Simultaneously reduced NKCC1 and Na,K-ATPase expression in murine cochlear lateral wall contribute to conservation of endocochlear potential following a sensorineural hearing loss

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• 作者：Hao Xiong^a ; Hanqi Chu^a ; ^{qi7chu@163.com} ; Xiaoqin Zhou^b ; Xiaowen Huang^a ; Yonghua Cui^a ; Liangqiang Zhou^a ; Jin Chen^a ; Jianling Li^a ; Yan Wang^a ; Qingguo Chen^a ; Zhiyong Li^a
• 关键词：Stria vascularis ; Endocochlear potential ; Aminoglycoside ; Potassium transport
• 刊名：Neuroscience Letters
• 出版年：2011
• 出版时间：20 January 2011
• 年：2011
• 卷：488
• 期：2
• 页码：204-209
• 全文大小：628 K

文摘

The mechanisms of the response in the murine cochlear lateral wall following sensorineural hearing loss (SNHL) are poorly understood. We focused on comparing the endocochlear potential (EP) with morphological changes in the lateral wall and expression of four important potassium (K⁺) transporters in a mouse model of SNHL induced by co-administration of aminoglycoside and loop diuretic. The expression of the α1 and α2 isoforms of Na,K-ATPase, Na–K–2Cl-Cotransporter-1 (NKCC1) and potassium channel KCNQ1 was assessed. The EP showed a significant decline at 12 h post-treatment followed by complete recovery by 2 days post-treatment. The EP was maintained at near normal levels in animals deafened for periods up to 112 days. Despite this recovery, there was a significant and progressive decrease in the thickness of the stria vascularis, which was predominantly due to atrophy of marginal cells. Both protein and mRNA expression of α1 and α2 isoforms of Na,K-ATPase and NKCC1 in the lateral wall were dramatically reduced following a long-term deafening. KCNQ1 expression remained unchanged. These observations provide insight into the detailed mechanisms of EP modulation following SNHL and may have crucial implications in the future treatment of aminoglycoside-induced hearing loss.