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PubMed1991

Ototoxic effect of potassium canrenoate on the guinea pig cochlea.

Potassium canrenoate (PC) is a diuretic with antialdosterone action, reducing the reabsorption of sodium in the efferent renal tubules. This drug has been reported to damage only the marginal cells of the stria vascularis in the cochlea. The perilymphatic space of the guinea pig cochlea was perfused with an artificial perilymph containing 5 x 10(-3) M potassium canrenoate. Following the onset of perfusion, the endocochlear dc potential (EP) gradually declined to around 10 mV but did not become negative even when the perfusion was continued. A similar decrease in EP was observed in kanamycin-deafened guinea pigs. When the respirator was turned off and perfusion discontinued, a large negative EP appeared during 5 min of anoxia in normal guinea pigs but not in the kanamycin-deafened guinea pigs. The decreased EP recovered to preanoxic level after resumption of ventilation. The cochlear microphonics (CM) also gradually declined in parallel with the EP. The summating potential (SP) showed only a minor change. The potassium ion activity in the endolymph decreased slightly but the sodium ion activity remained unchanged during perfusion. These findings suggest that the main target of the PC is the cells of the stria vascularis.

Animals↗
PubMed1981

Specificity of action of vanadate to the organ of corti.

Although vanadate strongly inhibits Na/K-ATPase activity of the stria vascularis in vitro, it initially causes no depression of the ouabain-sensitive endocochlear potential (EP) when perfused perilymphatically or via the vasculature. However, when the perilymph of scala tympani is replaced with artificial media containing 0.1 to 1 mM vanadate, there is a large (about 17 mV) increase in the EP of the second cochlear turn. Further experiments showed that the cochlear microphonics declined during the time in which the EP increased, and that the response of these two potentials to vanadate is greater in the second turn than in the first. Injection of 50 n1 of 1 mM vanadate (in artificial endolymph) into the endolymphatic space of the second turn caused no increase in the EP. These results support the notion that the early effects of vanadate are on the contra-luminal membranes of cells of the organ of Corti rather than on the stria vascularis. By superimposing anoxia or furosemide (i.v.) upon vanadate intoxication, we determined that the initial increase of the compound EP due to vanadate alone was due to a reduction in magnitude of the negative component of the EP. It is argued that of the three prevalent theories concerning the generation of the negative EP, the data tend to support the hypothesis that the intracellular potential of the hair cells gives rise to the negative EP.

Adenosine Triphosphatases↗
PubMedDate not supplied

Brainstem responses in the quivering mutant mouse.

The recessive quivering gene in mice produces general neurological abnormalities and deafness. Previous work indicated that cochlear responses (microphonics and compound action potentials) were normal in the quivering (qv/qv) mouse, but inferior colliculus evoked potentials had poor thresholds and abnormal latencies. The object of the present study was to record evoked potentials from the cochlear nucleus (CN) in quivering and control mice, and also to record surface responses. The CN evoked response in control mice consisted of two prominent positive peaks. The first peak appeared normal in the quivering CN, resulting in normal thresholds for detection of the response. However, the second peak in mutants was smaller and of longer latency. Surface responses in quivering showed a normal first wave followed by an abnormal wave pattern. It was concluded that the input from auditory nerve to CN in quivering is probably normal and that the central deficit in quivering is evident at the level of CN.

Animals↗
PubMed1996

Tuning curves of the difference tone auditory nerve neurophonic.

When a pair of tonal stimuli of different frequencies (F1 and F2, where F2 > F1) are simultaneously presented to the ear, an electrical response with a frequency of F2-F1 can be recorded from the round window (RW) of the gerbil's cochlea. By using phase-locked tones of alternating polarity, the cochlear microphonics are canceled, leaving a time-averaged difference tone-auditory nerve neurophonic (DT-ANN). When the F1 frequency ranges from 1.25 to 30 kHz and F2-F1 approximately 900 Hz, a DT-ANN audiogram can be constructed which parallels (but is at least 10 dB more sensitive than) the compound action potential (CAP) audiogram. In addition to this DT response, a smaller magnitude, higher threshold response having a frequency of 2 DT can often be measured. Both the DT-ANN and the 2 DT-ANN show non-monotonic amplitude input-output functions. The DT- and 2 DT-ANN responses can be forward masked. Masking of low level (e.g., 30 dB SPL) probe stimuli results in DT- and 2 DT-ANN V-shaped tuning curves (TC) with low tip thresholds (approximately 20-30 dB SPL) and a tip frequency close to that of F1 and F2. The Q10 dB values of the forward masked DT-ANN TCs ranges from 1.54 to 20.0 for F1 frequencies varying from 2 to 20 kHz, respectively. The V-shaped DT-ANN TCs generated with simultaneous maskers are often flanked, outside their high- and low-frequency slopes, by frequency-intensity domains where the masker enhances the amplitude of the DT-ANN response. These data (1) provide evidence that, in response to low-intensity tones, the DT-ANN is generated by a restricted population of neurons that have characteristic frequencies close to F1 and F2, and (2) provide evidence for sharply tuned, phase-locked activity occurring in response to low-intensity stimuli, by cochlear axons having characteristic frequencies as high as 20 kHz.

Acoustic Stimulation↗
PubMed1987

Strial dysfunction in mice with cochleo-saccular abnormalities.

Most viable dominant spotting (Wv/Wv) mutant mice, which show cochleo-saccular degeneration, were found to have an endocochlear potential (EP) around zero together with a structurally abnormal stria vascularis. Inner hair cells were well preserved, but outer hair cells in the basal half of the cochlea were degenerating, possibly as a result of primary strial dysfunction. Thresholds for the detection of a compound action potential were raised to around 100 dB SPL in the mutants with no EP, and there was little if any cochlear microphonic at the round window. Of the 20 Wv/Wv mice studied, five partially escaped the effects of the mutation and had measurable positive potentials (15-86 mV) in scala media in the basal turn; responses in these animals were intermediate between control responses and those of mutants with no EP. These findings confirm that the pathological processes in this mutant, with cochleo-saccular abnormalities, are fundamentally different from the pathological processes in animals with neuroepithelial abnormalities reported previously [see Steel and Bock (1983) Arch. Otolaryngol. 109, 22-29, for references].

Animals↗
PubMed1989

The quinoxalinediones DNOX, CNOX and two related congeners suppress hair cell-to-auditory nerve transmission.

We tested 6,7-dinitroquinoxaline-2,3-dione (DNQX); 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX); 6,7-dichloro-3-hydroxy-2-quinoxalinecarboxylic acid (DHQC); and 3-hydroxy-2-quinoxalinecarboxylic acid (3HQC), new kainate and quisqualate receptor antagonists, upon cochlear potentials in guinea pig. Perilymph spaces of guinea pig cochleae were perfused with artificial perilymph solutions containing up to 1000 microM concentrations of DHQC and 3HQC, and 500 microM concentrations of DNQX and CNQX, at a rate of 2.5 microliters/min for 10 min. Cochlear potentials evoked by 10 kHz tone bursts of varying intensity were recorded from the basal turn scala vestibuli. Cochlear perfusion of the four drugs resulted in a dose-related suppression of the compound action potential of the auditory nerve (CAP; N1-P1), a prolongation of N1 latency at suprathreshold levels, an elevated CAP threshold, and a decreased N1 latency at CAP threshold. None of the drugs had significant effects on cochlear microphonics (CM) or the summating potential (SP). EC50 values (concentrations causing a 50% reduction in CAP amplitude at 68 dB SPL) were 8 microM for DNQX, 30 microM for DHQC, 35 microM for CNQX, and 1 mM for 3HQC. Results support the hypothesis that kainate and quisqualate receptors are involved in neurotransmission between the hair cell and afferent nerve.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1999

Intermittent noise-induced hearing loss and the influence of carbon monoxide.

Intermittent noise causes less hearing loss than continuous noise of equal intensity. The reduction in damage observed with intermittent noise may be explained by the fact that the auditory system has time to recover between the noise phases. Simultaneous carbon monoxide (CO) exposure produces greater noise-induced hearing loss than does noise alone (Chen and Fechter, 1999). In the present study, intermittent noise (octave-band with a center frequency of 13.6 kHz, 100 dB) of a 2 h total duration but with a different duty cycle (% of noise during exposure) was used. The intermittent exposure that had a shorter noise duty cycle induced a less permanent threshold shift (PTS) than those that had a longer noise duty cycle (or less rest periods). This relation between the loss in compound action potential (CAP) sensitivity and the noise duty cycle (or rest period) was abolished by the presence of CO. The cochlear microphonic (CM) amplitude revealed similar results to those seen using the CAP. While intermittent noise that had a short noise duty cycle did not cause hair cell loss by itself, the combined exposure to noise and CO (1200 ppm) caused remarkable OHC loss in the basal turn.

Action Potentials↗
PubMed1986

Effect of click spectrum and polarity on round window N1N2 response in the rat.

The effect of the duration of click stimuli on the compound action potential recorded from the round window in the rat and the effect of low-pass filtering of short click sounds were studied. Thus the intensity functions of the round window N1 potential have a two-segment course and there is a difference in the response to rarefaction and condensation clicks, depending upon the content of low-frequency components in the click stimulus. The intensity function of the rat's response to broadband clicks does not show the same two-segment course as has been reported in experiments in other animals, and there is little difference between the response to condensation clicks and that to rarefaction clicks in this animal. However, when the duration of the click is increased or when broadband clicks are subjected to low-pass filtering, the intensity functions in response to condensation clicks do show a change in course, while the response to rarefaction clicks remains essentially unchanged. A similar change in the response to a broadband click can be induced by adding a low-pass-filtered click to the broadband click. The response to such a combination is not only a linear summation of the neural response to the individual components of the stimuli and the cochlear microphonics, but the low-frequency components that are added also affect the response to the broadband click, mainly by reducing the amplitude of the response.

Acoustic Stimulation↗
PubMed1980

Immediate effects of intravenous tobramycin and gentamicin on human cochlear function.

Immediate electrocochleographic changes have been studied in a series of patients following intravenous infusion of either tobramycin or gentamicin. In patients receiving tobramycin, as soon as peak serum levels of antibiotic were reached, a dramatic decrease occurred in the magnitude of the compound VIII nerve action potential (AP), and of the cochlear microphonic (CM). The shape of the AP also changed. The N1 component of the waveform became very small, and N2 increased in size; this is the dissociated pattern of basal coil cochlear damage. The speed of onset of these electrical changes and their apparent reversibility suggests a temporary metabolic block caused by tobramycin. No such changes were observed following infusion of gentamicin.

Action Potentials↗
PubMed1994

Stimulus biasing: a comparison between cochlear hair cell and organ of Corti response patterns.

Responses from the organ of Corti (OC) fluid space and from individual hair cells are collected for short duration tone pips measured alone and in the presence of a 20 Hz bias tone. Because of the relatively long period of the acoustic bias signal, a probe can be selectively placed at precise locations within a single response period. Since bias effects produced during maximum basilar membrane velocity are negligible, this report documents changes associated with basilar membrane displacements to scala vestibuli and scala tympani. Hair cell response patterns are compared with those measured nearby in the OC to determine the degree to which inner (IHC) and outer hair cells (OHC) contribute to the gross cochlear potentials. It is shown that intracellular OHC and OC dc responses are strongly influenced by the bias while intracellular IHC dc responses are minimally affected. Although an association has been established between the cochlear microphonic and outer hair cell ac receptor potentials, the well correlated changes in the outer hair cell dc receptor potential and the organ of Corti summating potential suggest that gross cochlear potentials reflect dc as well as ac contributions from nearby OHCs. Since IHC responses are not influenced by the bias, they appear to contribute less than OHCs to extracellular potentials. These conclusions, however, are restricted to the moderately high input levels required to produce these effects (Durrant and Dallos, 1974) and to the central region of the cochlea where the recordings are made. Finally, the degree to which bias effects are contaminated by two-tone suppression is discussed.

Acoustic Stimulation↗
PubMed1989

Effects of sodium bromate on ionic concentrations and osmolalities of the cochlear fluids in guinea pigs.

Effects of sodium bromate on cochlear potentials and electrolyte composition of the cochlear fluids in guinea pigs were investigated following administration of sodium bromate into the cochlea, using perilymphatic perfusion. Cochlear microphonics and the whole nerve action potential of the auditory nerve were markedly suppressed. The K+ and Cl- activities in the endolymph as well as the endocochlear dc potential (EP) decreased significantly and irreversibly, in proportion to the concentration of sodium bromate. A negative EP never developed during the monitoring of 120 min. Microsamples of the endolymph showed substantial decreases of K+ and Cl- concentrations and an increase in the concentration of Na+. Osmolality of the endolymph was much lower than that of the perilymph. The severe edema of the stria vascularis and collapse of Reissner's membrane were histologically evident. These events suggest a breakdown of the endolymph-perilymph barrier, coincident with an inhibition of the strial active transport, as a result of the ototoxic action of sodium bromate. The possible ion and water movement across the endolymph-perilymph barrier in the presence of sodium bromate is discussed.

Acoustic Stimulation↗
PubMed1978

Distribution of the crossed olivocochlear bundle in the chinchilla's cochlea.

The efferent crossed olivocochlear bundle (COCB) was transected in the brain stem of the chinchilla, and the animals sacrificed 7 to 96 days later. Electron microscopy revealed that all the large efferent nerve endings on outer hair cells in the basalmost 2 mm (round window region) of the cochlea had degenerated, 87.5% in the remainder of the first turn, 70% in the second turn and 43% in the third turn. Only a few degenerating nerve fibers were seen in the medial spiral tract (inner spiral and tunnel bundles) of the experimental animals. Nerve fibers were counted in the medial spiral tracts of the cochleas of control animals as well as in those animals whose COCB had been transected. There were considerable individual variations in the fiber numbers, and statistical analysis showed no significant difference between the numbers of nerve fibers in normal and experimental animals. The cochlear microphonics (CM) and nerve action potentials (AP) of acute animals were assessed before and after COCB section. The CM and AP of the chronic experimental animals were compared with responses from normals. Overall, no changes in a physiological response of the anesthetized chinchilla could be attributed to complete section of the COCB.

Acetylcholinesterase↗
PubMed1998

Protection against aminoglycoside otic drop-induced ototoxicity by a spin trap: I. Acute effects.

Topical administration of aminoglycoside antibiotic drops containing neomycin and polymyxin B disrupts cochlear structure and function in rodents, possibly as a result of reactive oxygen species generation. This study investigated the ability of a spin trap, alpha-phenyl-tert-butyl-nitrone (PBN), to prevent acute aminoglycoside antibiotic drop-induced cochlear dysfunction. Guinea pigs were monitored for compound action potential thresholds and 1.0 microV root-mean-square cochlear microphonic isopotential curve values, then injected intraperitoneally with PBN (60 mg/kg) or saline solution. After 10 minutes, 50 microl of PBN (100 mmol/L) or artificial perilymph was applied to the round window membrane, followed after 10 minutes with artificial perilymph or aminoglycoside antibiotic drops (50 microl). From 10 to 60 minutes after exposure, mean compound action potential thresholds progressively increased in the artificial perilymph-aminoglycoside antibiotic drop group, beginning with high frequencies and later including ever-lower frequencies. These threshold shifts in compound action potentials were significantly greater (p<0.05) than those seen in the artificial perilymph-artificial perilymph or PBN-aminoglycoside antibiotic drop groups. This finding indicates that PBN provided protection against acute aminoglycoside antibiotic drop-induced compound action potential threshold sensitivity loss. Mean cochlear microphonic shift values at 60 minutes in the artificial perilymph-aminoglycoside antibiotic drop group significantly exceeded those of the other groups only at the highest frequencies. These data suggest that acute aminoglycoside antibiotic drop-induced cochlear disruption primarily affects high frequency compound action potential function and may be partially reactive oxygen species-mediated and preventable.

Action Potentials↗
PubMed2005

Ca2+ current-driven nonlinear amplification by the mammalian cochlea in vitro.

An active process in the inner ear expends energy to enhance the sensitivity and frequency selectivity of hearing. Two mechanisms have been proposed to underlie this process in the mammalian cochlea: receptor potential-based electromotility and Ca(2+)-driven active hair-bundle motility. To link the phenomenology of the cochlear amplifier with these cellular mechanisms, we developed an in vitro cochlear preparation from Meriones unguiculatus that affords optical access to the sensory epithelium while mimicking its in vivo environment. Acoustic and electrical stimulation elicited microphonic potentials and electrically evoked hair-bundle movement, demonstrating intact forward and reverse mechanotransduction. The mechanical responses of hair bundles from inner hair cells revealed a characteristic resonance and a compressive nonlinearity diagnostic of the active process. Blocking transduction with amiloride abolished nonlinear amplification, whereas eliminating all but the Ca(2+) component of the transduction current did not. These results suggest that the Ca(2+) current drives the cochlear active process, and they support the hypothesis that active hair-bundle motility underlies cochlear amplification.

Acoustic Stimulation↗
PubMed2000

The contribution of phospholipase A2 to the cochlear dysfunction induced by transient ischemia.

The objective of the present study was to examine whether mepacrine, a commonly used phospholipase A2 inhibitor, decreases ischemic damage to the cochlea. Transient ischemia of the cochlea was induced in albino guinea pigs for 15, 30 or 60 min by pressing the labyrinthine artery at the porus acusticus internus. The animals were intraperitoneally given mepacrine or physiological saline solution (PSS) 20 min prior to ischemia. Although mepacrine failed to alleviate the post-ischemic threshold shift of compound action potential (CAP) in case of 60 min ischemia, a statistically significant reduction in the CAP threshold shift was observed in the mepacrine-treated animals after 15 and 30 min ischemia. However, there was no statistically significant difference in the post-ischemic threshold shift of cochlear microphonic between the mepacrine-given and the PSS-given animals. Furthermore, mepacrine partially alleviated ischemia-induced swelling of radial afferent dendrites of primary auditory neurons. These results suggest that excessive activation of phospholipase A2 plays an injury-producing role at least by enhancing excitotoxicity in ischemia-reperfusion injury of the cochlea.

Action Potentials↗