[The relationship of endocochlear DC potential to cochlear microphonics elucidated by the change of resistance of basal membrane in guinea-pig cochlea (author's transl)].
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Animals↗
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Results for “Cochlear Microphonic Potentials”
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Reversible cisplatin ototoxicity in the albino guinea pig.
Guinea pigs implanted with round window electrodes received daily doses (2.0 mg/kg) of cisplatin until a profound hearing loss occurred (> 40 dB at 8 kHz). Afterwards, pronounced recovery occurred. Recovery progressed over intervals up to 3 weeks before it saturated. Loss and recovery involved both the compound action potential and, less pronounced, the cochlear microphonics. Cochlear potentials evoked by lower frequencies recovered more fully than those evoked by higher frequencies. Loss and recovery was found also in the endocochlear potential. Outer hair cell counts did not change over the recovery period. These findings confirm our previously reported results on the reversibility of cisplatin damage. Further, they implicate the vascular stria as an important target for cisplatin in the cochlea.
Action Potentials↗
Non-linear aspects of outer hair cell transduction and the temporary threshold shifts after acoustic trauma.
The 200-Hz cochlear microphonic potential (CM) and the compound action potential (CAP) of the auditory nerve evoked by tone-bursts were recorded in the basal turn of the cochlea of anaesthetised guinea pigs, before and after exposure to traumatic high-frequency tones that produce a temporary threshold shift (TTS) in this cochlear region. The drop in CM and the TTS were highly correlated, suggesting that it is the disruption of the outer hair cells generating the CM that causes the TTS. The previously measured rise in endocochlear potential and drop in organ of Corti K+ levels suggest that the TTS is due to a temporary closure of outer hair cell mechanoelectrical transduction (MET) channels, which produces a drop in the mechanical sensitivity of the organ of Corti, due to disruption of the active process provided by outer hair cells. The time course of the onset and recovery of TTS is consistent with a kinetic folding and refolding of MET channels over a time course of hours and days. Mathematical modelling of this putative channel folding suggests that TTS recovery may be accelerated by the presentation of additional sounds during the recovery period. We present electrophysiological data (CM and CAP measurements) showing that this accelerated recovery occurs. Using two-tone complexes (phase-locked 5- and 10-kHz traumatic tones, and 10-kHz traumatic tones with 25-Hz bias tones), we also show that the mechanisms producing TTS are non-linear and asymmetric, and that the greatest 'trauma' occurs when the hair bundles of outer hair cells are deflected away from the basal body of these cells (i.e. in the direction normally causing hyperpolarisation of the cell membrane potential).
Animals↗
[Changes of cochlear electrical activities in early experimental hydrolabyrinth].
Changes of endocochlear potential (EP), cochlear microphonic potential (CM) and summating potential (SP) were studied in guinea pig cochlea after four weeks blockade of the endolymphatic sac and duct. The EP, CM and SP were measured with a microelectrode through the spiral ligament of the first turn. EP was decreased by 15%. The minimum CM output produced by tone burst of six frequencies (0.5, 1, 2, 4, 5 and 8 KHz) had reduced by 83.1%, 82.4%, 84.5%, 84.2%, 47.2% and 54.2% respectively, and the maximum CM output had declined by 54.3%, 41%, 43.2%, 21.1%, 26% and 24% separately. The minimum SP output caused by 4, 5 KHz tone burst had declined by 62.4% and 70.5%, and the maximum SP output had decreased by 41.5%, 45.2% in the early experiments. These results indicate that EP, CM and SP all underwent decreases. The extent of CM declination at low frequencies was larger than that at the high frequencies in the early experiments. The mechanisms of influence on EP, CM and SP in early experimental endolymphatic hydrops are discussed.
Action Potentials↗
Changes of the action potential, the summating potential and cochlear microphonics in experimental endolymphatic hydrops.
The changes of the action potential (AP), the summating potential (SP) and cochlear microphonics (CM) were investigated in reference to the grade of endolymphatic hydrops produced by endolymphatic sac obliteration in guinea pigs. In a few cases with minimum endolymphatic hydrops, super-normal AP was obtained. With an increase of endolymphatic hydrops, CM responses were reduced although AP responses at intensive stimulation were maintained relatively well. It is thought that the polarity of positive SP, as observed in control, was influenced to deflect towards negative SP by an interaction between the increased degree of endolymphatic hydrops and the changes of the biochemical components of the inner ear fluids.
Action Potentials↗
The effects of intracochlear and systemic furosemide on the properties of single cochlear nerve fibres in the cat.
1. Tuning properties and spontaneous discharge rate of single cochlear fibres in the anaesthetized cat were determined during short- and long-term poisoning of the cochlea by locally and systemically applied furosemide.2. With intra-arterial administration of furosemide, short-term reversible elevation occurred of the low threshold sharply tuned ;tip' segment of the frequency threshold (;tuning') curve (f.t.c.) by up to 40 db, without substantial changes in the threshold of the low frequency ;tail' segment of the f.t.c. These changes could occur in part without changes in the spontaneous activity and entirely without changes in the maximal evoked activity. These effects were observed in all fibres examined, the characteristic frequencies of which ranged from 3.5 to 31 kHz.3. Intracochlear administration of furosemide in 0.9 mM concentrations produced similar changes, but these were not reversible.4. The changes correlated with the depression of the amplitude of the gross cochlear action potential. The cochlear microphonic potential, however, was either unchanged, or only slightly reduced.5. In long-term furosemide poisoning of the cochlea, fibres with anomalous response properties were found alongside fibres having normal tuning. The former exhibited either reduced excitability of the low threshold tip segment, or a tip segment attenuated in both excitability and threshold.6. It is concluded that the selective effects of furosemide on the tip segment of cochlear fibre f.t.c.s offer further evidence for a physiologically vulnerable ;second filter' in the cochlea. The selective influence of the furosemide on the low threshold tip segment provides support for the hypothesis that the normal f.t.c. is generated by two largely independent processes: one vulnerable, low threshold and sharply tuned, and the other less vulnerable, but high threshold and more broadly tuned.7. The findings, obtained with an agent known to produce reversible impairment of hearing in man, provide direct physiological evidence in support of the hypothesis that in sensorineural hearing loss of cochlear origin the frequency selectivity of cochlear nerve fibres is impaired.
Action Potentials↗
[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↗
Compound action potential and cochlear microphonic extracted from electrocochleographic responses to condensation or rarefaction clicks.
In electrocochleography (ECochG) compound action potential (CAP) and summation potential (SP) are usually separated from the cochlear microphonic (CM) by the CM cancellation technique consisting in averaging the responses evoked by rarefaction and condensation clicks. With the aim of analysing the ECochG responses evoked by monophasic clicks, we developed a numerical method based on the theory of optimal filtering, which makes no assumptions about the unknown potentials. The application of the filtering technique to the ECochG recordings obtained from 6 normally hearing children and 10 children with cochlear hearing loss allowed us to perform CAP extraction in cases where CM was not cancelled by the conventional method. Differences in SP amplitude and polarity were found between rarefaction and condensation click-evoked responses in cochlear hearing losses.
Acoustic Stimulation↗
Phosphorothioate oligodeoxynucleotides can selectively alter neuronal activity in the cochlea.
A growing body of evidence indicates that extracellular adenosine triphosphate (ATP) may have a major role in cochlear function. Antagonists of ionotropic ATP receptors (P2X2) have significant effects on cochlear potentials and distortion product otoacoustic emissions (DPOAEs). We tested whether antisense oligodeoxynucleotides (ODNs) would mimic the functional deficiencies induced by the ATP antagonists through binding to P2X2 ATP receptor mRNA and thereby reduce the number of ATP receptors expressed in the membrane of the cells. Both a phosphorothioate ODN (S-ODN) antisense and a phosphodiester ODN (P-ODN) antisense to the P2X2 sequence and random sense ODNs containing 21 nucleotides were administered chronically (7 days) to the guinea pig cochlea via the perilymph compartment. Sound evoked cochlear potentials (cochlear microphonic; summating potential; compound action potential of the auditory nerve, CAP; latency of the first negative peak in the CAP, N1 latency) and DPOAEs were monitored to assess the effects of the ODNs. Results indicate that the phosphorothioate derivatives of both the antisense and random sense ODNs suppressed the CAP and prolonged the N1 latency with no significant effect on the other parameters. The P-ODNs had no effect. Since both the antisense and random sense S-ODNs had the same effect, we conclude that the S-ODNs affected neuronal function in a manner that did not involve binding to the ATP receptor mRNA.
Adenosine Triphosphate↗
Brainstem auditory evoked potentials and cochlear microphonics in the HMSN family with auditory neuropathy.
UNLABELLED: The aim of this work was to assess the hearing impairment in patients with hereditary motor and sensory neuropathy (HMSN). Elevation of pure tone thresholds in the presence of preserved inner ear function as suggested by cochlear microphonics (CM), absent or markedly abnormal brainstem auditory evoked potentials (BAEP), and elevation of speech perception out of proportion to the pure tone loss were found in the patients. From 28 members of a Gypsy family, we examined two siblings aged 31 and 30 years and their nephew aged 20 years, all suffering from HMSN that was associated with auditory neuropathy. All three affected members with difficulty of understanding speech had following investigations: pure tone and speech audiograms, BAEP, cochlear microphonics, and nerve conduction studies (NCV). RESULTS: the older two siblings had a flat 80 dB audiogram, whereas the younger one has flat 20 dB audiogram on the Lt. ear and 30 dB audiogram on the Rt. ear. All had no speech comprehension and no BAEP. Two patients had preserved cochlear microphonics on one ear. Peripheral nerves were electrically not elicitable, however, at the beginning of the disease nerve conduction was slow. CONCLUSION: in all three affected members with distinct clinical picture of HMSN their hearing impairment was proved to be due to severe auditory neuropathy in the presence of preserved inner ear function.
Adult↗
Effects of perilymphatically perfused gentamicin on microphonic potential, lipid labeling and morphology of cochlear tissues.
The perilymphatic space of the guinea pig was perfused in situ with artificial perilymph containing [32P] orthophosphate and 3H-glycerol while cochlear microphonic potentials (CM) were monitored. The perfusion of 10 mM gentamicin suppressed CM by 62% within 30 min. 32P-incorporation into phosphatidylinositol bisphosphate in the organ of Corti was decreased but distribution of 3H-glycerol in neutral lipids and phospholipids was not affected by gentamicin. The morphological evaluation included all structures lining the scala media, the spiral ligament, the basal membrane and the vestibular organs. Hair cells sometimes contained small intracellular 'precipitation' lines but, in general, ultrastructure of all tissues was essentially normal and no overt histopathological changes were evident. The observed biochemical changes should, therefore, represent early and primary actions of the drug. This confirms the hypothesis that an interaction with the acidic phospholipid, phosphatidylinositol bisphosphate, is an important step in the ototoxic mechanism of amino-glycoside antibiotics.
Animals↗
Additional pharmacological evidence that endogenous ATP modulates cochlear mechanics.
In the cochlea, outer hair cells (OHCs) generate the active cochlear mechanics whereas the supporting cells, such as Deiters' cells and Hensen's cells, may play a role in both the active and passive cochlear mechanics. The presence of receptors for adenosine triphosphate (ATP) on OHCs, Deiters' cells and Hensen's cells indicates that endogenous ATP may have a role in cochlear mechanics. To explore this possibility, the effects of the ATP antagonist, pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS), were studied in guinea pig both in vitro on isolated OHCs, Deiters' cells, Hensen's cells and pillar cells using the whole-cell configuration of the patch-clamp technique, and in vivo on sound evoked cochlear potentials (cochlear microphonic, CM; summating potential, SP; compound action potential, CAP) and distortion product otoacoustic emissions (DPOAEs) using cochlear perilymphatic perfusion. Results show that PPADS (100 microM) reduced the inward current evoked by 5-10 microM ATP in OHCs, Deiters' cells, Hensen's cells and pillar cells. This effect of PPADS was slow in onset and was slowly reversed to a varying degree in the different cell types. In vivo application of PPADS in increasing concentrations reduced the sound evoked CAP, SP and increased N1 latency starting at about 0.33 mM (SP) and 1 mM (CAP and N1 latency). PPADS (0.33-1 mM) reversibly suppressed the initial value of the quadratic DPOAE and reversed the 'slow decline' in the quadratic DPOAE that occurs during continuous stimulation with moderate level primaries. These results, together with the similar effects of the ATP antagonist suramin reported previously (Skellett et al., 1997), may be evidence that endogenous ATP acting on cells in the organ of Corti alters cochlear mechanics.
Action Potentials↗
Hearing loss in multiple sclerosis: localization of the auditory pathway lesion according to electrocochleographic findings.
Multiple sclerosis is known to affect the myelin of the auditory pathway resulting in acute hearing loss. Two cases of sudden deafness due to multiple sclerosis have been evaluated by conventional audiometry, brainstem auditory evoked response audiometry and transtympanic electrocochleography. The abnormalities of the compound action potential in both patients (enhanced latency, abnormal adaptation using fast stimulus rate) and the normal receptor potentials (cochlear microphonic, summating potential), as well as the absence of brainstem responses suggest a disturbance of synchronization at the level of the first auditory neurone. The electrocochleography provides valuable information for the topodiagnosis of this and other neural hearing losses, especially in the absence of reliable brainstem responses.
Adult↗
Glutamate transporters in the guinea-pig cochlea: partial mRNA sequences, cellular expression and functional implications.
In the cochlea, glutamate plays a major role in synaptic transmission between the inner hair cell and the primary auditory neurons. Extracellular glutamate concentration must be regulated to prevent excitotoxicity. This regulation is mediated by excitatory amino acid transporters, membrane proteins that remove glutamate from the synaptic cleft. In this study, we investigated the distribution and activity of three excitatory amino acid transporters subtypes in the guinea-pig cochlea: glutamate aspartate transporter, glutamate transporter and excitatory amino acid carrier. A partial messenger ribonucleic acid sequence was determined for each of these transporters, by polymerase chain reaction with degenerate primers, using guinea-pig brain complementary deoxyribonucleic acid as the template. Primers specific for each transporter were then designed and used to screen a dissected organ of Corti complementary deoxyribonucleic acid library. The cellular distribution of each transporter was examined by immunocytochemistry. We investigated the functional consequences of inhibiting glutamate uptake by recording cochlear potentials during intracochlear perfusion with either l-trans-pyrrolidine-2,4-dicarboxylic acid or dihydrokainate. At the end of the electrophysiological session, cochleas were processed for electron microscopy. Only the glutamate aspartate transporter messenger ribonucleic acid was detected in the organ of Corti. Consistently, glutamate aspartate transporter protein was detected in the inner hair cell-supporting cells and in the ganglion of Corti satellite cells. Glutamate transporter and excitatory amino acid carrier were found in the afferent auditory neurons. Only intracochlear perfusions with l-trans-pyrrolidine-2,4-dicarboxylic acid resulted in a dose-dependent decrease in the amplitude of the cochlear compound action potential, leaving cochlear microphonic potential unaffected. After l-trans-pyrrolidine-2,4-dicarboxylic acid perfusion, cochleas displayed a swelling of the afferent endings typical of excitotoxicity. [(-)1-(4-aminophenyl)-4-methyl-7,8-methylenedioxy-4,5-dihydro-3-methylcarbamyl-2,3-benzodiazepine], a selective alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor antagonist protects the cochlea against l-trans-pyrrolidine-2,4-dicarboxylic acid effect.
Afferent Pathways↗
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↗
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↗
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↗
Cochlear microphonics and action potentials mature and decline at different rates in the normal and pathologic mouse cochlea.
A technique is described that can nontraumatically assess cochlear microphonic (CM) and cochlear action potential (AP) thresholds to pure tones in the intact mouse. This method was applied to the normal hearing CBA/J, and to the C57BL/6J, which has early-onset hearing loss. CM thresholds are most sensitive in both mice by 23 days of age, and the C57BL/6J CM responses degenerate rapidly thereafter, especially at the high-frequency end. The CMs of the CBA/J continue to change past 23 days, developing a threshold dip at 24 kHz, and becoming slightly less sensitive at 32 kHz. The AP of the C57BL/6J is also most sensitive at 23 days, and becomes gradually less sensitive to 32- and 64-kHz tones over the next 36 days. The CBA/J AP thresholds are not maximally sensitive until 41 days of age.
Age Factors↗