A novel animal model of acute cochlear mitochondrial dysfunction.

Abstract:

:Acute mitochondrial dysfunction in the cochlea is likely to result in hearing loss as a consequence of local energy shortage, similar to ischemia- or noise-induced hearing loss. To establish an animal model of acute cochlear mitochondrial dysfunction, we applied a mitochondrial toxin, 3-nitropropionic acid (3-NP) in the rat cochlea. Rats treated with 500mM 3-NP exhibited permanent threshold shifts in acoustic brainstem response while the same volume of 300mM 3-NP caused temporary threshold shifts. Histological examination in the permanent threshold shift model revealed severe degeneration of fibrocytes within spiral ligament and spiral limbus, indicating these cells are vulnerable to acute mitochondrial dysfunction. This model represents a novel tool for investigating the pathophysiology of acute cochlear mitochondrial dysfunction.

journal_name

Neuroreport

journal_title

Neuroreport

authors

Hoya N,Okamoto Y,Kamiya K,Fujii M,Matsunaga T

doi

10.1097/01.wnr.0000133226.94662.80

subject

Has Abstract

pub_date

2004-07-19 00:00:00

pages

1597-600

issue

10

eissn

0959-4965

issn

1473-558X

pii

00001756-200407190-00013

journal_volume

15

pub_type

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