Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Acute changes in cochlear potentials due to cisplatin.

N Tsukasaki1, C A Whitworth, L P Rybak

  • 1Department of Surgery, Southern Illinois University School of Medicine,Springfield, IL 62794-9638, USA.

Hearing Research
|October 18, 2000
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Short interfering RNA against STAT1 attenuates cisplatin-induced ototoxicity in the rat by suppressing inflammation.

Cell death & disease·2011
Same author

Ototoxicity.

Kidney international·2007
Same author

Expression of the kidney injury molecule 1 in the rat cochlea and induction by cisplatin.

Neuroscience·2006
Same author

Time response of carboplatin-induced hearing loss in rat.

Hearing research·2004
Same author

Carboplatin-induced oxidative stress in rat cochlea.

Hearing research·2001
Same author

Pharmacological antagonism of the slow-activating delayed rectifying potassium channel (I(Ks)) has no effect on cochlear structure and function in vivo.

Pharmacology & toxicology·2001
Same journal

Multivariate prediction of conductive dysfunction in well and NICU newborns using wideband acoustic immittance with acoustic reflex tests.

Hearing research·2026
Same journal

TGF-β signaling regulates flat epithelium formation in severely injured adult mouse utricle through epithelial-mesenchymal transition.

Hearing research·2026
Same journal

Membrane scaffolding in auditory hair cells - a molecular tightrope walk enables lateral wall stiffness and flexibility.

Hearing research·2026
Same journal

Speech-in-noise recognition during hearing protector use: Human performance and acoustic prediction.

Hearing research·2026
Same journal

Estimation of hair cell loss from audiograms.

Hearing research·2026
Same journal

Cochlear size variation in a large-scale international multicentre cohort.

Hearing research·2026
See all related articles

Cisplatin ototoxicity rapidly reduces cochlear function, indicated by decreased endocochlear potential (EP) and cochlear microphonics (CM). Early changes stem from stria vascularis alterations, preceding significant hair cell damage.

Area of Science:

  • Ototoxicity research
  • Auditory neuroscience
  • Inner ear physiology

Background:

  • Cisplatin is a common chemotherapy agent with known ototoxic side effects.
  • The precise early mechanisms of cisplatin-induced hearing loss are not fully understood.
  • Hair cells and stria vascularis are critical for auditory function and are potential targets of ototoxicity.

Purpose of the Study:

  • To investigate the early effects of cisplatin on hair cells and the stria vascularis.
  • To simultaneously observe the impact of cisplatin on endocochlear potential (EP) and cochlear microphonics (CM).
  • To correlate electrophysiological changes with morphological alterations in the cochlea.

Main Methods:

  • Adult chinchillas were treated with topical cisplatin or saline on the round window.

Related Experiment Videos

  • Endocochlear potential (EP) and cochlear microphonics (CM) were recorded for 12-14 hours.
  • Scanning electron microscopy was used to assess morphological changes in cochlear structures.
  • Main Results:

    • A profound reduction in both EP and CM amplitudes was observed within 12-14 hours.
    • A strong correlation existed between EP and CM amplitude reductions.
    • Minimal outer hair cell degeneration was noted at 12-14 hours, despite significant functional decline.

    Conclusions:

    • Early cisplatin ototoxicity primarily affects cochlear function through stria vascularis alterations, leading to EP reduction.
    • Subsequent hair cell damage contributes to later-stage cochlear dysfunction.
    • These findings highlight the stria vascularis as an early target in cisplatin-induced ototoxicity.