耳聋是重要的感觉系统疾病，严重影响人们的工作生活。1978年Kemp发现耳声发射，即人耳在听到声音的同时也向外发出特定的声音。随后的研究发现，耳声发射由耳蜗外毛细胞的电运动产生，Presin是电运动的分子基础，但目前老化耳蜗Prestin在相互作用、动力传递及功能调控等方面仍缺乏直接实验依据。本研究拟以Prestin功能调控为切入点，通过综合运用免疫电镜、原子力显微镜、基因转染、膜片钳及高速影像系统等病理生理学的技术手段，动态观察老化耳蜗外毛细胞及与正常外毛细胞在动力蛋白表达、细胞结构、电运动的强度和频率特性上的异同，揭示老化耳蜗与正常耳蜗主动放大机制功能与结构的异同，阐明老化对听器功能调控方式。以老化耳蜗主动放大机制的研究入手，可以为老年性耳聋的发生机制及治疗提供新理论依据和思路，对提高国民健康水平、改善老年耳聋人群的生活质量具有重要意义。

Age-related hearing loss, or presbycusis, is the cumulative effect of aging on hearing. Also known as presbyacusis, it is defined as a progressive bilateral symmetrical age-related sensorineural hearing loss. The hearing loss is most marked at higher frequencies. Hearing loss that accumulates with age but is caused by factors other than normal aging is not presbycusis, although differentiating the individual effects of multiple causes of hearing loss can be difficult. The detection of high-pitched sounds becomes more difficult, and speech perception is affected, particularly of sibilantsand fricatives. Both ears tend to be affected. Despite this, age-related hearing loss may only become noticeable later in life. The effects of age can be exacerbated by exposure to environmental noise, whether at work or in leisure time (shooting, music, etc). Examples of microscopic changes seen in this condition are hair cell degeneration of the cochlea and giant stereociliary degeneration..Siting above the basllar membrane, outer hair cells（OHCs）appear able to perceive its vibration through their mechanosensitive hair bundles and to feed back mechanical forces that enhance both auditory system's sensitivity and its frsquency selectivity．They are mechanical components of the cochlea and have been the subject of many experiments designed to discover just exactly how they generate mechanical forces and how these forces contribute to the micromechanics of the cochlea.Prestin is required for OHC motility and plays a central role in OHC electromotility. Today, we still have no knowledge of Prestin's most nature to the active cochlear. Without definitive information, it is difficult to understand how is alters electromechanical coupleing the OHC in the aged cochlea, how is involved in the mammalian cochlear amplifier. .In this study, we verified whether the function of Deiters cells (DCs) can induce aged cochlear OHCs movement and mediate OHCs electromotility or not. These findings could provide new possible understandings of age-related hearing control and gap junction function in the inner ear.