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作 者:夏寅[1] 龙海珊[1] 韩德民[1,2] 龚树生[1] 雷厉[1] 史金凤[1] 范尔仲[2] 李颖[2] 赵庆[3]
机构地区:[1]首都医科大学附属北京同仁医院耳鼻咽喉头颈外科首都医科大学耳鼻咽喉头颈科学教育部重点实验室,北京100730 [2]北京市耳鼻咽喉科研究所 [3]中国医学科学院基础研究所
出 处:《临床耳鼻咽喉头颈外科杂志》2009年第4期174-177,共4页Journal of Clinical Otorhinolaryngology Head And Neck Surgery
基 金:国家“十五”科技攻关项目(No:2004BA720A18-02);北京市自然科学基金资助项目(No:7031001,No:7212008);首都医学发展科研基金资助项目(No:2003-1013)
摘 要:目的:通过神经损伤性噪声引起4周昆明小鼠出现暂时性阈移(TTS)和永久性阈移(PTS),探讨听觉通路N-甲基D-天冬氨酸受体(NMDAR)活性调节耳蜗螺旋神经节(CG)磷酸化c-Jun变化。方法:采用30只昆明小鼠制作噪声性聋动物模型,进行听觉脑干诱发反应听力检测,并采用免疫组织化学对耳蜗听觉通路中NMDAR关键成分(磷酸化c-Jun)的表达进行检测。结果:噪声性聋诱导PTS后8h、48h、7d、14dCG磷酸化c-Jun的相对吸收度值明显增加,而阳性细胞数依次减少。噪声性聋诱导PTS前后立即腹膜腔注射MK-801引起相似改变。而诱导TTS后48h则降至正常水平。结论:磷酸化c-Jun在噪声性聋后表达的增加具有时间相关性;MK-801通过阻断噪声暴露后传入神经递质谷氨酸,减少突触后钙内流所致的兴奋性毒性,从而保护听觉神经。因此,NMDAR可能参与了内耳损伤。Objective: To investigate the mechanism of hearing pathway NMDAR regulating the changes of phosphorylated c- Jun expression in spiral ganglion after exposed Kunming mice to neural injury noise stimulation to induce permanent or temporary threshold shift. Method:To compare the different expressions of the key compo- nents (phosphorylated c-Jun) of NMDAR signal pathway during neural iniury stimulation by Immunohistoehemistry in CG. Result:The levels of phosphorylated c-Jun remarkably increased in the spiral ganglion after 8 h, 48 h, 7 d and 14 d following noise trauma induced permanent threshold shift (PTS), and the numbers of positive cells reduced gradually. The similar changes occur in mice treated with MK-801 30 minutes before and after 3 h trauma induced PTS. After 48 h of noise induced TTS, the expression of Phosphorylated c -Jun return the level of normal control. Conclusion:The expressions of phosphorylated c-Jun are time-related and uniform in the time and position in CG after noise trauma. MK-801 can alleviate the damage of noise trauma by altered the NMDA receptor-media ted calcium influx. Therefore, the NMDA receptors may involved in the damage of inner ear in common.
关 键 词:噪声性聋 暂时性阈移 永久性阈移 免疫细胞化学 螺旋神经节
分 类 号:R764.43[医药卫生—耳鼻咽喉科]
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