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

Department of Otolaryngology-Head and Neck Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Neuroscience Letters (Impact Factor: 2.03). 01/2011; 488(2):204-9. DOI: 10.1016/j.neulet.2010.11.030
Source: PubMed


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 12h 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.

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    • "d Schmiedt , 1992 ) . Morphological changes in the stria may also be associated with treatment by drugs and noise but may not be causal to hearing loss . Strial pathology can be observed after aminoglycoside challenge ( Forge et al . , 1987 ) , but the endocochlear potential remains stable until late in ototoxic treatment ( Komune et al . , 1987 ; Xiong et al . , 2011 ) , negating a functional consequence of such alterations . Cisplatin may affect both strial morphology and function ( Laurell et al . , 2007 ) but at least some of these changes are reversible ( Klis et al . , 2000 ) and therefore not a direct cause of hair cell loss . The effects of noise on lateral wall tissues are variable , probabl"
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