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PubMed1976

Basis and some diagnostic implications of electrocochleography.

Electrocochleography (ECoG) involves the recording of electrical responses to sound from the vicinity of the cochlea. The technique, as we practice it, utilizes a trans-tympanic recording needle situated on the promontory of the middle ear. Filtered clicks in the frequency range between 500 and 8,000 Hz are presented to the ear under test at a rate of 10/sec. Repetitive clicks of a given frequency are first presented at high intensity and the responses summed (averaged) in a computer. The click is systematically lowered in intensity, and an average is collected at each level until the normal dynamic range of hearing has been explored. Two major electrical indices are present in the recording: these are 1. the whole-nerve action potential (AP) derived from the first-order auditory neurons, and 2. the cochlear microphonic (CM) derived from the hair cells. Inspection of the whole nerve AP as intensity is lowered allows the estimation of the response threshold, which correlates well with behavioral threshold. Inspection of the relation between the CM and the AP allows qualitative differentiation to be made between pathology arising in the hair cell (sensory) and in the nerve (neural).

Acoustic Stimulation↗
PubMed1980

Further remarks on the mechanism producing the symptoms of Ménière's disease.

The characteristic symptoms of a Ménière attack--low-tone hearing loss; and nystagmus of long duration, often beating in an ipsilateral direction, eventually changing to a contralateral direction, with a return to normal function between attacks--have all been reproduced in animal experiments by increasing the potassium concentration of the interstitial fluid surrounding the afferent nerve branches from the sensory areas of the inner ear. Several recent experiments of other investigators have shown that a low potassium concentration may increase the action potential frequency. This would explain an ipsilateral nystagmus. Raising the concentration further depresses the action potential frequency, resulting in a contralateral nystagmus. Furthermore, there is evidence indicating that cochlear microphonics might not be affected by increases in the potassium concentration. This seems to indicate that the nerves, and not the hair cells, are engaged in the production of those symptoms dependent on potassium increase. The clinical signs of a similar reaction of the cochlear hair cells in Ménière's cases seem to support the assumption of a similar cause. All the objective symptoms of a Ménière attack, thus, seem to comply with the experimental findings of an endolymphatic potassium contamination of the perilymph spaces around the afferent nerve branches.

Action Potentials↗
PubMed1997

Co-administration of the neurotrophic ACTH(4-9) analogue, ORG 2766, may reduce the cochleotoxic effects of cisplatin.

In this study the effect of the neurotrophic ACTH(4-9) analogue, ORG 2766, on cisplatin cochleotoxicity was investigated with both light- and transmission electron microscopy. Guinea pigs were treated with either cisplatin+ORG 2766 (n = 11) or cisplatin + physiological saline (n = 9). All animals treated with cisplatin + physiological saline showed complete loss of outer hair cells (OHC) and degeneration of the organ of Corti in the basal cochlear turns, while partial OHC loss was found in the middle and apical turns. The inner hair cells (IHC) and other cochlear tissues were not affected. Eight animals from the group treated with cisplatin + ORG 2766 demonstrated similar pathological changes, but to a lesser degree, especially in the middle turns. The three remaining animals demonstrated no cochlear alterations at all, light-microscopically, and only minor subcellular changes in the OHCs at the ultrastructural level. Electrophysiologically, these three animals showed normals compound action potential (CAP) amplitudes at stimulus frequencies from 0.5 to 16 kHz and normal cochlear microphonics (CM) in the frequency range from 0.5 to 8 kHz. The other animals treated with cisplatin + ORG 2766 showed a severe loss in their CAPs and CM, except for one showing intermediate loss. All animals from the group treated with cisplatin alone showed a severe loss in their CAPs and CM. Endolymphatic hydrops was present in all animals from the cisplatin- and the cisplatin + ORG 2766-treated groups. These data indicate that daily, concomitant administration of ORG 2766 may reduce OHC loss and subsequent degeneration of the organ of Corti in cisplatin-treated guinea pig cochleas.

Acoustic Stimulation↗
PubMedDate not supplied

Low-frequency biasing of round window responses in guinea pigs and chinchillas.

The acoustic biasing technique using low-frequency sound is of increasing interest to investigators, not only as a means of studying cochlear transduction but also as a promising tool for assessing cochlear pathology such as endolymphatic hydrops. We compared normal modulation patterns of round window responses in guinea pigs and chinchillas, whose low-frequency auditory characteristics are known to be different. A 50-Hz sine wave (90 dB SPL for guinea pigs and 80 dB SPL for chinchillas), which evoked an equivalent magnitude of cochlear microphonics (CM) in both species, was used to modulate the compound action potential (CAP) and the summating potential (SP) elicited by 8-kHz tone bursts. Overall patterns of CAP and SP modulation were almost identical between the two species except for a difference in the phase of 50 Hz CM. The phase of maximum SP enlargement was in accord with that of maximum CAP suppression, which led to inferred basilar membrane (BM) position at maximum scala tympani displacement by between 45 and 90 degrees. More complex or hysteresis effects seemed to be involved in the modulation of CAP and SP magnitude, in addition to the biasing effect owing solely to BM displacement.

Acoustic Stimulation↗
PubMed1984

Short-latency auditory responses obtained by cross correlation.

Short-latency auditory responses were derived by cross correlation of pseudorandom white noise with averaged scalp potentials in guinea pigs. The cross-correlation functions were characterized by distinct cochlear microphonic and neural components, as distinguished by susceptibility to hypothermia and masking noise. This technique detects only linear, frequency-following responses of the auditory system, and demonstrated neural frequency following up to 3-4 kHz; thresholds were about 30-40 dB spectrum level. While conventional auditory brain stem responses reflect onset neural activity and are most responsive to high-frequency stimuli, cross-correlation responses reflect frequency-following activity, primarily to low frequencies, and thus may represent a complementary method of electrophysiologic assessment of the auditory system. Data are very rapidly acquired, and estimation of responses of limited areas of the cochlea may be possible by off-line digital filtering of cross-correlation functions obtained with broadband noise stimuli.

Animals↗
PubMed1978

Intracellular studies of hair cells in the mammalian cochlea.

1. Intracellular recordings were made from inner hair cells in the first turn of the guinea-pig cochlea, the recording sites being confirmed by the injection of Procion yellow dye and subsequent histology. 2. The receptor potential, in response to a pure tone burst, consisted of an AC response which followed the wave form of the stimulus and was analogous to the extracellularly recorded cochlear microphonic and a depolarizating DC response which followed the envelope of the tone burst and was analogous to the extracellularly recorded summating potential. 3. The DC response was broadly tuned at high sound pressure having a maximal amplitude of 27 mV at a sound pressure level of ca. 100 db; however the bandwidth of the response was reduced at lower sound pressure level. Isoamplitude curves for the DC response were indistinguishable from the threshold curves for auditory nerve fibres. 4. The AC response was tuned in a similar fashion to the DC response except that it was attenuated at 6-9 db/octave with respect to the DC response. It is suggested that this difference was due to the effect of membrane capacitance and resistance on the AC response. In contrast the extracellularly recorded AC component was not subject to this attenuation. 5. The total resistance and capacitance in three cells were found to be 46-61 Momega and 7.8-15.8 muF respectively. 6. Intracellular resistance changes were measured during sound stimulation, the resistance change being proportional to the DC receptor potential, indicating constant current flow through the hair cell. The current varied between 0.37 and 0.81 nA between cells. The time constant for seven cells was found to lie between 0.31 and 0.76 msec. 7. A map of the basilar membrane showing position of hair cells against characteristic frequency corresponded to the cut-off frequencies of the basilar membrane mechanical measurements and the innervation sites of spiral ganglion cells.

Animals↗
PubMed1984

Impairment in cochlear function produced by chloramphenicol and noise.

Ototoxic interaction between chloramphenicol and noise was studied in two separate investigations. In the first study, permanent ototoxicity was demonstrated in a group of rats which were subjected to short-duration, high-intensity noise and were then given chloramphenicol orally. The anatomical damage in this group was consistent with observed changes in cochlear round window recordings of cochlear microphonics at 4 kHz and of the N1 component of the eighth nerve action potential. In the second study, a temporary depression in the function of the cochlea was observed in rats subjected to the noise-chloramphenicol regimen used in the first study. Depressions in recordings of the round window similar to those in the first study were seen only during the first five days of recordings. After the fifth day, the recordings of the round window were normal, indicating recovery from a temporary shift in threshold produced by chloramphenicol and noise. Incidence of purulent otitis media was found in 57 and 0% of the animals in the first and second studies, respectively. The combination of chloramphenicol and noise appears to be responsible for the production of temporary cochlear deficits. The addition of the third variable, otitis media, appears to result in permanent impairment of the cochlea.

Animals↗
PubMed2006

Cochlear function after selective spiral ganglion cells degeneration induced by ouabain.

BACKGROUND: Ouabain, a cardiac glycoside that specifically binds to Na/K-ATPase and inhibits its activity, was applied to gerbils to develop a method for studying auditory neuropathy. METHODS: Ouabain was applied to the round window of the cochlea in each gerbil by using a piece of gelfoam with 3 microl or 24 microl (1 mmol/L) ouabain solution. The changes of the threshold of auditory brainstem response, cochlear function round window electrocochleography, as well as the morphological changes of the spiral ganglion cells of the cochlea were observed after application of ouabain for 24 hours or 96 hours. RESULTS: In ouabain treated gerbils, auditory brainstem response and compound action potential thresholds showed either elevation or no response at all. However, the thresholds of cochlear microphonic and distortion product otoacoustic emissions were not affected. Degeneration and necrosis of some spiral ganglion cells in ears with applications of ouabain (24 hours, 3 microl, 1 mmol/L; 96 hours, 24 microl, 1 mmol/L ouabain). The number of spiral ganglion cells was decreased (24 hours, 3 microl, 1 mmol/L ouabain) or near to a total loss (96 hours, 24 microl, 1 mmol/L ouabain). CONCLUSIONS: These results indicate a high degree of independence between the spiral ganglion cells and the outer hair cell systems in the cochlear transduction mechanism. The method used in this study would provide a valuable tool for studying auditory neuropathy.

Action Potentials↗
PubMedDate not supplied

[Mechanism of the effect of neuronal response suppression in the auditory nerve during exposure to bitonal stimuli].

It is supposed that interreceptor currents existing due to microphonic and summating potentials are the exiting factors for the neuron endings of the cochlear nerve. A model is proposed of the formation of the cochlear neuron responses under the stimulation of the hearing system by a tone signal with a changing frequency and by a signal consisting of two tones. It is shown that the proposed model explains the effect of inhibition of the neuron response to a given tone signal when another tone signal of proper intensity arises in a definite frequency region.

Hearing↗
PubMed1991

The protective effects of allopurinol and superoxide dismutase-polyethylene glycol on ischemic and reperfusion-induced cochlear damage.

The purpose of this study was to assess the protective effects of allopurinol, a blocker of free oxygen radical (FOR) formation, and superoxide dismutase-polyethylene glycol (SOD-PEG), a scavenger of FORs, on ischemic and reperfusion-induced cochlear damage. Fifteen Wistar Kyoto rats (WKY) were randomly assigned to three groups: (1) a control group (5 animals) that was exposed to 15 minutes of cochlear ischemia by clamping the anterior inferior cerebellar artery (AICA), followed by 15 minutes of reperfusion as documented by laser Doppler flowmetry; (2) a drug-treated group (5 animals) that received allopurinol before ischemia/reperfusion; and (3) a drug-treated group (5 animals) that received SOD-PEG before ischemia/reperfusion. In the control group, the tone burst-evoked compound action potential (CAP) recorded from the round window (RW) of the cochlea was abolished, and the cochlear microphonic (CM) was reduced after ischemia. In contrast, both allopurinol and SOD-PEG-treated animals showed post-reperfusion sensitivity in CAP and CM measures. We interpret these results to indicate that damage to the cochlear from ischemia and subsequent reperfusion can be attenuated by pretreatment with allopurinol or SOD-PEG. This provides indirect evidence that FORs may be partially responsible for cochlear damage resulting from ischemic conditions.

Action Potentials↗
PubMed2005

Auditory processing in individuals with auditory neuropathy.

BACKGROUND: Auditory neuropathy is a disorder characterized by no or severely impaired auditory brainstem responses in presence of normal otoacoustic emissions and/or cochlear microphonics. Speech perception abilities in these individuals are disproportionate to their hearing sensitivity and reported to be dependent on cortical evoked potentials and temporal processing abilities. The disproportionate loss of auditory percept in presence of normal cochlear function is suggestive of impairment of auditory neural synchrony. METHODS: We studied the auditory evoked potentials and psychophysical abilities in 14 adults with auditory neuropathy to characterize their perceptual capabilities. Psychophysical tests included measurement of open set speech identification scores, just noticeable difference for transition duration of syllable /da/ and temporal modulation transfer function. Auditory evoked potentials measures were, recording of P1/N1, P2/N2 complex and mismatch negativity (MMN). RESULTS: Results revealed a significant correlation between temporal processing deficits and speech perception abilities. In majority of individuals with auditory neuropathy P1/N1, P2/N2 complex and mismatch negativity could be elicited with normal amplitude and latency. None of the measured evoked potential parameters correlated with the speech perception scores. Many of the subjects with auditory neuropathy showed normal MMN even though they could not discriminate the stimulus contrast behaviorally. CONCLUSION: Conclusions drawn from the study are: 1. Individuals with auditory neuropathy have severely affected temporal processing. 2. The presence of MMN may not be directly linked to presence of behavioral discrimination and to speech perception capabilities at least in adults with auditory neuropathy.

Journal Article↗
PubMed1978

Carbonic anhydrase in the generation of cochlear potentials.

The experiments on 18 guinea pigs were divided into two groups and each group was arranged in such a way that the effect of hypercapnia (generated by breathing 10% CO2-90% O2) was investigated with and without inhibition of carbonic anhydrase by methazolamide, 25 mg/kg, in the first group and acetazolamide, 50 mg/kg, in the second group, administered intravenously. The endocochlear potentials (EP) and endocochlear PO2 were recorded by microelectrodes introduced into the scala media, and cochlear microphonics (CM) were monitored by a silver-wire electrode from the round window. In the first exposure to hypercapnia (20-40 min) EP increased about + 6 mV. At the same time CM decreased; the reason for this is not yet known. During the second period of hypercapnia (80-100 min) when carbonic anhydrase was inhibited with methazolamide and acetazolamide, EP did not elevate as during the first period when carbonic anhydrase was not inhibited. In this work, under specific conditions, it was observed for the first time that carbonic anhydrase affects the generation of EP.

Acetazolamide↗