Early changes in the cochlear duct from ethacrynic ACID: An electronmicroscopic evaluation

Quick, Cedric A.; Duvall, Arndt J.

doi:10.1288/00005537-197006000-00009

Cited by 133 publications

(29 citation statements)

References 11 publications

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“…For example, inhibition of the Na-K-Cl cotransporter with loop diuretics or mutations in the gene encoding the Na-K-Cl cotransporter reduces endocochlear potential, results in hearing loss and in an enlarged intrastrial space much like we found in the present study [Flagella et al, 1999;Quick and Duvall, 1970]. Another example that parallels our results is the Brn-4 gene-deficient mouse, which exhibits reduced endocochlear potential and hearing loss and shows severe ultrastructural alterations in spiral ligament fibrocytes, including cellular atrophy and a reduction in the number of mitochondria in these cells [Minowa et al, 1999].…”

Section: Discussionsupporting

confidence: 72%

Permanent Threshold Shift Caused by Acute Cochlear Mitochondrial Dysfunction Is Primarily Mediated by Degeneration of the Lateral Wall of the Cochlea

et al. 2005

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Mitochondrial dysfunction in the cochlea is thought to be an important cause of sensorineural hearing loss. Recently, we have established a novel rat model with acute hearing impairment caused by exposure to the mitochondrial toxin 3-nitropropionic acid (3-NP) to analyze the mechanism of cochlear mitochondrial dysfunction. Both permanent and temporary threshold shifts were observed in this model depending on the amount of 3-NP used to induce hearing impairment. In this study, we demonstrate cochlear morphological changes in the permanent threshold shift model. Marked degeneration was detected in type 2 fibrocytes in the spiral prominence, type 4 fibrocytes in the spiral ligament, marginal cells and intermediate cells in the stria vascularis 3 h after 3-NP administration; these changes were progressive for at least 14 days. Less prominent degeneration was detected in type 1 and type 3 fibrocytes in the spiral ligament. These results indicate that permanent threshold shift caused by acute cochlear mitochondrial dysfunction is primarily mediated by cellular degeneration in the lateral wall of the cochlea, and suggest that therapy of cochlear hearing loss due to acute energy failure may be achieved through protection and regeneration of the cochlear lateral wall.

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Section: Discussionsupporting

confidence: 72%

Permanent Threshold Shift Caused by Acute Cochlear Mitochondrial Dysfunction Is Primarily Mediated by Degeneration of the Lateral Wall of the Cochlea

et al. 2005

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“…injection of 40-50 mg/kg furosemide in the guinea pig (Forge, 1976). Ethacrynic acid produces cytopathological changes in the stria vascularis and in the outer hair cells of the basal part of the cochlea in a number of species, including cat (Quick & Duvall, 1970;Mathog, Thomas & Hudson, 1970;Nakai, 1971;Bosher, Smith & Warren, 1973a, b, Silverstein & Begin, 1974Bosher, 1980b). The question therefore arises whether the effect of furosemide on the organ of Corti are secondary to primary effects on the stria, mediated via the endocochlear potential (e.p.).…”

Section: E F Evans and R Klinkementioning

confidence: 99%

The effects of intracochlear and systemic furosemide on the properties of single cochlear nerve fibres in the cat

Evans

Klinke

1982

The Journal of Physiology

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SUMMARY1. 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 offurosemide, 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.

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“…These cells maintain a very high metabolical rate and low energy reserves (10). The electrophysiological data is supported by the morphological picture (11), where cystic changes in the stria vascularis are observed as early as the changes of the EP potentials. The decline of CM and AP is possibly secondary because the polarization of hair cells is lowered (decline of EP).…”

Section: Discussionmentioning

confidence: 69%

“…This experimental information which indicates a rapid onset of EA action manifested in reduction of cochlear potentials may be correlated with clinical observations in which sudden hearing loss results shortly after EA administration. Electron microscope photomicrographs show extensive morphological changes in the stria vascularis shortly after drug administration (vacuolization and cystic swelling) (11). The descriptive diagram of the anatomy and electrophysiology (Fig.…”

Section: Dichloro-4-(2-methylenebutyryl)-phenoxy]acetic Acid Has Beenmentioning

confidence: 99%

Ethacrynic Acid EFFECTS ON THE COCHLEAR POTENTIALS IN NORMAL AND HIGH BLOOD OXYGEN

Prazma¹,

Pecorak²

1975

J. Clin. Invest.

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(Po2), the partial pressure of carbon dioxide (Pco2), and the pH of the blood were measured before EA administration and at the end of the experiment (3 h later) by drawing blood samples from the contralateral carotid artery. Cochlear potentials-endocochlear potential (EP), cochlear microphonics (CM), and action potentials (AP)-were recorded by standard methods from the first turn of the cochlea. Experimental data seem to indicate that elevation of the Po2 to 174-179 mm Hg during relatively high doses of EA treatment prevents the declines in cochlear potentials which were observed in the first and second groups (normal and lower Po.), and preserves active ion transport which is responsible for the generation of cochlear potentials. These data suggest a means by which to reduce the ototoxic effect of EA and possibly indicates a method of treatment for hearing loss which developed after the administration of EA.

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Early changes in the cochlear duct from ethacrynic ACID: An electronmicroscopic evaluation

Cited by 133 publications

References 11 publications

Permanent Threshold Shift Caused by Acute Cochlear Mitochondrial Dysfunction Is Primarily Mediated by Degeneration of the Lateral Wall of the Cochlea

Permanent Threshold Shift Caused by Acute Cochlear Mitochondrial Dysfunction Is Primarily Mediated by Degeneration of the Lateral Wall of the Cochlea

The effects of intracochlear and systemic furosemide on the properties of single cochlear nerve fibres in the cat

Ethacrynic Acid EFFECTS ON THE COCHLEAR POTENTIALS IN NORMAL AND HIGH BLOOD OXYGEN

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