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
Neuroreportjournal_title
Neuroreportauthors
Hoya N,Okamoto Y,Kamiya K,Fujii M,Matsunaga Tdoi
10.1097/01.wnr.0000133226.94662.80subject
Has Abstractpub_date
2004-07-19 00:00:00pages
1597-600issue
10eissn
0959-4965issn
1473-558Xpii
00001756-200407190-00013journal_volume
15pub_type
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