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PubMed1989

The effect of PAF in the cochlea of guinea pigs.

The influence of 10(-10) and 10(-9) M PAF/animal given into the jugular vein over 30 sec on inner ear potentials, i.e. endolymphatic potential (EP), summating potential (SP) and cochlear microphonics (CM) was investigated. The EP showed the most pronounced changes. When infusing a specific PAF receptor antagonist, ginkgolide B, or the TXA2 receptor antagonist, sulotraban, before the the infusion of PAF, the changes in cochlear potentials could be completely prevented. A second TXA2 receptor antagonist, daltroban, did not effectively prevent PAF actions. It is hypothesized that these PAF effects are due to an interference with ion transport in the non-sensory structures of the inner ear.

Acoustic Stimulation↗
PubMed1991

PAF receptor antagonists influence asphyxia-induced changes of the inner ear.

The influence of a transient asphyxia on cochlear potentials, i.e. endolymphatic potential (EP), summating potential (SP) and cochlear microphonics (CM) was investigated in guinea pigs which were injected with two different PAF receptor antagonists before. It could be shown that apafant (WEB 2086) and bepafant (WEB 2170) significantly reduced the asphyxia-induced potential changes compared to controls. The results suggest a mediating role of PAF in the asphyxia model. The impact of the findings for therapeutics is discussed.

Animals↗
PubMed1985

Auditory-evoked potential correlates of susceptibility to noise-induced hearing loss.

Correlations between changes in cochlear microphonics (CM) and auditory brainstem-evoked potentials (ABEP) resulting from transitory-threshold-shift (TTS)-inducing noise, in normally hearing subjects, and the eventual permanent threshold shift (PTS) which the same subjects developed after 9-14 months of well-quantified occupational noise were evaluated. In addition, the predictive value of pigmentation, as an indicator of eventual PTS, was assessed. Eleven CM and ABEP indices which showed significant correlation with the eventual hearing loss were identified. Eight of these indices reflect the effect of increased stimulus rate and experimental TTS-inducing noise. These results show that the difference in ABEP latencies as a result of increased stimulus rate is smaller in persons with large eventual PTS (high susceptibility to noise-induced hearing loss). The effect is larger in persons that eventually developed a small PTS (low susceptibility). Pigmentation, as reflected by iris and skin color, was found to have a negative correlation with susceptibility to noise, i.e. the more pigment the less PTS developed. The above indices may be useful to determine personal susceptibility to noise in normally hearing subjects.

Adolescent↗
PubMedDate not supplied

[Influence of a CNS pathology on the electrocochleography response].

This study analyzed 73 electrocochleographic recordings made in children with a normal hearing threshold, selected retrospectively from 1563 recordings made between 1973 and 1990. The aim of the study was to check the original findings for any correlation between the various response parameters which might be indicative of a pathological condition. Compound action potential (AP) latency and amplitude, presynaptic summation potential (SP) and cochlear microphonic (CM) amplitudes and AP rapid adaptation behavior were calculated and recordings were associated with clinical information on aetiologic diagnosis, otoscopic examination, impedance measurement data and the finding of any central nervous system (CNS) pathology. The trend of the amplitudes as a function of the intensity of all three potentials (input-output functions), CM and SP in particular, demonstrated unexpected scattered values especially towards the high intensities. This was found correlated to the presence of CNS pathology. The comparison between the two groups (with vs without CNS pathology) with the aid of the Student's t-test proved statically significant, especially for CM and SP amplitudes while rather less so for AP amplitude. In particular, all CM and SP amplitude values outside the confidence intervals (calculated as 95% of normal cases) revealed CNS pathology. It has been suggested that the influence of the CNS on cochlear function is due to a disturbed function of the olicocochlear bundle, which is known to have an inhibitory effect on cochlear dynamics; furthermore, there is also proof that it can be activated regardless of any ipso-and/or contra-lateral acoustic stimulation. The effects observed on the electrocochleography in cases with CNS disorders would thus be explained by an interruption of the olivocochlear bundle at the CNS level or a disruption of the CNS mechanism capable of controlling its activation.

Audiometry, Evoked Response↗
PubMed1986

Efferent tracts and cochlear frequency selectivity.

The cochlear innervation of guinea pigs was sectioned medially in a rostrocaudal direction at the level of the floor of the fourth ventricle, to study the effects of efferent pathways on cochlear microphonic (CM) suppression, the compound action potential (CAP) masking phenomenon, the input-output CAP function, and cochlear frequency selectivity estimated with tuning curves of single auditory nerve fibers. Sectioning reduced CM suppression without having any effect on absolute CM amplitude; it also reduced CAP masking. The input-output CAP function was not changed at intensities below 75 dB, and the single-unit tuning curves recorded before and after nerve sectioning were unaffected. Thus, the crossed efferent tracts (i.e., mainly the medial system) seems to be involved in the masking function itself, rather than one of the mechanisms responsible for high frequency cochlear selectivity.

Acoustic Stimulation↗
PubMed1990

Electrophysiological determinations of the effects of 1 kHz noise exposure on the high-frequency hearing of guinea pigs.

The effects of noise were studied in 90 5-week-old albino Hartley guinea pigs with normal hearing. The following experimental setup was used: (1) exposure to 1 kHz tones at 100 dB for 4 h, 20 h and 40 h; (2) exposure to 1 kHz tones at 110 dB for 20 h and 40 h. In order to investigate the effects of the noise exposures on the hearing of the guinea pigs, cochlear microphonics (CM), whole nerve action potentials (AP) and endocochlear potentials (EP) were examined. We obtained the following results. With a high sound pressure, a decrease was observed in the CM maximum output voltage in the test frequencies from 2 kHz to 6 kHz while the CM threshold increased ("pseudo threshold"). Intensity function of the N1 potential of the AP using a 7 kHz tone burst decreased; the threshold of the N1 potential also increased considerably by exposure to chronic high sound pressure. An extension of latency and a decrease in the absolute value of the negative potential in EP were induced by chronic noise exposure.

Animals↗
PubMed2000

Mathematical decomposition of the round window potential.

We present an algorithm called the median transform which can be used to decompose the round window auditory potential into AC and DC components. The first of these is identified with the cochlear microphonic, and the second with the combined summating and compound action potentials. Elsewhere in this volume, the algorithm is employed as an intermediate step in obtaining the instantaneous frequency of the CM. Since the algorithm is easily implemented and operates entirely in the time domain, it may prove useful to clinicians as well as researchers.

Action Potentials↗
PubMed1980

Ototoxicity of propylene glycol in experimental animals.

The ototoxicity of antibiotics given either systemically or topically has been recently recognized. However, the ototoxicity of topically applied alcohols and other solvents used as vehicles for drugs has not been well recognized. One of the most common solvents, propylene glycol, was chosen for this study, and this agent in various concentrations was instilled into the middle ear of guinea pigs and chinchillas for various periods of time. Its effect on the function of the cochlea was studied as well as the histopathologic changes in the temporal bones. Deterioration of the cochlear microphonics and the endocochlear direct current potential was found. A 10 per cent solution applied for six days caused a reduction in the cochlear microphonics. Fifty per cent or stronger solution always caused a reduction in the cochlear microphonics. The deterioration in the cochlear microphonics persisted one month. Dose related changes in the endocochlear potential were noted. Morphologic changes were severe and included granulation tissue in the middle ear and destruction and ossification of the auditory bulla and bony cochlea. Propylene glycol should not be used in the ear that has a perforation of the tympanic membrane.

Animals↗
PubMed1986

Electrocochleography recorded non-invasively from the external ear.

A method is described to record cochlear evoked potentials in humans (ECochG) with a low impedance electrode on the external ear near the opening of the external auditory canal. A piezoelectric click stimulus was delivered to the ear through a polyethylene tube creating diminution of stimulus artifact and a signal delay. Wave forms resembling the cochlear microphonic (CM), summating potential (SP) and the eighth nerve action potential (N1) were differentially accentuated by changes in stimulation and recording parameters. The addition or subtraction of condensation and rarefaction click wave forms further clarified the N1 and SP, or the CM potential, respectively. These responses can be recorded with most contemporary evoked response equipment. This non-invasive method of ECochG lends itself well to the study of hearing loss and possibly other neurologic disorders, and may complement BAER examination especially when wave I is poorly delineated.

Audiometry, Evoked Response↗
PubMed1988

Evolution of recruitment at different frequencies during the development of endolymphatic hydrops in the guinea pig.

The study of human temporal bones has identified endolymphatic hydrops as a common feature of several diseases. In particular it is systematically found in those bones removed from patients with premortem Menière's disease. Menière's disease is known to induce sensorineural pathology with recruitment, which changes with the evolution of the hearing loss, and is suspected to induce a cochlear conductive loss by a possible increase in static pressure of endolymph. Amplitude/intensity functions of sensorineural responses can reflect recruitment and/or conduction loss. Experimentally induced hydrops in animals provokes cochlear physiological alterations, some of which closely resemble certain features of Menière's disease. In the present study using a guinea-pig animal model, we have examined amplitude/intensity functions at the round window for cochlear microphonics (RWCM), summating potentials (RWSP) and action potentials (CAP) at different stages of hearing loss in experimentally induced hydrops. During the period of fluctuating thresholds there was reduction of maximal RWCM amplitude, no change in RWSP and recruitment on the CAP. At a later stage when the audiogram was flat and fluctuations were no longer seen, RWCM remained unchanged. At this time RWSP could show recruitment while CAP amplitudes at all intensities were reduced, indicating either a cochlear conductive loss and/or a general depression of neural activity.

Animals↗
PubMed1989

The origin of the low-frequency microphonic in the first cochlear turn of guinea-pig.

Low-frequency microphonic potentials (100 Hz to 2000 Hz) have been measured in the first turn of the guinea pig cochlea before and after a variety of manipulations of the cochlea. These included ablation of the apical turns, iontophoresis of streptomycin, dc current injection into the first turn, acoustic trauma and two-tone interference with pure tones. These manipulations indicate that the low-frequency microphonic measured in the first turn and at the round window is generated predominantly by the hair cells of this region. It is a convenient and relatively uncomplicated indicator of the integrity of the mechano-electrical transduction process of these cells.

Acoustic Stimulation↗
PubMedDate not supplied

Evoked potential correlates of genetic progressive hearing loss. Age-related changes from the ear to the inferior colliculus of C57BL/6 and CBA/J mice.

Volume-conducted auditory evoked potentials were simultaneously measured from the level of the ear to the inferior colliculus of mice. The C57BL/6 mouse, which displays genetic sensorineural progressive hearing loss, was compared with the CBA/J mouse. At 50 days post partum, amplitudes of the summating potential (SP) and cochlear microphonic (CM) were lower in the C57BL/6 genotype, and they decreased progressively with age. Fifty days later, changes were seen in responses from the auditory nerve and cochlear nucleus of this mouse. By 200 days of age, the C57BL/6 had a "recruitment" pattern at CNS regions, but not at the auditory nerve.

Acoustic Stimulation↗
PubMed1992

Intensity-dependent changes in oxygenation of cochlear perilymph during acoustic exposure.

This study examined the effects of acoustic exposure at different intensities on local oxygenation of the cochlea. The oxygen partial pressure (pO2) of perilymph in the basal scala tympani was measured polarographically in anesthetized guinea pigs exposed to either wide-band noise at 85 dB SPL or a 10 kHz pure tone at 90, 105, or 125 dB SPL for 1 h. Cochlear temperature, heart rate, arterial blood pressure and acid-base status were monitored. The cochlear microphonics (CM) and compound action potentials (CAP) were recorded before and after exposure. There were clear intensity-dependent differences in the effect of acoustic exposure on perilymphatic oxygenation. Moderate exposure intensities (85-90 dB SPL) were found to increase the pO2 by an average of about 20% of the initial level. In contrast, high intensity acoustic exposure (125 dB SPL) resulted in a mean decrease of about 20%. These changes persisted within a subsequent 30-min post-exposure period. There was no significant change in cochlear temperature and cardiorespiratory variables during and after any of the exposures as compared to the controls. CM and CAP amplitudes showed an extensive loss after acoustic overstimulation (125 dB SPL), but no permanent change with lower exposure intensities. These findings suggest that intracochlear oxygenation plays an important role in inner ear physiology during acoustic stimulation.

Acoustic Stimulation↗
PubMedDate not supplied

Cochlear electrical activity in the C57BL/6 laboratory mouse: volume-conducted vertex and round window responses.

Remote (vertex-positive, volume-conducted) and local (round window, or RW) responses were simultaneously recorded from the C57BL/6 mouse. Volume-conducted responses were obtained which corresponded to the cochlear microphonic (CM), summating potential (SP), and action potential (AP), as measured at the RW. The vertex PI, corresponding to the AP, had a shorter latency to rarefaction than to condensation clicks. At higher SPL's bimodal PI peaks (a and b) were observed. PIb amplitudes were greater at lower, and PIa amplitudes were greater at higher SPL'S. Responses subsequent to the RW N1 and the volume-conducted P1 were eliminated after the ear was isolated from the brainstem.

Acoustic Stimulation↗
PubMed1993

Intensity-related changes in cochlear blood flow in the guinea pig during and following acoustic exposure.

This study examined the effects of acoustic exposure at different intensities on cochlear blood flow (CBF) using laser Doppler flowmetry. CBF was measured in anesthetized guinea pigs exposed to either a 10 kHz pure tone at 125, 105, or 90 dB SPL, or wide-band noise at 85 dB SPL for 1 h. Mean arterial blood pressure and heart rate were recorded continuously. Arterial acid-base status, cochlear temperature, cochlear microphonics (CM), and compound action potentials (CAP) were measured before and after exposure. There was a small, but significant, steady decline in basal CBF after 40 min loud sound exposure (125 dB SPL), but no change in basal CBF occurred with the lower intensities (85-105 dB SPL). In contrast, there was a significant increase in apical CBF after 1 h exposure to either moderate wideband noise (85 dB SPL) or a 10 kHz tone at 105 dB SPL. These changes persisted during a 20-min post-exposure period. In most cases, the cochlear temperature and cardiorespiratory variables monitored remained unchanged during and after the exposures as compared to the controls. CM and CAP amplitudes showed extensive losses after acoustic overstimulation (125 dB SPL), but no permanent changes were found at the lower intensities used. The present findings confirm the occurrence of intensity-related effects of acoustic exposure on the cochlear microcirculation.

Animals↗
PubMed1994

Effects of adenosine 5'-triphosphate and related agonists on cochlear function.

Several lines of evidence implicate a neurotransmitter/modulator role for ATP in the cochlea. Most of the work supporting such a notion has been accomplished using in vitro preparations of sensory hair cells or other cochlear tissues. Little is known regarding the functional consequences of ATP receptor activation in vivo. In the present experiments, we tested ATP and related agonist analogs for their effects on sound-evoked responses of the cochlea (cochlear microphonic, CM; summating potential, SP; distortion product otoacoustic emissions, DPOAE) and auditory nerve (compound action potential, CAP) in vivo and on outer hair cell (OHC) currents and cell length in vitro. In vivo, local application of these compounds was associated with concentration- and intensity-dependent response alterations. The slowly-hydrolyzable P2y agonist, ATP-gamma-S, was clearly of greatest in vivo potency: At low to moderate stimulus intensities, micromolar concentrations of this drug reduced all responses, in particular CAP and DPOAEs, which fell to the level of the noise floor. At high intensities, response suppression was smaller and SP was increased. In vivo effects of ATP, ATP-alpha-S and 2-Me-S-ATP were qualitatively similar to, but smaller in magnitude and requiring higher concentrations than those observed for ATP-gamma-S. Adenosine was without significant effect on responses of the cochlea and auditory nerve. In vitro, effects of ATP-gamma-S and ATP were similar: both induced inward currents in OHCs held at -60 mV without producing observable (> 0.3 micron) changes in OHC length. Results suggest that endogenous ATP influences cochlear function through receptors at several sites in the cochlea. Results suggest further that these response alterations are mediated, at least in part, by receptors of the P2y subtype.

Action Potentials↗
PubMed1997

The mechanism and site of action of lidocaine hydrochloride in guinea pig inner ear.

Lidocaine was applied to the round window (RW) in order to localize its site of action in the cochlea. Cochlear microphonic (CM), summating potential (SP), and compound action potential (CAP) input/output functions were measured to a 16 kHz tone burst to assess the functional changes of the cochlea. In separate experiments, the effect of lidocaine on the whole cell current of isolated outer hair cells (OHC) was studied. A dose of 2 microliters of 40 mM lidocaine in saline solution, when applied to the RW, caused a small change in all measured variables, indicating a passage of the drug through the RW membrane to sites of action. However, 160 mM of lidocaine further decreased CM, SP, and CAP by a total of 40% from the control. A partial recovery occurred for CM during the 30 min follow-up period. CAP and SP continued to decline. In isolated OHCs, lidocaine decreased the whole cell current in a dose-dependent fashion. The KD for lidocaine effect on OHCs was 7 mM. Our in vivo results indicate that lidocaine affects OHCs and reduces CM, causing a subsequent reduction in SP and CAP. The increased effect of lidocaine on CAP and SP, while CM is recovering, suggests an additional specific effect of lidocaine on the cochlear nerve and/or on inner hair cells. Considering that lidocaine alters OHC current (in isolated hair cells) and that lidocaine does not affect endocochlear potential [Laurikainen et al. Acta Otolaryngol (Stockh) 1991: 112: 800-9], the observed CM changes are most likely due to an in vivo effect on OHCs. Thus, the early effect of lidocaine on the cochlea appears to be due to a significant change in organ of Corti function, rather than to direct anesthesia of the cochlear nerve. Later, an independent effect of the drug may occur on neural tissues in the inner ear.

Animals↗
PubMed1985

A possible site of production of the negative endocochlear DC potential.

The scala vestibuli or the scala tympani of guinea pigs was perfused with artificial perilymph containing 1, 5, 10, 20, 30, 40 and 50 mM of potassium chloride in a total concentration of 150 mM with the background composed of sodium chloride. With the perfusion of the scala vestibuli, each concentration failed to alter the magnitude of the negative endocochlear DC potential produced by anoxia or the intravenous injection of 100 mg/kg of body weight of furosemide. With the perfusion of the scala tympani, the negative endocochlear DC potential disappeared precipitously and the maximum output of the cochlear microphonic was severely depressed with concentrations of potassium chloride of 30 mM or greater. The magnitude of the negative endocochlear DC potential appears to be closely related to the maximum output of the cochlear microphonic. These results suggest that the site of production of the negative EP is in the hair cells of the organ of Corti.

Animals↗