Identification of the nonlinearity governing even-order distortion products in cochlear potentials

Emst, Maarten G. van; Klis, Sjaak F.L.; Smoorenburg, Guido F.

doi:10.1016/s0378-5955(97)00156-1

Cited by 21 publications

(11 citation statements)

References 26 publications

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“…A drop of the endocochlear potential is thought to cause the decline of hair cell current (CM) and cochlear nerve activity. Recording cochlear potentials, West et al (1973), Nourski et al (2004) and McFadden et al (2004) found a recovery of the response within 1 h, which can be attributed to a recovery of the endocochlear potential (Sewell, 1984;Van Emst et al, 1997). This recovery typically lasted only briefly (less than 4 h) and, subsequently, a second decline of the response occurred.…”

Section: First-day Thresholdsmentioning

confidence: 89%

“…This early decline of the cochlear response is attributed to the reversible effect of furosemide, including the smaller effect on the CM than on the CAP (CAP: Sewell, 1984;Hu et al, 2003;CM: West et al, 1973;Van Emst et al, 1997). A drop of the endocochlear potential is thought to cause the decline of hair cell current (CM) and cochlear nerve activity.…”

Section: First-day Thresholdsmentioning

confidence: 99%

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Time course of cochlear electrophysiology and morphology after combined administration of kanamycin and furosemide

et al. 2007

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In animal models of deafness, administration of an aminoglycoside in combination with a loop diuretic is often applied to produce a rapid loss of cochlear hair cells. However, the extent to which surviving hair cells remain functional after such a deafening procedure varies. In a longitudinal electrocochleographical study, we investigated the variability of cochlear function between and within guinea pigs after combined administration of kanamycin and furosemide. Concurrently, histological data were obtained at 1, 2, 4 and 8 weeks after deafening treatment. The main measures in our study were compound action potential (CAP) thresholds, percentage of surviving hair cells and packing density of spiral ganglion cells (SGCs). One day after deafening treatment, we found threshold shifts widely varying among animals from 0 to 100 dB. The variability decreased after 2 days, and in 18 out of 20 animals threshold shifts greater than 55 dB were found 4-7 days after deafening. Remarkably, in the majority of animals, thresholds decreased by up to 25 dB after 7 days indicating functional recovery. As expected, final thresholds were negatively correlated to the percentage of surviving hair cells. Notably, the percentage of surviving hair cells might be predicted on the basis of thresholds observed one day after deafening. SGC packing density, which rapidly decreased with the period after deafening treatment and correlated to the percentage of surviving inner hair cells, was not a determining factor for the CAP thresholds.

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Section: First-day Thresholdsmentioning

confidence: 89%

Section: First-day Thresholdsmentioning

confidence: 99%

Time course of cochlear electrophysiology and morphology after combined administration of kanamycin and furosemide

et al. 2007

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“…The EP was measured as described elsewhere [van Emst et al, 1997]. Briefly, animals were anesthetized with halothane and the bulla was approached ventrolaterally.…”

Section: Electrocochleographymentioning

confidence: 99%

Cisplatin Ototoxicity Involves Organ of Corti, Stria Vascularis and Spiral Ganglion: Modulation by αMSH and ORG 2766

et al. 2003

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It has been shown that αMSH and the nonmelanotropic ACTH/MSH(4–9) analog ORG 2766 can ameliorate cisplatin-induced neurotoxicity and ototoxicity. Here, we investigated whether these peptides delay the occurrence of the cisplatin-induced shift in auditory threshold, and whether they affect the subsequent recovery of cochlear potentials. Chronically implanted round window electrodes were used to obtain daily recordings of auditory nerve compound action potentials (CAP) and cochlear microphonics at frequencies ranging from 2 to 16 kHz. Cisplatin (1.5 mg/kg i.p.) plus αMSH, ORG 2766 (75 µg/kg s.c.), or saline were injected daily until the 40-dB CAP threshold shift at 8 kHz was reached. Endocochlear potential (EP) was measured either 1–2 days or 28 days later, followed by morphometric analysis of the cochlea. Peptide cotreatment did not consistently delay the threshold shift; however, the CAP threshold recovered faster and to a greater extent, with the potency order being αMSH > ORG 2766 > saline. Significant recovery at the 2 highest frequencies was seen in the αMSH-treated animals only. CAP amplitude at high sound pressures, which depends more on nerve function than on outer hair cell (OHC) function, decreased severely in all groups but recovered significantly in the αMSH- and completely in the ORG-2766-cotreated group. EP was significantly lower in the first days after the threshold shift but had completely recovered at 28 days. Morphometric analysis of the spiral ganglion also indicated involvement of ganglion cells. OHC loss was most severe in the basal turn of saline-cotreated animals. These data suggest that the cisplatin-induced acute threshold shift might be due to reversible strial failure, whereas subsequent OHC survival determines the final degree of functional recovery. Both OHC loss and neuronal function were ameliorated by peptide cotreatment.

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“…The addition of a loop diuretic to an aminoglycoside administration has a more than additive ototoxic effect because diuretics facilitate aminoglycosides to pass the blood-cochlea barrier (3Y5); they allow aminoglycosides to more effectively spread through the cochlea by altering the endolymphatic potential (6,7), and they decrease the renal kanamycin clearance (8).…”

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confidence: 99%

Deafness Induction in Mice

Jansen

Bremer²,

Topsakal

et al. 2013

Otology &Amp; Neurotology

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Identification of the nonlinearity governing even-order distortion products in cochlear potentials

Cited by 21 publications

References 26 publications

Time course of cochlear electrophysiology and morphology after combined administration of kanamycin and furosemide

Time course of cochlear electrophysiology and morphology after combined administration of kanamycin and furosemide

Cisplatin Ototoxicity Involves Organ of Corti, Stria Vascularis and Spiral Ganglion: Modulation by αMSH and ORG 2766

Deafness Induction in Mice

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