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Results for “Cochlear Microphonic Potentials”

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PubMed1991

[Effects of heavy metal ions in endocochlear DC potential and cochlear microphonics in the guinea pig--the influence of calcium on the cochlea].

Endocochlear DC potential (EP) and cochlear microphonics (CM) in the guinea pig under the influence of the divalent heavy metal cations of manganese, nickel, cobalt and cadmium, and the trivalent cation of lanthanum were investigated. The area from the scala tympani to the scala vestibuli was perfused with control and test solutions. CM decreased gradually to 50-80%, but EP showed no change after perfusion with a solution containing 1 mM of metal ions. At a concentration of 10 mM, EP decreased from 80 mV to 10-20 mV and CM decreased to 15-55%. At 100 mM, EP increased by about 10 mV at the beginning of perfusion, remained steady for 1 min, and then rapidly decreased to 0-10 mV. Meanwhile, CM continued to decrease, finally sustaining a 10-56% reduction. The decrease in EP and CM were irreversible, and perfusion of the area with the standard solution for 20 min had no effect. The osmolarity of the artificial perilymph containing 100 mM of metal ions was twice as high as that of the normal physiological solution. The effects of osmolarity, however, were excluded because perfusion with an artificial perilymphatic solution made hypertonic by either NaCl or sucrose changed neither EP nor CM. The application of 100 mM of metal ions topically to the round window membrane caused no change in EP. The alkali metal ions are known to inhibit inward Ca2+ current. Therefore, the present results suggest that Ca2+ ions play a role in maintaining EP generation in the stria vascularis and CM generation in the organ of Corti.

Animals↗
PubMed1985

Dissociation of the cochlear microphonics and endocochlear potential after injection of ethacrynic acid.

The cochlear microphonics (CM), endocochlear potential (EP) and summating potential (SP) were simultaneously recorded for 60 min after injection of 30 mg/kg body weight of ethacrynic acid. The EP decreased parallel with the CM for about 20 min after injection, but they differed in the recovery stage. Even when the EP was still negative, the output of CM for 500 Hz acoustic stimulus recovered to its original level and was supernormal. A large SP observed in the recovery stage of CM and EP seemed to suggest that some functional change in the hair cells might be connected with the supernormal CM. Four minutes of anoxia during the supernormal CM decreased CM to only 68% of its level prior to anoxia. A cathodal polarization of the scala media, to change the polarity of the dc potential gradient, reversed the polarity of CM in the anoxic guinea-pig cochlea but not in the guinea-pig cochlea administered ethacrynic acid. These results suggest that supernormal CM observed in this experiment may not be dependent on the dc potential gradient, but due to some functional change in the hair cells after the injection of ethacrynic acid, although CM is essentially dependent on the dc potential gradient between the scala media and the inside of the hair cells.

Acoustic Stimulation↗
PubMed1988

Effects of various vanadium compounds on cochlear potentials.

The effects of vanadium compounds, sodium vanadate, ammonium vanadate, potassium vanadate, vanadium oxysulfate, vanadium acetylacetonate, and vanadium trichloride, on endocochlear potential (EP) and cochlear microphonic potential (CM) were examined in the guinea pig cochlea. The perilymphatic space was perfused for 30 min with 1 mM solution of each compound and changes of EP, CM, and negative EP were observed. Upon perfusion with pentavalent vanadium solutions, such as sodium vanadate, ammonium vanadate, and potassium vanadate, the EP showed an overshoot at the beginning of perfusion and then a gradual decrease, while the CM showed only a gradual decrease. The other compounds had no effects on EP and CM. Since the negative EP showed no differences due to perfusion of any compound, it is concluded that the vanadate compounds have inhibitory effects on EP primarily, and on CM only secondarily. The chemical mechanism of the effects of vanadates was discussed concerning the function of the stria vascularis and also its participation in acute hearing loss.

Animals↗
PubMed1988

Effects of vanadate on EP and its distribution in guinea pig cochlea.

Effects of sigma-sodium vanadate on endocochlear d.c. potential (EP) and cochlear microphonic potential (CM) were examined and its distribution was observed by an X-ray microanalyzer in the guinea pig cochlea. The perilymphatic space was perfused with 1, 5, and 10 mM solutions of sodium vanadate, using a Harvard Microperfusion pump. By perfusing the scala vestibuli, EP and CM showed a rapid decrease. On the other hand, by perfusing the scala tympani, EP showed an overshoot at first, then a gradual decrease, while CM showed only a gradual decrease. The rates of decrease of EP and CM were dependent upon perfusion time and vanadate concentration. After the electrophysiological examinations, the specimen of the cochlea was observed by X-ray microanalyzer. An accumulation of vanadium was confirmed, especially in the stria vascularis and the hair cells. From the results obtained, the possibility of the responsibility of vanadate for a hypothetical sudden deafness originating in the stria vascularis was discussed.

Animals↗
PubMed1986

The depression of the auditory nerve-brain-stem evoked response in hypoxaemia--mechanism and site of effect.

During severe hypoxaemia in the cat the ABR was depressed in 2 different patterns: if mean arterial blood pressure (MAP) was maintained then all other evoked potentials (EPs--somatosensory and visual) remained. If MAP was not maintained, all of these EPs were depressed. This study sought to document these different patterns of ABR depression and to ascertain their mechanisms. When MAP fell, the ABR loss began with the later waves and progressed to the earlier waves. These are signs of a central brain lesion. The hypoxaemia, detrimental to normal function of the cardiovascular system, leads to depression of MAP, to a fall in cerebral perfusion pressure and blood flow, to cerebral ischaemia and ABR loss. On the other hand, when MAP was maintained, severe hypoxaemia was accompanied by a depression of all of the ABR waves at the same time. The cochlear microphonic potential was also simultaneously depressed. These are signs of a peripheral, cochlear effect similar to the demonstrated depression of the positive endocochlear resting potential of the scala media and of the cochlear microphonic potential during hypoxaemia. This leads to interference with the cochlear transduction mechanism so that all of the auditory evoked potentials, including the ABR, are simultaneously depressed. These results lead to the suggestion that the ABR abnormalities seen in patients who suffered a hypoxic (anoxic) insult or an ischaemic episode (prolonged interpeak latencies, loss of later waves and finally all waves absent or only the first wave remaining) is always due to ischaemia even when the initial insult was hypoxic.

Animals↗
PubMedDate not supplied

Central auditory fatigue.

The results of this study, based on evoked responses and single-neuronal responses, reveal that there is a central involvement in auditory fatigue. In these experiments, cochlear potentials (microphonic and whole-nerve action potential) and inferior colliculus electrical responses were simultaneously obtained before and after excessive sound exposure. In general, sound exposure produced a greater reduction of the collicular evoked responses than of the cochlear microphonics and action potentials. Recordings from single neurons support the evoked-response findings.

Animals↗
PubMed1990

[Effects of perilymphatic perfusion with cisplatin on the cochlear potential in guinea pigs].

The effects of three concentrations of cisplatin, administered by acute perilymphatic perfusion on the endocochlear potential (EP) and the cochlear microphonic potential (CM) of the guinea pig cochleae, at 1 kHz are reported. No change in EP magnitude was discovered and a concentration-dependent reduction in CM amplitude occurred during 60 minutes' perfusion period. The results suggest that cisplatin-induced hearing loss is not necessarily progressive degradation of EP.

Animals↗
PubMed1975

Ionic mechanism of the efferent olivo-cochlear inhibition studied by cochlear perfusion in the cat.

1. A method for perfusing the scala tympani of the cat's cochlea from basal turn to apex is described. The perfusion with modified Krebs solution did not interfere with the recording of cochlear microphonic (CM) and neural responses to sound, nor with the efferent inhibition elicited by stereotaxic stimulation of the crossed olivo-cochlear bundle (COCB) in the medulla. 2. Cochlear perfusion with solutions in which most of the chloride was replaced by large anions (sulphate or gluconate) decreased or eliminated auditory nerve or the ventral cochlear nucleus. These effects were reversible. They were only observed if the rate of perfusion (2-20 mul/min) was adequate to reduce the chloride concentration in perilymph below about 80 mM, this being estimated, in different perfusion of the same cochlea, by a chloride-selective electrode. 3. The COCB-induced negative shift of the endocochlear potential recorded with a glass micro-electrode inserted into the scala media was abolished by I.V. strychnine o.2 mg/kg. It was decreased when the perilymph chloride was reduced to 50-70 mM and could be abolished when the perilymph chloride dropped to about 5 mM. 4. The COCB-induced potentiation of the cochlear microphonic potential was also reduced by chloride substitution but the pattern of this effect differed from that of neural inhibition. 5. Similar cochlear perfusions with a solution in which the small diameter bromide anion was substituted for chloride did not affect the COCB-efferent effects. 6. The data indicate that the inhibitory transmitter released by COCB terminals elicits an increased conductance to small anions (normally to chloride) in the membrane of the auditory dendrite and of the outer hair cell. The significance of the COCB-induced negative shift of endocochlear potential and of the potentiation of CM is discussed, as well as the pre- and post-synaptic mechanisms involved in the efferent gating exerted on the auditory input. The latter would seem to involve primarily a post-synaptic mechanism at efferent axo-dendritic synapses.

Acoustic Stimulation↗
PubMed1992

[The use of 6-flavor Rehmannia decoction with additives in the prevention of ototoxic deafness induced by gentamicin in guinea pigs].

The purpose of this study is to discuss the effects of the Chinese medicine six-flavor Rehmannia Decoction with additives on preventing deafness induced by gentamicin (GM) in guinea pig by means of testing the thresholds of Preyer's reflex (PR) cochlear microphonic potential (CM), action potential of the auditory nerve (N1) and scanning electron microscope of inner ear (SEM). The results showed that the medicine is effective in reducing the ototoxic effect of GM on inner ear.

Action Potentials↗
PubMed1988

[Microperforation and removal of the round window membrane. Short- and long-term study in animal experiments using electrocochleography and evoked response audiometry].

Our earlier animal experiments on guinea pigs showed that instrumental perforation of the round window membrane by a 0.2 mm platinum wire leads to an instant loss of the inner ear functions. The membrane defect healed in a few days, the cochlear structures remained intact, and the compound action potential of the auditory nerve and the brain-stem responses could be evoked again with normal latency times within 2 weeks. 1. In the studies reported here we first carried out microperforations with a 1 micron needle electrode, which caused no changes of the hearing potentials (cochlear microphonics, compound action potential of the auditory nerve, brain-stem responses), and no visible defect of the round window membrane and no perilymph outflow. 2. The removal of the round window membrane and the withdrawal of the perilymph led to a loss of the cochlear microphonics and to a considerable increase of the latency times of wave I (Jewett). The hearing potential regained their original values after 2 weeks without closure of the round window niche. The round window membrane had regenerated spontaneously and the scala tympani was again filled with perilymph. After covering the round window niche with a connective tissue graft, the hearing potentials regained their original values after 2 weeks, as they had done without cover of the round window niche. The round window membrane regenerated below the tissue graft and the scala tympani was also filled again with perilymph.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Cytochalasin D suppresses sound evoked potentials in the guinea pig cochlea.

Cytochalasin D (CD), an inhibitor of actin polymerization, was perfused through the guinea pig cochlea while monitoring various cochlear potentials. CD (10(-7)-10(-5) M) reduced the magnitude of the compound action potential of the cochlear nerve and the summating potential, and increased N1 latency. The cochlear microphonic potential was the least sensitive potential with only a slight effect being observed at 10(-5) M. The results are consistent with the hypothesis that actin has a role in cochlear function.

Actins↗
PubMed1990

[Narrow-band action potentials of the guinea-pig cochlea as compared with the ordinary electrocochleograms under normal and pathological conditions].

The narrow-band action potentials (NAP) and the ordinary electrocochleograms were recorded from the guinea-pig cochlea under normal and pathological conditions in order to study whether the NAP could be a useful measure to detect cochlear dysfunctions. The cochlea damaged either by the administration of kanamycin or by a mechanical lesion of the round window served as pathological materials. Recordings showed that the threshold and amplitude measured for the N1 potential of NAPs ran in parallel with those of the cochlear microphonic potentials (CM), under both normal and pathological conditions of the cochlea. This implies that the CM could be replaced by the NAP when difficulties were present in recording CMs. It may be inferred that the NAP reflects responses of the inner hair-cells and cochlear nerves, while the CM would mainly be derived from responses of the outer hair-cells to the frequency-specific movements of the basilar membrane. If so, the NAP should offer a good means for the objective audiometry. Recording NAPs is also superior to the ordinary electrocochleography in that the method makes it possible to obtain responses generated near the apex of the cochlea, i.e., responses to low-pitch sound stimuli.

Action Potentials↗