Vulnerability of the Organ of Corti in Poisoning

Koide, Yasushi; Hata, Atsuo; Hando, Rkiko

doi:10.3109/00016486609127069

Cited by 45 publications

(10 citation statements)

References 8 publications

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“…At no time, however, were respiratory enzyme activity levels in CBA mice as low as those observed in 1.5-month-old C57 mice. These results might not be predicted based on several previous studies that have argued for a direct relationship between cell vulnerability and metabolic activity [Hancock, 1961;Koide et al, 1966]. Hancock [1961], for instance, found that susceptibility to streptomycin damage was reduced in the presence of carbon monoxide or 2-heptyl-4-hydroquinoline-N-oxide, both of which inhibit cellular respiration via the cytochrome system.…”

Section: Dehydrogenase Activity In Ihcs Versus Ohcscontrasting

confidence: 44%

“…Hancock [1961], for instance, found that susceptibility to streptomycin damage was reduced in the presence of carbon monoxide or 2-heptyl-4-hydroquinoline-N-oxide, both of which inhibit cellular respiration via the cytochrome system. One interpretation of these results is that metabolically active cells are more susceptible to damage than cells with low levels of activity [Koide et al, 1964[Koide et al, , 1966. If decreased aerobic metabolism protects HCs from age-related damage as well as from ototoxicity, then C57 mice would be expected to show less HC loss than CBA mice, and HCs of older CBA mice would be less vulnerable than HCs of young CBA mice.…”

Section: Dehydrogenase Activity In Ihcs Versus Ohcsmentioning

confidence: 98%

“…Numerous studies of oxygen metabolism in the cochlea [Hsu, 1992;Koide et al, 1964Koide et al, , 1966Mizukoshi and Daly, 1967;Saito et al, 1995;Spoendlin and Balogh, 1963;Vosteen, 1960;Yang and Han, 1991;Yang et al, 1990] have shown that succinate dehydrogenase (SDH) and other mitochondrial respiratory enzymes, such as cytochrome oxidase, are active in inner hair cells (IHCs), OHCs, Deiters' cells, other supporting cells, spiral ligament, stria vascularis (SV) and spiral ganglion neurons. Acoustic overstimulation [Vosteen, 1960] or administration of ototoxic drugs [Kaku et al, 1973;Koide et al, 1966;Mizukoshi and Daly, 1967] decreases oxygen consumption and reduces SDH activity levels in hair cells (HCs) and/or nerve fibers prior to HC loss.…”

Section: Introductionmentioning

confidence: 99%

“…Acoustic overstimulation [Vosteen, 1960] or administration of ototoxic drugs [Kaku et al, 1973;Koide et al, 1966;Mizukoshi and Daly, 1967] decreases oxygen consumption and reduces SDH activity levels in hair cells (HCs) and/or nerve fibers prior to HC loss. If presbycusis is associated with disturbances of respiratory enzymes in the cochlea, then differences may be observed between C57 mice and CBA mice, and between young, normalhearing CBA mice and old CBA mice with hearing loss.…”

Section: Introductionmentioning

confidence: 99%

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Age- and Strain-Related Differences in Dehydrogenase Activity and Glycogen Levels in CBA and C57 Mouse Cochleas

Ding¹,

McFadden²,

Wang³

et al. 1999

Audiol Neurotol

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In the C57 mouse strain, loss of sensory hair cells (HCs) begins during early adulthood, starting in the base of the cochlea and progressing toward the apex as aging continues. In contrast, the CBA mouse strain exhibits no significant cochlear histopathology until relatively late in life. These strain and age differences may be related to differences in cochlear energy metabolism. To examine this possibility, we used dehydrogenase and glycogen histochemistry to evaluate the metabolic capacities of HCs and stria vascularis (SV) in cochleas of C57 and CBA mice. Reaction product density was quantified and compared as a function of strain (1.5-month-old C57 mice vs. CBA mice) and age (CBA mice, 1.5, 18 and 36 months). Young C57 mice had significantly less HC dehydrogenase activity than CBA mice of any age, lower HC glycogen levels than 18-month-old CBA mice and lower SV glycogen levels than 18- or 36-month-old CBA animals. Within the CBA strain, HC dehydrogenase activity decreased significantly between 1.5 and 18 months of age, while glycogen levels in both HCs and SV increased over the same time period. Between 18 and 36 months, HC dehydrogenase activity and SV glycogen levels remained stable. The results show that there are significant age-related changes in energy metabolism in the inner ear of CBA mice that are correlated with age-related hearing loss. Genetically determined deficits in cochlear metabolic capacity in C57 mice could be linked to the early onset of hearing loss in this strain.

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Section: Dehydrogenase Activity In Ihcs Versus Ohcscontrasting

confidence: 44%

Section: Dehydrogenase Activity In Ihcs Versus Ohcsmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Age- and Strain-Related Differences in Dehydrogenase Activity and Glycogen Levels in CBA and C57 Mouse Cochleas

Ding¹,

McFadden²,

Wang³

et al. 1999

Audiol Neurotol

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“…Also, Bowman, Dolgin & Coulson (1973) found that diuretic doses of ethacrynic acid were insufficient to block glycolysis. As far as oxidative processes are concerned, Brown (1975) argues that because chloramphenicol produces suppression of cochlear respiratory enzyme activity (Koide, Hata & Hando, 1966) without substantial ototoxic effects in guinea pig and cat (e.g. Patterson & Gulick, 1963), it is unlikely that suppression of cochlear respiratory enzyme activity is the primary mechanism whereby ethacrynic acid (and by implication, furosemide) exerts ototoxic effects.…”

Section: Discussionmentioning

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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