Aging outer hair cells (OHCs) in the Fischer 344 rat cochlea: Function and morphology
Aging outer hair cells (OHCs) in the Fischer 344 rat cochlea: Function and morphology
复制标题
DOI：
10.1016/j.heares.2008.11.010
复制
发表时间：
2009-02-01
期刊：
影响因子：
2.8
通讯作者：
Henderson, Donald
中科院分区：
文献类型：
--
作者：
Chen, Guang-Di;Li, Manna;Henderson, Donald
如先前报道的[Popelar，J.，Groh，D.，Pelanova，J.，Canlon，B.，Syka，J.，2006. Fischer 344大鼠耳蜗和脑干听觉功能的变化Neurobiol. Aging 27，490-500; Buckiova，D.，Popelar，J.，Syka，J.，2007. F344大鼠老化耳蜗：形态和功能变化。Exp. Gerontol。42，629-638;比勒费尔德，E.C.，Coling，D.，陈光诚Li，M.N.，Tanaka，C.，Hu，B.H.，亨德森博士，2008. Fischer 344/NHsd大鼠亚系中的听力损失。听Res. 241，26-33]，患有严重听力损失的老年Fischer 344（17344）大鼠保留了许多外毛细胞（OHC），特别是在耳蜗的中间转弯处。目前的研究证实了以前的发现，即老年OHC存在，但功能障碍。畸变产物耳声发射（DPOAE），这被认为是反映在体内OHC的运动，在老年大鼠中是不存在的，而大多数OHC（>80%）的存在和形态完整。肌动蛋白染色及光镜检查未见OHC静纤毛损伤。从中间圈记录的12 kHz处的耳蜗微音（CM）仅显示出轻微的年龄相关性降低，表明耳蜗区域中剩余OHC中的正常机械电转导装置具有10-20%的OHC损失。琥珀酸脱氢酶（SDH）的活性，柠檬酸循环和线粒体电子传递链（METC）共享的酶，也在老年OHC的正常水平。重要的是，与年轻对照组相比，老年OHC显示普雷斯廷免疫标记水平降低。结合我们先前的发现，显示血管纹和耳蜗内电位在老年F344大鼠中基本正常[比勒费尔德，E.C.，Coling，D.，陈光诚Li，M.N.，Tanaka，C.，Hu，B.H.，亨德森博士，2008. Fischer 344/NHsd大鼠亚系中的听力损失。听Res. 241，26-33]，结果提示，普雷斯廷的破坏是DPOAE丧失和耳蜗敏感性丧失的主要原因。(C)2008 Elsevier B. V.保留所有权利。
As previously reported [Popelar, J., Groh, D., Pelanova, J., Canlon, B., Syka, J., 2006. Age-related changes in cochlear and brainstern auditory functions in Fischer 344 rats. Neurobiol. Aging 27, 490-500; Buckiova, D., Popelar, J., Syka, J., 2007. Aging cochleas in the F344 rat: morphological and functional changes. Exp. Gerontol. 42, 629-638; Bielefeld, E.C., Coling, D., Chen, G.D., Li, M.N., Tanaka, C., Hu, B.H., Henderson, D., 2008. Age-related hearing loss in the Fischer 344/NHsd rat substrain. Hear. Res. 241, 26-33], aged Fischer 344 (17344) rats with severe hearing loss retain many outer hair cells (OHCs) especially in the middle turn of the cochlea. The current Study confirmed the previous findings showing that aged OHCs were present, but dysfunctional. Distortion product otoacoustic emissions (DPOAE), which are believed to reflect in vivo OHC motility, were absent in the aged rats while the majority of OHCs (>80%) were present and morphologically intact. There was no detectable injury of OHC stereocilia as assessed by actin-staining and examination under the light microscope. Cochlear microphonics (CM) at 12 kHz, recorded from the middle turn, only showed a slight age-related reduction, indicating a normal mechanoelectrical transduction apparatus in the remaining OHCs in the cochlear regions with 10-20% OHC loss. Activities of succinate dehydrogenase (SDH), an enzyme shared by the citric acid cycle and the mitochondrial electron transport chain (METC), were also at normal levels in aged OHCs. Importantly, aged OHCs showed reduced levels of prestin immunolabeling compared to young controls. Together with our previous finding showing that the stria vascularis and endocochlear potential were essentially normal in aged F344 rats [Bielefeld, E.C., Coling, D., Chen, G.D., Li, M.N., Tanaka, C., Hu, B.H., Henderson, D., 2008. Age-related hearing loss in the Fischer 344/NHsd rat substrain. Hear. Res. 241, 26-33], the results Suggest that disruption of prestin is the major cause of DPOAE loss and loss of cochlear sensitivity. (C) 2008 Elsevier B.V. All rights reserved.