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

过高的声压会被认为是疼痛。这通常发生在120 dB声压级以上。如果明显低于这个水平，就可以说是听觉亢进。这种对声音的过度敏感可能是由于内耳结构的损伤。在哺乳动物的内耳中，传递到大脑的神经元信号是在内耳力学和传出控制之间极其复杂的相互作用中产生的。在本项目中，除了传入连接的变化外，我们将研究噪音创伤后传出连接的退化是否会导致传入事件神经元活动的变化，从而导致听觉亢进？在哺乳动物的内耳中，有两种感觉细胞，内耳毛细胞和外耳毛细胞（OHC）。OHC具有压电特性（电动力），可以在低声压级放大机械信号，也可以在高声压级衰减机械信号。因此，OHCs与哺乳动物极其敏感的听觉有关，并有助于在声压过高时保护听力功能。在高声压级时，OHC的压电性通过与OHC的基孔连接的输出来降低。噪音损伤造成的神经纤维的损失可能会扰乱这种保护机制，并产生深远的后果，包括听觉亢进的发展。利用单耳诱发脑干电位和耳声发射（f2-f1），我们将研究蒙古沙鼠的传出神经纤维可能的退化及其对神经元加工的影响。在这些实验中，传出系统被对侧噪声激活，由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激值，以便将力学和神经生理学数据与惊吓反射的行为研究相关联，这将为我们提供关于听觉亢进的信息。最后，通过纤维染色测定内耳传出纤维的变性和再生程度。考虑到动物的年龄，我们希望通过这些噪声损伤的力学、神经生理和行为学的综合研究，更好地了解听觉亢进的发生机制，并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.