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PubMed2004

Perilymphatic application of alpha-melanocyte stimulating hormone ameliorates hearing loss caused by systemic administration of cisplatin.

It has previously been demonstrated that ototoxicity induced by systemic administration of cisplatin is reduced by concomitant systemic administration of alpha-melanocyte stimulating hormone (alpha-MSH). In this study we investigated the effects of cochlear, perilymphatic application of alpha-MSH during intraperitoneal administration of cisplatin. Guinea pigs, implanted with a round-window electrode, allowing daily monitoring of the compound action potential (CAP), and also implanted with a mini-osmotic pump, pumping at a rate of 0.25 microl/h either physiological saline or alpha-MSH solution (0.02, 2, and 20 microg/ml), were treated daily with a bolus injection of cisplatin (2 mg/kg) until the electrocochleogram showed a persistent decrease in CAP amplitude (> or = 40 dB threshold shift at 8 kHz). Then, cisplatin treatment was stopped, but intracochlear perfusion of alpha-MSH or physiological saline was continued for 10 days to evaluate possible effects of alpha-MSH on the expected recovery. On day 10, the animals were killed and the cochleas were fixed and processed for histological analysis. All groups required 6-7 days of cisplatin to reach the criterion CAP threshold shift. Ten days after cessation of the cisplatin treatment, recovery of the CAP was observed in all groups and at all frequencies, although it was more pronounced at the lower frequencies. With respect to recovery, small statistically significant differences were found between the saline and the alpha-MSH co-treated groups. Histological results showed significantly less outer hair cell (OHC) loss in the group co-treated with 2 microg/ml alpha-MSH as compared to the group co-treated with saline. Since alpha-MSH was directly delivered to the cochlea, the ameliorating effect of alpha-MSH on OHC survival is likely to involve a cochlear target.

Action Potentials↗
PubMed1999

The effects of tone exposure on the inner ear functions in the guinea pig: impact tone vs. steady state tone.

The damage-risk criterion (DRC) for hearing supposes that sound exposure with equal energy implies equal risk for noise-induced hearing loss (NIHL). We measured cochlear microphonics (CM), compound action potential (CAP), endocochlear potential (EP) and K+ ion concentration in the scala media, to see if the same level of Leq24h (impact tone and steady state tone) induced the same physiological changes in the inner ear function or not. Regarding the equal energy principle (EEP), we also examined if the EEP is appropriate or not at exposure of moderate level tone. We also checked how the time interval between impact tones affects or not the inner ear functions at the same Leq24h tone exposure. Therefore we used exposure at 1 pulse/second or 1 pulse/3 seconds and steady state tone exposure at Leq24h=90, 85 and 80 dB. The results are the following. Both steady state and impact tone exposure causes change of the electrophysiological data. First, CM maximum output voltage after exposure to impact tone of 115 dB (Leq24h=90 dB) was lower than after exposure to a 8 kHz steady state tone of 90 dB. CAP threshold (below 10 microV) obtained after the 115 and 110 dB exposure of impact tone were 5-10 dB higher than that of steady state tone of 90 dB. The negative EP induced by impact tone exposures showed the same tendency as the CM experiments. Having more frequent pulses (1 pulse/second vs. to 1 pulse/3 seconds) showed more inhibition. The K+ concentration time course remained similar to the control when the Leq24h was low (80 dB). Impact tone exposure induced stronger effects to the inner ear at exposure of moderate level tone than that of steady state tone of Leq24h.

Acoustic Stimulation↗
PubMed1997

Up-regulation of adenosine receptors in the cochlea by cisplatin.

In a previous study, we have demonstrated the presence of two adenosine receptor (AR) subtypes, namely A1 and A3AR, in the chinchilla cochlea. One or both of these receptors couple to activation of antioxidant enzymes, with resulting decreases in lipid peroxidation. The chemotherapeutic agent, cisplatin, was shown to produce ototoxicity within a few days of administration presumably by generating reactive oxygen species (ROS) and thereby increasing lipid peroxidation. In this study, we focused on whether lipid peroxidation induces hearing loss by assessing the cochlear antioxidant defense system over a shorter time period (24 h) following cisplatin administration. Cisplatin was administered to anesthetized chinchillas by round window membrane application and hearing loss was determined by compound action potential (CAP) and endocochlear potential (EP) 24 and 72 h post-treatment. Elevations in CAP thresholds in response to click and to 2, 4, 8 and 16 kHz tones and decreases in EP were obtained within 24 h of cisplatin treatment. These changes persisted for at least up to 72 h. Measurements of antioxidant enzymes indicate no change in the activities of superoxide dismutase, catalase or glutathione peroxidase, either 24 or 72 h following cisplatin treatment. The levels of malondialdehyde obtained at these time points were equivalent to those obtained from the controls. Furthermore, no difference in cochlear morphology was detectable by scanning electron microscopy at the basal, middle or apical turns of the cochlea within 24 h. By 72 h, however, losses in both inner and outer hair cells were observed in the basal and middle turns of the cochlea. A major finding of this study is that exposure to cisplatin led to a 5-fold up-regulation of [125I]N6-2-[4-amino-3-phenyl]ethyladenosine binding in the cochlea within 24 h, reflecting increases in expression of AR(s) in this tissue. These data indicate a dissociation between cisplatin acute (within 24 h) ototoxicity and lipid peroxidation. Furthermore, up-regulation of AR(s) may represent a rapid compensatory mechanism by the cochlea to counter the toxic effects of increased ROS generated by cisplatin.

Acoustic Stimulation↗
PubMed1987

Endolymph formation in the inner ear of pigeons.

The endolymphatic space of pigeons was studied by using double-barrelled electrodes with a potassium liquid ion exchanger. The K+ activity of the endolymph was 155 mM in the cochlea and 133 mM in the ampulla, respectively. Positive DC potential in the cochlea (+14.5 mV) was much lower than in guinea pigs (+80 mV) whereas in the ampulla of pigeons the DC potential (+7.4 mV) was 2 times higher than that of guinea pigs (+3.9 mV). General application of ethacrynic acid in pigeons induced a weak change in DC potential and no typical intercellular edema in the cochlea and ampulla. Local application of ethacrynic acid and ouabain in the cochlea and ampulla of pigeons induced a negative DC potential of between -30 and -40 mV. This negative DC potential was higher than the anoxia-induced negative potential. Short hypoxia during a drug-induced DC potential resulted in a decrease in DC potential above the diffusion potential. Below the diffusion potential additional hypoxia increased the DC potential independent of the cause of intoxication.

Animals↗
PubMedDate not supplied

Validity of the two-component theory in the production of endocochlear potential.

To evaluate the mechanism of endocochlear potential (EP) and the validity of the two-component theory in its production, we perfused the endolymphatic space of normal and kanamycin-deafened guinea pigs with artificial endolymph containing 50 mM K+. The K+ activities and EP were simultaneously measured with a double-barreled K+ electrode during and after perfusion. The relationship between the magnitude of the electrogenic potential and K+ active transport was calculated and compared between the two groups of animals. The results showed that the positive component of the EP (positive EP) was mainly dependent on K+ active transport in the stria vascularis but included other electrogenic components not dependent on K+ active transport. The K+ and Na+ conductances (Gk and Gna) between the endolymph and perilymph were also calculated in the normal and kanamycin-deafened guinea pigs. The Gk was much lower in kanamycin-deafened guinea pigs but the Gna did not differ between the two groups of animals. The theoretical EP value during anoxia (negative EP) was consistent with that observed in each group. The difference in the negative EP was approximately 30 mV, but the steady-state EP did not differ between groups. It is concluded that EP is probably not the simple mathematical sum of the positive and negative potentials but involves more complex mechanisms.

Animals↗
PubMed1996

Direct effects of intraperilymphatic reactive oxygen species generation on cochlear function.

Reactive oxygen species (ROS) generation may play a role in ototoxicity, however, the specific effects of ROS generation upon cochlear function are unstudied. Therefore, guinea pig cochleas were instilled with artificial perilymph (AP), H2O2, or confirmed generating systems for the superoxide anion (O2-) or the hydroxyl radical (OH.), or with an ROS system plus its respective scavenger -catalase (CAT), superoxide dismutase (SOD) or deferoxamine (DEF). O2- generating system instillation led to significantly greater mean high frequency compound action potential (CAP) threshold shifts at 10 and 120 min post infusion than seen in AP control or SOD/O2- groups. H2O2 group CAP threshold shifts were significantly greater than control and CAT/H2O2 group values at 10 (16-30 kHz), and 120 min (above 12 kHz). OH generating system instillation led to significantly greater CAP threshold shifts at 10 (12-30 kHz) and 120 min (above 6 kHz) than seen in control or DEF/OH groups. No significant CAP differences were found between controls and scavenger/ROS groups. Mean 1.0 microV cochlear microphonic isopotential curve shift values did not systematically differ among groups. The rapid degradation of high frequency CAP threshold sensitivity seen here may provide insight into the portion of cochlear dysfunction which is ROS-mediated following noise, radiation or chemical exposures.

Action Potentials↗
PubMed1980

Effect of modulation of basilar membrane position on the cochlear microphonic.

Certain characteristics of the extracellular cochlear microphonic (CM) recorded by intracochlear electrodes change in a bimodal manner as a function of prior acoustic exposure, intensity of stimulation, or stimulus frequency. In the present study, it is shown that biasing the basilar membrane position toward scala tympani serves to enhance the CM amplitude when the cochlea is unfatigued, when low-intensity stimuli are used, or when frequencies below the best frequency of a differential electrode pair are used. Conversely, after acoustic fatigue, or during high-intensity or high-frequency stimulation, the microphonic potential is enhanced by a movement of the basilar membrane toward the scala vestibuli. The two populations of hair cells, whose responses are enhanced and diminished on opposing positions of the basilar membrane, are probably outer and inner hair cells.

Acoustic Stimulation↗
PubMed2005

The cochlear targets of cisplatin: an electrophysiological and morphological time-sequence study.

Cisplatin ototoxicity has at least three major targets in the cochlea: the stria vascularis, the organ of Corti, and the spiral ganglion. This study aims to differentiate between these three targets. In particular, we address the question of whether the effects at the level of the organ of Corti and spiral ganglion are mutually dependent or whether they develop in parallel. This question was approached by studying the ototoxic effects while they develop electrophysiologically and comparing these to earlier presented histological data [Van Ruijven et al., 2004. Hear. Res. 197, 44-54]. Guinea pigs were treated with intraperitoneal injections of cisplatin at a dose of 2 mg/kg/day for either 4, 6, or 8 consecutive days. This time sequence has not revealed any evidence of one ototoxic process triggering another. Therefore, we have to stay with the conclusion of Van Ruijven et al. (2004) that both processes run in parallel.

Action Potentials↗
PubMed1995

Nitroprusside suppresses cochlear potentials and outer hair cell responses.

Biochemical and pharmacological evidence supports a role for nitric oxide (NO) in the cochlea. In the present experiments, we tested sodium nitroprusside (SNP), an NO donor, applied by intracochlear perfusions on sound-evoked responses of the cochlea (CM, cochlear microphonic; SP, summating potential; EP, endocochlear potential; CAP, compound action potential) and in vitro on outer hair cell (OHC) voltage-induced length changes and current responses. In vivo application of SNP in increasing concentrations (10, 33, 100, 330 and 1000 microM) reduced all sound-evoked responses starting at about 300 microM. The responses continued to decline after a postdrug wash. At 1 mM SNP decreased EP slowly (approximately 80 min) whereas at 10 mM it reduced EP more rapidly (approximately 20 min). Ferricyanide (1 mM) and S-nitroso-N-acetylpenicillamine (SNAP; 1 mM) had no effect on sound-evoked cochlear potentials. Ferricyanide (1 mM and 10 mM) and ferrocyanide (10 mM) had no effect on EP. In vitro, SNP (10 mM) significantly reduced both OHC voltage-induced length changes and whole-cell outward currents. Results suggest that SNP, possibly acting by released NO, influences cochlear function through effects at the stria vascularis and at the OHCs.

Acoustic Stimulation↗