Electrically Evoked Otoacoustic Emissions Research Articles

Deficient forward transduction and enhanced reverse transduction in the alpha tectorin C1509G human hearing loss mutation

Most forms of hearing loss are associated with loss of cochlear outer hair cells (OHCs). OHCs require the tectorial membrane (TM) for stereociliary bundle stimulation (forward transduction) and active feedback (reverse transduction). Alpha tectorin is a protein constituent of the TM and the C1509G mutation in alpha tectorin in humans results in autosomal dominant hearing loss. We engineered and validated this mutation in mice and found that the TM was shortened in heterozygous Tecta(C1509G/+) mice, reaching only the first row of OHCs. Thus, deficient forward transduction renders OHCs within the second and third rows non-functional, producing partial hearing loss. Surprisingly, both Tecta(C1509G/+) and Tecta(C1509G/C1509G) mice were found to have increased reverse transduction as assessed by sound- and electrically-evoked otoacoustic emissions. We show that an increase in prestin, a protein necessary for electromotility, in all three rows of OHCs underlies this phenomenon. This mouse model demonstrates a human hearing loss mutation in which OHC function is altered through a non-cell-autonomous variation in prestin.

Long-Term Effects of Acoustic Trauma on Electrically Evoked Otoacoustic Emission

Electrically evoked otoacoustic emissions (EEOAEs) are sounds measured in the ear canal when alternating current (AC) stimulation is passed into the cochlea. These sounds are attributed to the motile responses of outer hair cells (OHCs). The EEOAE has characteristic amplitude, phase, and fine structure. Multicomponent analysis of the EEOAE shows short (SDC) and long delay components (LDC) that are thought to originate from OHCs near the AC stimulating site and from OHCs at more remote locations, respectively. We measured the effects of various loud noise exposures on the EEOAE and the cochlear whole-nerve action potential (CAP) in animals chronically implanted with a scala tympani electrode. Noise exposures that produced permanent (PTS) or temporary threshold shifts (TTS) were associated with frequency-specific changes in CAP thresholds, EEOAE fine structure, and reductions in the amplitude of the LDC. A frequent observation in this study was an increase in the overall EEOAE amplitude after the noise exposure. The increase was correlated with increased SDC amplitude. The SDC was present in animals chemically treated with ototoxic drugs and mechanical damage to the cochlea. The SDC was eliminated after disarticulation of the ossicular chain. The presence of EEOAE fine structure in the postexposure response is an indicator of TTS in advance of CAP recovery. The results suggest that the EEOAE might be used to differentiate the mechanisms associated with TTS and PTS.

Effect of salicylate on electrically evoked otoacoustic emissions elicited in the first and third turns of the guinea pig cochlea

Objective—Electrically evoked otoacoustic emissions (EEOAEs) are sounds emitted in the ear canal when an alternating current is delivered to the cochlea. Salicylate, which causes reversible hearing loss, decreases both the electromotility of the outer hair cells (OHCs) and the EEOAE output. The frequency response of EEOAEs is known to depend on the location of the stimulating electrode. Using electrodes placed in the first or third turn of the cochlea, we measured EEOAEs before and after salicylate administration in order to clarify the frequency range of EEOAEs from which exact information can be acquired.Material and Methods—A sinusoidal electrical signal (160 μA root-mean-square) at frequencies ranging from 500 Hz to 16 kHz was delivered to the first or third turn of the scala tympani of the guinea pig cochlea in order to determine EEOAEs. The EEOAE outputs were measured before and every 5 min after administration of salicylate (500 mg/kg) for 60 min. The threshold of the compound action potential (CAP) was measured before and 60 min after salicylate administration.Results—CAP thresholds were reduced at frequencies ranging from 2 to 12 kHz after salicylate administration. The maximum EEOAE output recorded with the first-turn electrode was obtained at 12 kHz with a gentle slope of low cutoff, whereas the frequency response of the EEOAE recorded with the third-turn electrode demonstrated a steep dip at 2 kHz.Conclusion—EEOAE reduction after salicylate administration was restricted to frequencies close to that of the characteristic frequency (CF) of the electrode position. This was probably related to the fact that the EEOAE is the sum of waves from the CF of the electrode position and the stimulus frequency. In terms of studying the electromotility of OHCs, useful information obtained from EEOAEs is restricted to the narrow frequency band close to the CF of the electrode location.

Interpreting electrically evoked emissions using a finite-element model of the cochlea

Electrically evoked otoacoustic emissions (EEOAEs) are used to investigate in vivo cochlear electromechanical function. Electrical stimulation through bipolar electrodes placed very close to the basilar membrane (in the scala vestibuli and scala tympani) gives rise to a narrow frequency range of EEOAEs, limited to around 20 kHz when the electrodes are placed near the 18-kHz best frequency place. Model predictions using a three-dimensional inviscid fluid model in conjunction with a middle ear model [S. Puria and J. B. Allen, J. Acoust. Soc. Am. 104, 3463–3481 (1998)] and a simple model for outer hair cell activity [S. Neely and D. Kim, J. Acoust. Soc. Am. 94, 137–146 (1993)] are used to interpret the experimental results. To estimate effect of viscosity, model results are compared with those obtained for a viscous fluid. The models are solved using a 2.5-D finite-element formulation. Predictions show that the high frequency limit of the excitation is determined by the spatial extent of the current stimulus. The global peaks in the EEOAE spectra are interpreted as constructive interference between electrically evoked backward traveling waves and forward traveling waves reflected from the stapes. Steady state response predictions of the model are presented.

The sources of electrically evoked otoacoustic emissions

It has been hypothesized that electrically evoked otoacoustic emissions (EEOAEs) are generated at a site on the basilar membrane near the stimulating electrode. From this original site, the energy propagates towards the oval window, giving rise to the short time delay component (SDC) of EEOAEs. The energy also propagates towards its characteristic frequency (CF) location, and the emission reflected from the CF location forms a long time delay component (LDC). This hypothesis is directly tested in this study by using an acoustical swept tone to modulate the EEOAEs generated by alternating electric current delivered to the round window niche in gerbils. An acoustical tone with a high sound pressure level or a small frequency separation from the EEOAE frequency induced a strong suppression of the EEOAE LDC, but no obvious suppression of the SDC. When the electrical current frequency was fixed, the swept acoustic tone induced a slight suppression, an enhanced peak, and a strong suppression of EEOAEs as the acoustic frequency was swept from the low to high frequency. These data indicate that the electrical current induced cochlear partition vibration near the stimulating electrode. One part of this energy propagates directly to the ear canal, forming the SDC, and the other part propagates to its CF place and is reflected from there to the ear canal, forming the LDC.

Acoustic Modulation of Electrically Evoked Otoacoustic Emission in Chickens

Electrically evoked otoacoustic emissions (EEOAEs) can be elicited from the chicken inner ear. Since lesion studies implicate hair cells are the source of EEOAEs, we hypothesized that acoustic stimuli would modulate EEOAE amplitude at cochlear locations where the acoustic and electrical stimuli overlap. To assess this interaction, EEOAEs were measured as the frequency and amplitude of the acoustic stimuli were varied. EEOAEs, evoked by AC current (3–250 µA rms) delivered to the round window had a broad band pass response (1–6 kHz) with a peak between 3 and 4 kHz and maximum amplitude of 27 dB SPL. EEOAE suppression/enhancement tuning curves were measured at 2, 3, 4 and 6 kHz by varying the frequency of a 70 dB SPL tone and measuring the change in EEOAE amplitude. EEOAE tuning curves were characterized by a tip; a narrow range of frequencies where EEOAE amplitude was suppressed by as much as 5 dB, and by sidebands, a range of frequencies above and below the tip where EEOAE amplitude was enhanced by as much as 1.5 dB. The best suppression frequency, or characteristic frequency, was close to the frequency of the EEOAE elicited by the 3- or 4-kHz electric stimulus. However, the characteristic frequency was displaced towards higher frequencies for the 2-kHz electric stimulus, and towards lower frequencies for the 6-kHz electric stimulus. EEOAE suppression increased approximately linearly with acoustic level. These results suggest that EEOAEs evoked by round window stimulation are predominantly generated by hair cells near the 3- to 4-kHz region of the cochlea.

Interaction between adenosine triphosphate and mechanically induced modulation of electrically evoked otoacoustic emissions.

It was shown previously that electrically evoked otoacoustic emissions (EEOAEs) can be amplitude modulated by low-frequency bias tones and enhanced by application of adenosine triphosphate (ATP) to scala media. These effects were attributed, respectively, to the mechano-electrical transduction (MET) channels and ATP-gated ion channels on outer hair cell (OHC) stereocilia, two conductance pathways that appear to be functionally independent and additive in their effects on ionic current through the OHC. In the experiments described here, the separate influences of ATP and MET channel bias on EEOAEs did not combine linearly. Modulated EEOAEs increased in amplitude, but lost modulation at the phase and frequency of the bias tone (except at very high sound levels) after application of ATP to scala media, even though spectral components at the modulation sideband frequencies were still present. Some sidebands underwent phase shifts after ATP. In EEOAEs modulated by tones at lower sound levels, substitution of the original phase values restored modulation to the waveform, which then resembled a linear summation of the separate effects of ATP and low-frequency bias. While the physiological meaning of this procedure is not clear, the result raises the possibility that a secondary effect of ATP on one or more nonlinear stages in the transduction process, which may have caused the phase shifts, obscured linear summation at lower sound levels. In addition, "acoustic enhancement" of the EEOAE may have introduced nonlinear interaction at higher levels of the bias tones.

Electrically evoked otoacoustic emissions from the chicken ear

The outer hair cell electromotile response is believed to underlie the sharp tuning and exquisite sensitivity of the mammalian inner ear, and contribute to the production of electrically evoked otoacoustic emissions (EEOAEs) and sound-evoked otoacoustic emissions (OAEs). Avian ears are also sharply tuned, extremely sensitive and generate spontaneous and sound-evoked OAEs, but avian hair cells do not exhibit somatic electromotility. However, stereocilia bundle movements have been observed in avian and amphibian hair cells suggesting that EEOAEs might arise from electrically evoked bundle movements. Here, we demonstrate for the first time that AC current applied to the round window of the chicken evokes EEOAE of up to 18 dB SPL. The EEOAE produces a bandpass response with maximum amplitude in the 1000–3000 Hz range; the response drops off rapidly above 4000 Hz and below 500 Hz. The impulse response to current pulses is characterized by a large peak sometimes followed by a damped oscillation with a frequency around 2000 Hz. EEOAEs decreased significantly after anoxia and paraformaldehyde damage of the cochlea. Kanamycin-induced hair cell loss also caused a significant reduction in EEOAE and distortion product OAE; these emissions showed only a small recovery at long recovery times, when most hair cells should have regenerated. These results suggest that the EEOAE has a biological origin in the cochlea, which could presumably involve electrically evoked stereocilia bundle movements.

Effects of 4-aminopyridine on electrically evoked cochlear emissions and mechano-transduction in guinea pig outer hair cells

Stimulation of the cochlea with alternating current produces sound in the ear canal. These electrically evoked oto-acoustic emissions (EEOAEs) are attributed to electro-motility of outer hair cells (OHCs). Earlier work suggested EEOAEs were sensitive to the open probability of OHC mechano-electrical transduction (MET) channels. They were attenuated by 4-aminopyridine (4-AP) and amplitude-modulated by low frequency sound, consistent with current gaining access to a motility source via the MET conductance. However, inconsistencies in the behaviour as well as physical considerations argued against this simple interpretation. In this study the behaviour of EEOAEs in the presence of 4-AP in scala media was examined along with OHC transfer functions derived from low frequency cochlear microphonic (CM) waveforms. Both the level and the modulation of the EEOAEs were reduced by 4-AP, but disproportionately more so than the 4-AP-induced loss of CM. In addition, the modulation as well as the level of the EEOAEs recovered more rapidly than the CM. Both these results indicated that 4-AP modified the process of EEOAE generation independently of its effect on the gross receptor current through the MET conductance. Changes in the derived OHC transfer functions, specifically shifts in the estimated operating bias of the MET channels, indicated the effects of 4-AP applied to the endolymphatic surface of OHCs were complex. It is suggested that both direct and indirect consequences of a 4-AP blockade may have contributed. 4-AP was ineffective when applied to scala tympani.

Effect of inner and outer hair cell lesions on electrically evoked otoacoustic emissions

When the cochlea is stimulated by a sinusoidal current, the inner ear emits an acoustic signal at the stimulus frequency, termed the electrically evoked otoacoustic emission (EEOAE). Recent studies have found EEOAEs in birds lacking outer hair cells (OHCs), raising the possibility that other types of hair cells, including inner hair cells (IHCs), may generate EEOAEs. To determine the relative contribution of IHCs and OHCs to the generation of the EEOAE, we measured the amplitude of EEOAEs, distortion product otoacoustic emissions (DPOAEs), the cochlear microphonic (CM) and the compound action potential (CAP) in normal chinchillas and chinchillas with IHC lesions or IHC plus OHC lesions induced by carboplatin. Selective IHC loss had little or no effect on CM amplitude and caused a slight reduction in mean DPOAE amplitude. However, IHC loss resulted in a massive reduction in CAP amplitude. Importantly, selective IHC lesions did not reduce EEOAE amplitude, but instead, EEOAE amplitude increased at high frequencies. When both IHCs and OHCs were destroyed, the amplitude of the CM, DPOAE and EEOAE all decreased. The increase in EEOAE amplitude seen with IHC loss may be due to (1) loss of tonic efferent activity to the OHCs, (2) change in the mechanical properties of the cochlea or (3) elimination of EEOAEs produced by IHCs in phase opposition to those from OHCs.

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 μA 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 μM. CAP was significantly affected at 25 μM 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.

Electrically evoked otoacoustic emissions from apical and basal perilymphatic electrode positions in the guinea pig cochlea

Stimulation of the cochlea with sinusoidal current results in the production of an otoacoustic emission at the primary frequency of the stimulus current. In this study we test the hypothesis that the wide frequency response from round window (RW) stimulation is due to the involvement of a relatively large spatial segment of the organ of Corti. Tonotopically organized group delays would be evident from perilymphatic electrode locations that restrict the spatial extent of hair cell stimulation. Monopolar and bipolar-paired stimulus electrodes were placed in perilymphatic areas of the first or third cochlear turns and the electrically evoked otoacoustic emissions (EEOAE) produced by these electrodes were compared to that from the RW monopolar electrode in the anesthetized guinea pig. Current stimuli of 35 μA RMS were swept across the frequency range between 60 Hz and 100 kHz. The EEOAE was measured using a microphone coupled to the ear canal. It was found that the bandwidth of EEOAEs from RW stimulation extended to at least 40 kHz and was a relatively insensitive to electrode location on the RW. The group delay of the EEOAE from stimulation at the RW membrane (corrected to stapes motion) was about 53 μs. First and third turn stimulations from electrode placements in perilymph near the bony wall of cochlea yielded narrower band EEOAE magnitude spectra but which had the same short group delays as for RW stimulation. A confined current (from a bipolar electrode pair) applied close to the basilar membrane (BM) in the first turn produced the narrowest frequency-band magnitude emissions and a mean corrected group delay of 176 μs for a location approximately 3 mm from the high frequency end of the BM (corresponding to about the 18 kHz best frequency location). Bipolar electrodes in the third turn scala tympani produced low pass EEOAE magnitude functions with corrected group delays ranging between approximately 0.3 and 1 ms. The average phase slopes did not change with altered cochlear sensitivity and postmortem. These data indicate that the EEOAE from RW stimulation is the summed response from a wide-tonotopic distribution of outer hair cells. A preliminary model study indicates that short time delayed emissions are the result of a large spatial distribution of current applied to perilymphatic locations possibly giving rise to ‘wave-fixed’ emissions.

Effect of Salicylate and Short-term Sound Exposure on Extracochlear Electrically-evoked Otoacoustic Emissions

The effects of salicylate and acoustic overstimulation on the electromotility of the cochlear outer hair cells (OHCs) were assessed in vivo using electrically-evoked otoacoustic emissions (EEOAEs). Alternating currents to evoke the EEOAE were delivered by means of an extracochlear electrode on the round window, with which the compound action potentials (CAPs) were also monitored before and after the manipulations. The EEOAE outputs were a linear function of the injected currents between 52 and 267 w A rms. Administration of salicylate (500 mg kg) reduced the EEOAE outputs significantly at 5 and 8 kHz ( p <0.005), while no change in EEOAEs was observed at any frequency after exposure to a 4 kHz pure tone at 100 dB SPL for 10 min or at 120 dB SPL for 30 min. These results indicate that administration of salicylate reduces the electromotility of the OHCs, and thus produces losses in neural sensitivity of the cochlea. In contrast, the electromotility of OHCs appears to be protected against short-term intense sound exposure.

Fine structure and multicomponents of the electrically evoked otoacoustic emission in gerbil

Like the acoustically evoked distortion product otoacoustic emissions (DPOAE), the amplitude spectrum of the extracochlear electrically evoked otoacoustic emission (EEOAE) also shows peaks and valleys, which are termed the fine structure (FS) of the EEOAE. The hypothesis that the FS of the EEOAE is generated by multiple wave interactions in the cochlea is investigated by examining the relationship between the FS and the multiple-delay components of the EEOAE. The bulla of the gerbil was exposed using a ventral surgical approach. One pole of a bipolar electrode was placed in the round window niche, and the other pole on the surface of the first cochlear turn. A microphone was used to measure electrically evoked sound pressure change in the ear canal. A recently developed multicomponent analysis method was used to detect the EEOAE multiple delays. It was found that the FS is the spectral representation of the multiple-delay components. The relative power of a prominent long delay component (LDC) shows a negative relationship to the electrical stimulus level. Both the FS and the LDC were abolished by intravenous furosemide. Reconstructed signals showed that mathematical removal of the EEOAE LDC also completely eliminated the FS. These data demonstrate that the FS and the EEOAE multicomponents are properties of normal cochlear mechanics in a healthy ear and that the FS is a manifestation of the multicomponents. The findings in this study strongly indicate that the FS of the EEOAE evoked by extracochlear electrical stimulation is generated by wave interaction in the cochlea. The similarity between the EEOAE FS and the DPOAE FS suggests that they may share the same mechanism.

Quantitative measure of multicomponents of otoacoustic emissions

A method for quantitatively measuring measuring multicomponents of otoacoustic emissions (OAE) was developed in this study. The method is based on the rationale that, if the acoustic emission is a vector sum of multicomponents coming from different locations in the cochlea, each component will show a delay. The proposed method consists of the following steps: (1) the amplitude and phase of the emission is measured when the emission frequency is swept; (2) the real part of the spectrum is obtained based on the amplitude and phase spectra; and (3) the real part of the emission spectrum is then analyzed using a Fourier transform to extract the multiple components. The theoretical basis and practical procedure of this method are described, and in vitro and in vivo tests are used to demonstrate the validity of the method. Preliminary data demonstrate the multicomponents of the extracochlear electrically evoked otoacoustic emission (EEOAE).

Effects of salicylate on electrically evoked otoacoustic emissions in the guinea pig

Clinically, salicylates have been known to have a ototoxic side effect of reversible hearing loss and to reduce the voltage-dependent length change (electromotility) in experiments on isolated outer hair cells (OHC). In order to clarify how the reduction of OHC electromotility due to salicylates contributes to cochlear dysfunction in vivo, we observed compound action potentials (CAP) threshold as well as the outputs of the electrically evoked otoacoustic emissions (EEOAE) before and after intravenous administration of 500 mg/kg sodium salicylate in a guinea pig model. A silver ball electrode placed on the round window membrane of the animal was used for both recording of the CAP and stimulation to elicit the EEOAE. The CAP threshold to tone bursts with frequencies from 2 to 10 kHz elevated by 13 to 22 dB, and outputs of the EEOAE decreased approximately 4 dB for 5 kHz stimulation, and 12 dB for 8 kHz after salicylate administration. These results suggested that systemically administered salicylate also reduced the electromotility of the OHC, and caused the hearing impairment in vivo.

Method for evaluating inner ear hearing loss

A method for evaluating the electromotility of hair cells within the cochlea of a mammalian ear by providing an electrode in proximate relation with the round window and applying electricity therethrough in order to electrically excite hair cells within the cochlea to produce electrically-evoked otoacoustic emissions therefrom. The electrically-evoked otoacoustic emissions further excite the internal structure of the cochlea which produces vibrations at the oval window that act through the bones of the middle ear to drive the tympanic membrane, producing corresponding acoustic sounds in the ear canal. The resulting acoustic sounds in the ear canal are subsequently detected with a microphone where they are later measured and characterized via readily available signal processing techniques. A hearing aid device is also provided by this invention utilizing the features of the before mentioned analysis technique wherein a traditional hearing aid device acoustically captures a sound adjacent the outer ear and converts it to an electrical signal which is fed to the electrode in order to excite the hair cells within the cochlea and produce electrically-evoked pressure waves therein. The resulting electrically-evoked pressure waves subsequently excite the cochlea and produce perceived hearing in the brain of the test subject through the normal hearing processes of hair cells and conducting neurons.

Enhancement of electrically evoked oto-acoustic emissions associated with low-frequency stimulus bias of the basilar membrane towards scala vestibuli.

Electrically evoked oto-acoustic emissions (EEOAEs) are sounds present in the ear canal when ac current is passed into the cochlea. EEOAEs are attributed to the activation of fast electromotile responses in outer hair cells (OHCs). An interesting property of EEOAEs is the phenomenon of "acoustic enhancement," where the emission amplitude is increased by moderate-level sound [D. C. Mountain and A. E. Hubbard, Hear. Res. 42, 195-202 (1989)]. In this report a form of enhancement is described which occurs with displacements of the basilar membrane toward scala vestibuli, during amplitude modulation of the EEOAE waveform by low-frequency tones. This "SV-bias enhancement" possibly consists of two components: (i) a low-level component induced by sound at levels which produce nonlinear growth of the cochlear microphonic and which may be equivalent to the "acoustic enhancement" described previously, and (ii) a high-level component which occurs at sound levels well above those which cause saturation of the cochlear microphonic. The low-level component could be explained by either an increased access of the extrinsically applied current to a membrane-based source of OHC motility, perhaps coupled with a reduction in negative feedback, or an increase in electromotile output during scala vestibuli displacements, but the origin of the high-level component is obscure.

Nonlinear characteristics of electrically evoked otoacoustic emissions

To further our knowledge of outer hair cell nonlinearities, we measured the dependence of the electrically-evoked otoacoustic emissions (EEOEs) on current level for a wide range of electrical frequencies. Alternating electrical current was delivered into the scala media of the gerbil cochlea while the EEOE was measured with a probe-tube microphone. While the EEOE scaled linearly with current level for many frequencies and current levels, notable exceptions occurred. For frequencies below 300 Hz and currents above 20–30 μA peak, the gain (primary EEOE magnitude divided by the current level) increased abruptly. For higher frequencies, the gain often increased slightly with increasing current of up to 30–50 μA peak, but decreased at even higher current levels. We also investigated the enhancement of the EEOE due to simultaneous acoustic stimulation. The enhancement of the EEOE was relatively insensitive to current level with little change in enhancement for current levels up to 20 μA peak. For current levels above approximately 40 μA peak, the enhancement decreased slightly.

ATP in endolymph enhances electrically-evoked oto-acoustic emissions from the guinea pig cochlea

ATP was iontophoresed into the scala media of the guinea pig cochlea. A reversible increase in the amplitude of electrically-evoked oto-acoustic emissions (EEOAEs), and reductions in the endocochlear potential (EP) and the cochlear microphonic (CM) were observed. These effects were consistent with an action of ATP on P 2X receptors on outer hair cells (OHC). The results confirm that endogenous endolymphatic ATP, acting via P 2X receptors on OHCs, may serve a regulatory function in the cochlea.