Ischemia-Reperfusion Injury of the Cochlea: Pharmacological Strategies for Cochlear Protection and Implications of Glutamate and Reactive Oxygen Species

Author(s): Keiji Tabuchi, Bungo Nishimura, Shuho Tanaka, Kentaro Hayashi, Yuki Hirose, Akira Hara.

Journal Name: Current Neuropharmacology

Volume 8 , Issue 2 , 2010

Become EABM
Become Reviewer


A large amount of energy produced by active aerobic metabolism is necessary for the cochlea to maintain its function. This makes the cochlea vulnerable to blockade of cochlear blood flow and interruption of the oxygen supply. Although certain forms of human idiopathic sudden sensorineural hearing loss reportedly arise from ischemic injury, the pathological mechanism of cochlear ischemia-reperfusion injury has not been fully elucidated. Recent animal studies have shed light on the mechanisms of cochlear ischemia-reperfusion injury. It will help in the understanding of the pathology of cochlear ischemia-reperfusion injury to classify this injury into ischemic injury and reperfusion injury. Excitotoxicity, mainly observed during the ischemic period, aggravates the injury of primary auditory neurons. On the other hand, oxidative damage induced by hydroxyl radicals and nitric oxide enhances cochlear reperfusion injury. This article briefly summarizes the generation mechanisms of cochlear ischemia-reperfusion injury and potential therapeutic targets that could be developed for the effective management of this injury type.

Keywords: Cochlea, Blood flow, Ischemia-reperfusion injury, Excitotoxicity, Oxidative damage

Rights & PermissionsPrintExport Cite as

Article Details

Year: 2010
Page: [128 - 134]
Pages: 7
DOI: 10.2174/157015910791233123
Price: $58

Article Metrics

PDF: 1