Permanent threshold shift caused by acute cochlear mitochondrial dysfunction is primarily mediated by degeneration of the lateral wall of the cochlea

Yasuhide Okamoto, Noriyuki Hoya, Kazusaku Kamiya, Masato Fujii, Kaoru Ogawa, Tatsuo Matsunaga

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)220-233
Number of pages14
JournalAudiology and Neurotology
Volume10
Issue number4
DOIs
Publication statusPublished - 2005 Jul 1

Keywords

  • 3-Nitropropionic acid
  • Cochlea
  • Mitochondrial dysfunction
  • Permanent threshold shift
  • Rat
  • Spiral ligament
  • Spiral prominence
  • Stria vascularis

ASJC Scopus subject areas

  • Physiology
  • Otorhinolaryngology
  • Sensory Systems
  • Speech and Hearing

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