independent measures commonly differed by approximately 180 degrees at lower SPLs. Although most data were collected using 160-Hz tonal stimulation, tones with frequencies up to 1280 Hz produced qualitatively similar results. The CM and the CR both varied slightly with the level of the alternating current used to probe the CR. Considered on a quantitative basis, consistent with the accuracy of our measurements, any model which reduces to a fixed source, a fixed resistance, and a single linear, time-varying resistance cannot mimic the most significant, commonly found aspects of our CM and CR data. An alternate model incorporating a nonlinear, time-invariant resistance is able to account for some of the data. The output of the model is correctly considered a (time) changing resistance, or apparent changing resistance; but the model demonstrates that similar experimental results are not necessarily evidence for a time-varying resistor as originally proposed by Davis.

Acoustic Stimulation↗
PubMed1996

Auditory neuropathy.

Ten patients presented as children or young adults with hearing impairments that, by behavioural and physiological testing, were compatible with a disorder of the auditory portion of the VIII cranial nerve. Evidence of normal cochlear outer hair cell function was provided by preservation of otoacoustic emissions and cochlear microphonics in all of the patients. Auditory brainstem potentials showed evidence of abnormal auditory pathway function beginning with the VIII nerve: the potentials were absent in nine patients and severely distorted in one patient. Auditory brainstem reflexes (middle ear muscles; crossed suppression of otoacoustic emissions) were absent in all of the tested patients. Behavioural audiometric testing showed a mild to moderate elevation of pure tone threshold in nine patients. The extent of the hearing loss, if due to cochlear receptor damage, should not have resulted in the loss of auditory brainstem potentials. The shape of the pure tone loss varied, being predominantly low frequency in five patients, flat across all frequencies in three patients and predominantly high frequency in two patients. Speech intelligibility was tested in eight patients, and in six was affected out of proportion to what would have been expected if the pure tone loss were of cochlear origin. The patients were otherwise neurologically normal when the hearing impairment was first manifest. Subsequently, eight of these patients developed evidence for a peripheral neuropathy. The neuropathy was hereditary in three and sporadic in five. We suggest that this type of hearing impairment is due to a disorder of auditory nerve function and may have, as one of its causes, a neuropathy of the auditory nerve, occurring either in isolation or as part of a generalized neuropathic process.

Adolescent↗
PubMed1998

An animal model of auditory neuropathy.

OBJECTIVE: We describe an animal model of auditory neuropathy in which subjects have extensive, scattered inner haircell loss but with a relatively intact outer haircell population. DESIGN: Such a pattern of cochlear haircell damage can be produced in the chinchilla by treatment with the anticancer agent carboplatin. RESULTS: In these subjects, otoacoustic emissions (OAEs) and cochlear microphonics remain normal while auditory brain stem evoked potential (ABR) thresholds are significantly elevated. However, in the same subjects, central auditory neurons (in the inferior colliculus) have response thresholds that are considerably lower (by up to 50 dB) than ABR thresholds. These findings parallel the characteristics of auditory neuropathy in humans, in which absent or abnormal ABRs are recorded in patients with only mild to moderate audiometric thresholds and preserved OAEs. CONCLUSIONS: We suggest that scattered inner haircell lesions also can result from long-term cochlear hypoxia, and we propose that this is a likely candidate for the etiology of many types of auditory neuropathy in human subjects.

Animals↗