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1.
The electrically evoked somatic motility of outer hair cells (OHC), briefly termed OHC electromotility, plays a crucial role in cochlear amplification that underlies the remarkably high sensitivity and frequency selectivity of the mammalian hearing. Accompanying OHC electromotility is a voltage-dependent gating charge movement within the cell lateral membrane, manifested as a measurable nonlinear capacitance (NLC) in OHCs. The electromotility and NLC of OHCs are highly correlated by sharing a common molecular substrate, the motor protein prestin. In this study, we systematically characterized the quantitative relationship between OHC electromotility and NLC in their voltage dependences for the purpose of further understanding the electromechanical transduction in OHCs. The results demonstrated that the two possess differing voltage dependences with the V1/2 of electromotility consistently being ~20 mV depolarized in comparison with that of NLC although their slope factors α are statistically identical. Further investigations showed that the initial state of OHCs influences the voltage dependence of electromotility but not that of NLC, indicating that some biophysical factors other than the motor protein per se are involved in the process of OHC length changes. We proposed that the cytoskeletal spectrin-actin framework underneath the OHC plasma membrane and the cell’s turgor are the two most probable factors that cause the voltage-dependence discrepancy between OHC electromotility and NLC.  相似文献   
2.
目的 探讨电离辐射下大鼠耳蜗外毛细胞Prestin蛋白表达的改变及意义.方法 建立大鼠耳放射损伤模型,检测其听力复合动作电位(CAP)阈值及畸变产物耳声发射(DPOAEs)幅值,验证其电离辐射晚期感音神经性耳聋(SNHL)的发生.提取大鼠耳蜗组织mRNA及蛋白,荧光实时定量PCR检测耳蜗Prestin蛋白mRNA水平的...  相似文献   
3.

Purpose

To evaluate prestin as a biomarker for the identification of early ototoxicity.

Materials and methods

Rats (n?=?47) were randomly assigned to five groups: low-dose (LAG) or high-dose (HAG) amikacin (200 and 600?mg/kg/day, respectively, for 10?days), low-dose (LCIS)or high-dose (HCIS) cisplatin (single doses of 5 and 15?mg/kg, respectively, for 3?days), and control (n?=?8). At the end of the experiment, measurement of distortion product-evoked otoacoustic emissions (DPOAE) were performed to evaluate hearing, then blood samples and both ear tissues were collected under anesthesia. Prestin levels were determined by ELISA. Cochlear damage was evaluated histologically using a 4-point scoring system.

Results

The mean serum prestin levels were 377.0?±?135.3, 411.3?±?73.1, 512.6?±?106.0, 455.0?±?74.2 and 555.3?±?47.9?pg/ml for control, LCIS, HCIS, LAG and HAG groups, respectively. There was significant difference between prestin levels of Control–LCIS-HCIS groups (p?=?0.031) and prestin levels of Control-LAG-HAG groups (p?=?0.003). There were also significant differences in prestin levels between the low- and high-dose cisplatin and amikacin groups (p?=?0.028 and p?=?0.011, respectively). Each group had significantly lower DPOAE results at 4, 6 and 8?kHz than control groups (p?<?0.001). The LAG, HAG, LCIS and HCIS groups had significantly higher cochlear damage scores than the control group (p?<?0.05).

Conclusions

Higher doses of cisplatin and amikacin were associated with the greatest increases in serum prestin level and cochlear damage score. The results of this study suggest that prestin is a promising early indicator of cochlear damage.  相似文献   
4.
目的探讨电离辐射下大鼠耳蜗外毛细胞Prestin蛋白表达的改变及意义。方法建立大鼠耳放射损伤模型,检测其听力复合动作电位(CAP)阈值及畸变产物耳声发射(DPOAEs)幅值,验证其电离辐射晚期感音神经性耳聋(SNHL)的发生。提取大鼠耳蜗组织mRNA及蛋白,荧光实时定量PCR检测耳蜗Prestin蛋白mRNA水平的表达,以及Western杂交检测Prestin蛋白水平的表达。结果成功建立了电离辐射晚期SNHL大鼠模型,其耳蜗Prestin蛋白无论是mRNA表达水平还是蛋白表达水平均较未照射组明显降低。结论放疗晚期感音神经性耳聋的发生机制可能与电离辐射导致内耳外毛细胞Prestin蛋白的表达异常有关。  相似文献   
5.
6.
目的探讨噪声性听力损失(NIHL)与耳蜗外毛细胞Prestin蛋白表达的关系。方法将60只成年豚鼠随机分5组,除对照组外分别予以不同噪声声压级(85、95、105、115 d B SPL)的高斯白噪声暴露(28 d,6 h/d),而后检测听性脑干反应(ABR)以确定听阈位移水平,同时进行耳蜗病理学检查,采用免疫组化法分析耳蜗外毛细胞Prestin蛋白表达水平。结果各组豚鼠平均永久性听阈位移水平变化随着噪声暴露声压级的增强而增加(F=308.655,P0.01),强噪声声压级组(105 d B SPL)豚鼠的病理形态学显示明显的毛细胞损失,Prestin蛋白表达水平在高于95 d B SPL时随着噪声暴露声压级的增加而上调(F=700.072,P0.01)。结论耳蜗外毛细胞Prestin的表达增高,与耳蜗外毛细胞损失程度有关。  相似文献   
7.

Objectives

To define the clinical association of serum prestin autoantibodies and their impact on prognosis, as specific serum diagnostic markers in patients with idiopathic sudden sensorineural hearing loss (ISSNHL).

Design

Sera from 63 patients with ISSNHL were screened prospectively for the presence of prestin autoantibodies by an enzyme-linked immunosorbent assay (Elisa) test. Serum was assayed for anti-prestin IgG antibodies using recombinant human prestin (SLC26 A5). Demographic, clinical, and audiometric variables were analyzed.

Results

Two patients (3.17%) had demonstrable anti-prestin antibodies in serum (exact 95% CI: ?1.16% to 7.5%). No statistically significant association was found between prestin autoantibodies and demographic or audiologic parameters.

Conclusions

This preliminary and novel study does not support the presence of an active humoral immune reaction against prestin in ISSNHL.  相似文献   
8.
Intracochlear ATP is an important mediator in regulating hearing function. ATP can activate ionotropic purinergic (P2x) and metabotropic purinergic (P2y) receptors to influence cell functions. In this paper, we report that ATP can activate P2x receptors directly to modify outer hair cell (OHC) electromotility, which is an active cochlear amplifier determining hearing sensitivity and frequency selectivity in mammals. We found that ATP, but not UTP, a P2y receptor agonist, reduced the OHC electromotility-associated nonlinear capacitance (NLC) and shifted its voltage dependence to the right (depolarizing) direction. Blockage of the activation of P2x receptors by pyridoxalphosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS), suramin, and 4,4′-diisothiocyanato-stilbene-2,2′-disulfonic acid (DIDS) could block the ATP effect. This modification also required extracellular Ca++ participation. Removal of extracellular Ca++ abolished the ATP effect. However, chelation of intracellular Ca++ concentration by a fast calcium-chelating reagent 1,2-bis(o-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (BAPTA, 10 mM) did not affect the effect of ATP on NLC. The effect is also independent of K+ ions. Substitution of Cs+ for intracellular or extracellular K+ did not affect the ATP effect. Our findings indicate that ATP activates P2x receptors instead of P2y receptors to modify OHC electromotility. Extracellular Ca++ is required for this modification.  相似文献   
9.
10.
Prestin基因敲除小鼠听力和毛细胞改变的相关性研究   总被引:1,自引:0,他引:1  
目的研究发育和成熟过程中的prestin基因敲除小鼠听力特征,比较其听力损害和外毛细胞(OHC)丧失的相关性,初步探讨OHC丧失的机制.方法利用听性脑干反应(ABR)、抗小鼠耳蜗毛细胞特异性的肌浆球蛋白7a(Mysojn 7a)抗体免疫染色和耳蜗连续切片观察出生后(postnatal,P)14天(P14)~P56的prestin基因敲除纯合子(prestin-/-)、杂合子(prestin /-)和野生型(prestin / )小鼠听阈、耳蜗毛细胞和Corti器的改变.结果P14的prestin-/-小鼠听阈较prestin / 升高25 dB SPL,至P21和P28,听阈分别提高49 dB和52 dB,P35后听阈改变不明显.在P21的prestin-/-小鼠,32 kHz听阈提高46 dB;prestin /-也显示约3.5 dB的听阈升高(p<0.0001).Prestin-/-小鼠在P28以前无明显的OHC丧失,但是,OHC的长度较prestin / 明显缩短,P28以后,OHC丧失进行性加重.内毛细胞(IHC)丧失明显延迟和轻于OHC.结论Prestin-/-小鼠在毛细胞丧失之前呈现明显的听力损害,OHC的丧失可能与其本身的结构改变和成熟过程中的代谢异常有关.  相似文献   
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