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PubMedDate not supplied

Variation of endocochlear PO2 and cochlear potentials by breathing carbon dioxide.

The effect of carbon dioxide on oxygen dioxide tension in the endolymph was determined by the micropolarographic technique. Different concentrations (5% and 10% CO2) and different exposure times (3, 5, and 20 minutes) were investigated. The highest levels of PO2 in the endolymph (101.7, 93.9 and 69.5 mm Hg) were accomplished by respiration of 10% CO2, 90% O2, for 20, 5 and 3 minutes consecutively. The lowest PO2 increase, 50.7 mm Hg was observed after breathing 5% CO2, 90% O2 for 20 minutes. Extreme hypercapnia caused an increase of endocochlear potentials (EP) in all groups. In the second group EP increased from +79.3 to +84.9 and in all groups they had returned to the pretreatment level after CO2 discontinuation. These results support the theory that carbonic anhydrase participates in the generation of EP. At the same time that EP increased, cochlear microphonics declined and opposite after the breathing mixture was discontinued. The results permit the conclusion that high levels of PO2 in endolymph is achievable even with short periods of respiration with high CO2 mixture, and suggest the role of carbonic anhydrase during EP generation.

Action Potentials↗
PubMed1992

[A short history of hearing research. IV: Physiology].

In 1863, Hensen concluded from measurements of the width of the basilar membrane that tones of high and low pitch were represented at the base and apex of the cochlea, respectively. According to his calculations on the tonotopic representation of sound stimuli in the cochlea Helmholtz proposed additional resonators that would transmit the amplified signal to the afferent nerve endings. He speculated that the pillar cells of the tunnel of Corti or strands of the basilar membrane might be these proposed resonators. The resonance theory was contradicted by Wien in 1905. However, further experiments by Held and Kleinknecht in 1927 and by Békésy in 1928 demonstrated that Helmholtz's ideas on the tonotopic dispersion of the vibration of the basilar membrane were correct. Békésy measured the vibration of the cochlear partition in human and animal cadavers and discovered the travelling-wave of the basilar membrane. At the turn of the century Ter Kuile noted that the vibration of the cochlear partition caused a deflection of the sensory hairs of the hair cells, the auditory receptor cells. Wever and Bray described in 1930 stimulus-evoked electrical currents near the cochlea with a wave form similar to that of the original sound stimulus. It was Adrian who later coined the term "cochlear microphonics" for this phenomenon. According to calculations of Gold (1948) and others active mechanical amplification would be required for such a sharp tuning in the cochlea. The first to measure action potentials of the afferent auditory nerve was Tasaki (1954).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Effects of opioid be drugs on auditory evoked potentials suggest a role of lateral olivocochlear dynorphins in auditory function.

Multiple gene products of opioid peptide families (e.g., enkephalins, dynorphins) with differing opioid receptor specificities are present within olivocochlear efferent terminals. Enkephalins activate mu- and delta-opioid receptors, and are generally inhibitory in the nervous system, and dynorphins are kappa-receptor agonists, which may be excitatory to postsynaptic neurons. We have examined the effects of intravenously administered opioid agonists and antagonists on click-evoked N1 and N2 amplitudes and latencies of the compound action potential in the chinchilla recorded at the round window. Parenteral administration of the opioid receptor antagonist naloxone or the potent mu-receptor agonist fentanyl did not alter N1 and N2 amplitudes or latencies. The kappa-receptor agonist, mu-receptor antagonist pentazocine caused marked increases in N1 and N2 amplitudes over baseline values at threshold intensities. These effects were not abolished by naloxone. No effects were seen on the cochlear microphonic, supporting a site of action of these effects at the lateral olivocochlear efferent terminals on auditory nerve dendrites under inner hair cells. Similar results were obtained when far field auditory evoked responses were recorded. Results were obtained under ketamine/pentobarbital anesthesia, which provided stable recording baselines in contrast to tiletamine/zolezepam/pentobarbital, with which an upward drift in auditory potentials was observed. This stimulatory action of kappa-agonists on auditory-evoked potential amplitudes appears to represent a physiological role of the lateral olivocochlear efferent innervation. The different neurotransmitters of the olivocochlear efferents (e.g. enkephalins, dynorphins, acetylcholine) may have antagonistic actions on auditory potentials, as may the lateral and medial systems themselves.

Animals↗
PubMed1977

The peripheral hearing mechanism: new biophysical concepts for transduction of the acoustic signal to an electrochemical event.

A theory of peripheral function in hearing is proposed. It accounts for temporal discrimination among simultaneously received wave and pulse signals, cochlear analysis of acoustic input, and transduction of acoustic energy into biochemical energy by means of resonance and ion-shuttling involving the tectorial membrane and hair-cell complex. The postulated mechanism is such that it can accommodate the enormous range of intensity accessible to the mammalian ear. Synthesized by the theory are numerous empirical observations and experimental results reported by a broad gamut of disciplines but hitherto not unified. Additional support derives from the characteristics of an artificial "cochlea" and an electret (protein) microphone or "ion exchange microphone" with implications for enzyme conformational change.

Acoustic Stimulation↗
PubMed1990

Neural sensitivity to phase of high frequency tones.

The response of fibres of the auditory nerve and neurons of the inferior colliculus of the cat to harmonic two-tone complexes was studied. The components (primaries) had frequencies which were integral multiples of the characteristic frequency of the cell under study. This gave rise to distortion products at the characteristic frequency of the cell. The response of these cells to distortion products at their characteristic frequency was found to be dependent upon the relative phase of the primaries. This was observed for primaries of high frequency as well as those of low frequency. The response to distortion in the cochlear microphonic was also dependent upon the relative phase between harmonic primaries.

Acoustic Stimulation↗
PubMed2001

Distinguishing cochlear pathophysiology in 4-aminopyridine and furosemide treated ears using a nonlinear systems identification technique.

To test the adequacy of physiologic indices derived from a third-order polynomial model quantifying cochlear mechano-electric transduction (MET), 24 Mongolian gerbils were exposed to either 250-mM glucose (control), 150-mM 4-aminopyridine (4-AP), or 30-mM furosemide solutions applied to the round window (RW) membrane. The cochlear microphonic (CM) was recorded from the RW in response to 68- and 88-dB SPL Gaussian noise. A nonlinear systems identification technique (NLID) provided the frequency-domain parameters and physiologic indices of the polynomial model of MET. The control group showed no change in both compound action potential (CAP) thresholds and CM. Exposure to 4-AP and furosemide resulted in a similar elevation in CAP thresholds and a reduction in CM. However, the polynomial model of MET showed different changes. The operating point, slope, and symmetry of the MET function, the polynomial model parameters, and related nonlinear coherences differed between the experimental groups. It is concluded that the NLID technique is sensitive and specific to alterations in the cochlear physiology.

4-Aminopyridine↗
PubMed1979

Normal short-latency electrophysiological filtered click responses recorded from vertex and external auditory meatus.

We recorded normal electrophysiological responses to third-octave filtered clicks from external auditory meatus (EAM) and vertex electrodes referred to coupled earlobe electrodes (forehead ground). From both vertex and EAM, polarity-sensitive responses predominated at low frequencies and exhibited characteristics of both phase-locked neural responses (frequency-following response or FFR) and cochlear microphonics (CM). The FFR-like response predominated at the vertex site and the CM-like response predominated at EAM. At high frequencies, polarity-insensitive responses closely resembled rectangular-pulse click action potentials and brainstem evoked potentials, with clearly defined N1 and V peaks recorded from EAM and vertex, respectively. As frequency was lowered, the N1 and V peak latencies increased, the peaks broadened, and the latency-intensity curves steepened with greater prolongation occurring at lower click intensities. Lowering click frequency also shortened the N1-V interval and caused the plot of N1-V interval versus click intensity to become steeper. Plots of polarity-insensitive response amplitudes and thresholds against frequency revealed a high frequency bias for both N1 and V, but the V "frequency response" was flatter. A possible explanation of the shortened N1-V interval at low click frequencies based on this flatter V "Frequency response" is presented.

Acoustic Impedance Tests↗
PubMedDate not supplied

Some observations on negative endocochlear potential during anoxia.

The effects of anoxia on the endocochlear potential (EP) and +K and +Na concentrations in the endolymph were studied in three groups of guinea pigs: kanamycin-treated guinea pigs, waltzing guinea pigs and normal guinea pigs. The magnitude of the EP in kanamycin-treated guinea pigs and waltzing guinea pigs did not show marked deviation from that observed in normal animals. The +K and +Na concentrations in the endolymph in those animals with severe suppression of sound-evoked cochlear potentials were also within the normal range. The changes in +K and +Na concentrations in the endolymph in anoxic condition were similar in the three groups of animals. However, the rate of decline of the EP was slower in kanamycin-treated guinea pigs and old waltzing guinea pigs. In young waltzing guinea pigs showing moderate suppression on the cochlear microphonics, the decline of the EP during anoxia was comparable to that observed in normal guinea pigs. The results indicate that anoxia decreases +K and increases +Na concentrations in the endolymph in a similar fashion in kanamycin-treated guinea pigs, waltzing guinea pigs and normal guinea pigs. It is suggested that the decline of the EP during anoxia is correlated with the +K conductance of the organ of Corti.

Action Potentials↗
PubMed2004

Cochlear function in Prestin knockout mice.

Gross-potential recordings in mice lacking the Prestin gene indicate that compound action potential (CAP) thresholds are shifted by approximately 45 dB at 5 kHz and by approximately 60 dB at 33 kHz. However, in order to conclude that outer hair cell (OHC) electromotility is associated with the cochlear amplifier, frequency selectivity must be evaluated and the integrity of the OHC's forward transducer ascertained. The present report demonstrates no frequency selectivity in CAP tuning curves recorded in homozygotes. In addition, CAP input-output functions indicate that responses in knockout mice approach those in controls at high levels where the amplifier has little influence. Although the cochlear microphonic in knockout mice remains approximately 12 dB below that in wild-type mice even at the highest levels, this deficit is thought to reflect hair cell losses in mice lacking prestin. A change in OHC forward transduction is not implied because knockout mice display non-linear responses similar to those in controls. For example, homozygotes exhibit a bipolar summating potential (SP) with positive responses at high frequencies; negative responses at low frequencies. Measurement of intermodulation distortion also shows that the cubic difference tone, 2f(1)-f(2), is approximately 20 dB down from the primaries in both homozygotes and their controls. Because OHCs are the sole generators of the negative SP and because 2f(1)-f(2) is also thought to originate in OHC transduction, these data support the idea that forward transduction is not degraded in OHCs lacking prestin. Finally, application of AM1-43, which initially enters hair cells through their transducer channels, produces fluorescence in wild-type and knockout mice indicating transducer channel activity in both inner and outer hair cells.

Acoustic Stimulation↗
PubMed1992

Low-frequency modulation of compound action potential in experimental perilymphatic fistula and endolymphatic hydrops.

We have tested the hypothesis that the cause of cochlear dysfunction associated with perilymphatic fistula (PLF) is closely related to endolymphatic hydrops (ELH). Using guinea pigs, we studied the tone-burst elicited compound action potential (CAP) and its modulation as caused by a 50 Hz biasing tone in experimental PLF. We compared these results with those of experimental ELH. Following perilymph aspiration through the perforated round window membrane, mild but significant elevations of CAP thresholds at tested frequencies were found. A reduction in the amplitude of cochlear microphonics (CM) for a 50 Hz sine wave appeared to correlate with these CAP threshold changes. However, there were no significant changes in the modulation effect of the 50 Hz biasing tone on the CAP elicited by an 8 kHz tone burst. This finding differed from that in ears with experimental ELH, in which significant reductions of both 50 Hz CM and the degree of CAP modulation were consistently observed. We concluded that it is unlikely that the underlying mechanisms of a modification to the low frequency response of the base of the cochlea following perilymph aspiration is linked to that of experimental ELH.

Acoustic Stimulation↗
PubMed1990

Saturation of outer hair cell receptor currents causes two-tone suppression.

Zwicker [Biol. Cybern. 35, 243-250, (1979); J. Acoust. Soc. Am. 80, 163-176 (1986)] has previously proposed that many nonlinear phenomena in the mammalian cochlea can be explained by saturation of a positive feedback process which enhances mechanical sensitivity, although the site of the nonlinearity producing this saturation has so far remained obscure. In this paper we present evidence suggesting that the nonlinearity of mechano-electrical transduction in the outer hair cells is the dominant nonlinearity producing two-tone suppression in the mammalian cochlea. In particular, we show that: (i) suppression of the extracellular summating potential (SP), recorded from a particular place within the organ of Corti, has characteristics similar to the suppression of activity in the auditory-nerve; (ii) that SP suppression occurs at approximately constant basilar membrane displacement, inferred from the SP iso-response contours; and that (iii) the onset of SP suppression with suppressor tones on the tail of the frequency tuning curve closely parallels the onset of nonlinearity in the local cochlear microphonic. Since previous studies (Patuzzi et al., 1989) have demonstrated that the vibration of the basilar membrane at its characteristic frequency is very sensitive to changes in outer hair cell receptor current, we consider that interference in outer hair cell currents caused by nonlinearity in mechano-electrical transduction is an adequate explanation of two-tone suppression. This requires that outer hair cell receptor currents deviate from linearity at a suppressor tone level below that required to produce a significant DC receptor potential within the inner hair cells, and that the active process within the cochlea is distributed along a local region of the cochlea, basal of the vibration peak.

Acoustic Stimulation↗
PubMed1984

Effect of kainic acid upon N1 latency.

Although the N1 latency of whole nerve action potential is one of the important pieces of information obtained from ECochG, there are some conflicting opinions as to whether or not it is prolonged in sensorineural hearing loss. Kainic acid (KA) is known to destroy neurons selectively through an action at glutamatergic synapses. Therefore, a model of "neural deafness" was made by perfusing the scala tympani with KA solution. The effect of KA upon cochlear microphonics was minimal. Although the N1 amplitude was markedly suppressed by KA, the N1 latency was neither prolonged nor shortened. The result obtained in the present study strongly suggests that the N1 latency is not prolonged in "neural deafness."

Animals↗
PubMed2003

Auditory neuropathy/dyssynchrony: its diagnosis and management.

Patients with auditory neuropathy/dyssynchrony exhibit no auditory brain stem response (ABR), no middle ear muscle response, and both normal otoacoustic emissions or normal cochlear microphonics. An absent or grossly abnormal ABR is not always associated with deafness. In contrast, a hearing loss of 30 dB or more usually predicts absent otoacoustic emissions, but normal emissions can be seen in some patients whose behavioral audiograms imply total deafness. This article reviews the underlying physiology that makes these tests both useful and potentially misleading, and recommends steps to be considered by primary care physicians and other professionals to compensate for the vulnerabilities of each of the procedures.

Audiometry, Pure-Tone↗
PubMed1999

Longitudinal endolymph movements and endocochlear potential changes induced by stimulation at infrasonic frequencies.

The inner ear is continually exposed to pressure fluctuations in the infrasonic frequency range (< 20 Hz) from external and internal body sources. The cochlea is generally regarded to be insensitive to such stimulation. The effects of stimulation at infrasonic frequencies (0.1 to 10 Hz) on endocochlear potential (EP) and endolymph movements in the guinea pig cochlea were studied. Stimuli were applied directly to the perilymph of scala tympani or scala vestibuli of the cochlea via a fluid-filled pipette. Stimuli, especially those near 1 Hz, elicited large EP changes which under some conditions exceeded 20 mV in amplitude and were equivalent to a cochlear microphonic (CM) response. Accompanying the electrical responses was a cyclical, longitudinal displacement of the endolymph. The amplitude and phase of the CM varied according to which perilymphatic scala the stimuli were applied to and whether a perforation was made in the opposing perilymphatic scala. Spontaneously occurring middle ear muscle contractions were also found to induce EP deflections and longitudinal endolymph movements comparable to those generated by perilymphatic injections. These findings suggest that cochlear fluid movements induced by pressure fluctuations at infrasonic frequencies could play a role in fluid homeostasis in the normal state and in fluid disturbances in pathological states.

Animals↗
PubMed1975

[Karyometric studies of the ventral cochlear nucleus in kanamycin treated guinea pigs (author's transl)].

The aim of these investigations was to study the effect of kanamycin on the nucleus ventralis cochleae in guinea pigs. The evaluation of the results was based on the karyometric method which is a very sensitive criterion of the cell activity. In the same animals, the microphonic potential (PM) and the nerve action potential (AP) were measured in order to detect changes in the peripheral auditory system. The results were statistically analysed. The studies showed that despite marked changes in the PM and AP values, there were no changes in the cell volume in the nucleus ventralis cochleae. The findings indicate that the injuries induced by kanamycin are localized peripherally and the later central morphological changes reported in the literature can be assumed to be secondary resulting from the damage to the peripheral auditory system by kanamycin.

Animals↗
PubMed1992

Modulation of cochlear nerve spike rate by cardiac activity in the gerbil.

Among primary auditory axons with characteristic frequencies (CFs) below 2500 Hz, a substantial subpopulation was found in which spike activity was driven by cardiac events. The presence of cardiac-driven activity was inferred from cycle histograms triggered on the peak of the electrocardiogram (ECG). This driven activity was either like a simple onset response (often followed by a reduction of spike activity to below background level), or as a longer lasting series of peaks and troughs. In two axons with high CFs (7 kHz and 12.5 kHz), cardiac-driven suppression was observed. Recordings made by a probe microphone revealed the presence of heart-related sound in the external ear canal. The onset of that sound coincided with the onset of cardiac-driven spike activity (and suppression).

Action Potentials↗
PubMed1978

A new theory of cochlear function based on quasi quantum considerations.

A new theory of cochlear function is proposed. It locates the 2nd filter in the IHC which are regarded as biological resonators. The OHC play no part in frequency discrimination. Confirmation of the theory is derived from the fact that it offers plausible explanations for many otherwise unexplained paradoxes in the distribution of cochlear microphonics. It also explains why combination tones only occur in very restricted frequency regions, and it predicts their relative audibility. Finally a test is proposed whereby the theory must stand or fall.

Cochlea↗