Investigation of noise-induced degeneration of efferent nerve fibers in the mammalian inner ear as cause of hyperacusis

太高的声压级可能会被认为是疼痛。这通常发生在120分贝SPL以上的电平。如果这明显低于这一水平，人们就会说是听觉过敏症。这种对声音的超敏可能是由于内耳结构的损害。在哺乳动物的内耳，神经元信号被转发到大脑，在内耳机械和传出控制之间的极其复杂的相互作用中产生。在本项目中，我们将调查，除了传入连接的变化外，噪声创伤后传出连接的退化是否会导致传入神经元活动的变化，从而导致听力亢进？在哺乳动物的内耳中，有两种感觉细胞，内毛细胞和外毛细胞。OHC具有压电性(电动)，可以在低声压级放大机械信号，或在高声压级衰减机械信号。因此，当声压过高时，OHC参与哺乳动物极其敏感的听力，并有助于保护听力功能。在高声压级的情况下，通过连接到OHC的基极的传出来降低OHC的压电性。噪音创伤导致的神经纤维丢失可能会扰乱这种保护机制，并会产生深远的后果，包括发展为听力过敏症。利用单耳诱发脑干电位和耳声发射(f2-f1)，研究幼年和老年蒙古沙土鼠传出神经纤维的可能变性及其对神经元加工的影响。在这些实验中，传出系统被对侧的噪声激活，因此我们将测试这种激活在噪声创伤前后的影响。此外，我们将记录动物的应力值，以便将机械和神经生理学数据与惊吓反射的行为学研究相关联，这将为我们提供有关听力过敏发展的信息。最后，内耳传出纤维的退化和再生程度将通过纤维染色来确定。考虑到动物的年龄，我们希望通过对噪声性损伤的力学、神经生理学和行为学等方面的综合研究，更好地了解噪声性听力障碍的发生机制，为制定治疗方法提供依据。

Too high sound pressure levels can be perceived as pain. This usually occurs above a level of 120 dB SPL. If this is clearly below this level, one speaks of a hyperacusis. This hypersensitivity to sound is probably due to damage to structures in the inner ear. In the inner ear of mammals neuronal signals, which are forwarded to the brain, are generated in an extremely complex interplay between inner ear mechanics and efferent control. In the present project, we will investigate, besides the changes in the afferent connections, whether the degeneration of efferent connections after a noise trauma causes a change in the neuronal activity of the afferents and is thus a cause of hyperacusis? In the inner ear of mammals, there are two types of sense cells, the inner hair cells and the outer hair cells (OHC). The OHC have piezoelectric properties (electromotility), which can amplify the mechanical signal at low sound pressure levels or attenuate the mechanical signal at high sound pressure levels. The OHCs are thus involved in the extremely sensitive hearing in mammals and contribute to the protection of the hearing function when the sound pressure is too high. The piezoelectricity of the OHCs at high sound pressure levels is reduced by means of efferents, which are connected to the basal pol of the OHC. A loss of these nerve fibers by a noise trauma could disturb this protective mechanism and have far-reaching consequences, including the development of hyperacusis. Using monaural-evoked brain stem potentials and otoacoustic emissions (f2-f1), we will investigate the possible degeneration of efferent nerve fibers and their effects on neuronal processing in young and old Mongolian gerbil. In these experiments, the efferent system is activated by a contralateral noise, whereby we will test the influence of this activation before and after the noise trauma. In addition, we will document the stress values of the animals in order to correlate the mechanical and neurophysiological data with the behavioral studies on the startle reflex, which will provide us information about the development of hyperacusis. Finally, the extent of degeneration and regeneration of the efferent fibers in the inner ear will be determined by fiber staining. Taking into account the age of the animals, we hope to understand better through these comprehensive mechanical, neurophysiological and behavioral studies of noise-induced damage the mechanisms of development of hyperacusis and to provide a basis for the development of treatment methods.