感音神经性聋严重影响患者生活质量，因其发生机制不清，目前尚缺乏有效的治疗手段。感音神经性聋的发生过程中，听觉传导通路尤其是初级中枢耳蜗核会发生不同程度的可塑性改变，这种改变与神经元和胶质细胞的相互作用密切相关。我们的前期研究提示：耳蜗核的神经元-胶质细胞的相互作用可能是噪声等因素刺激后导致的感音神经性聋的中枢机制的关键环节之一，而acrolein及相关的信号分子可能是介导其细胞通讯的关键分子。本课题拟从神经行为学、机能学和形态学等不同层次，深入研究神经元、胶质细胞释放的信号分子与感音神经性聋的相关性，阐述acrolein和相关的信号分子所介导的感音神经性聋的分子机制，以及其对听觉功能的影响。期望在初步阐明耳蜗核神经元-胶质细胞网络参与感音神经性聋的机制的同时，为其临床治疗提供新的靶点和策略。

Sensorineural hearing loss (SHL) significantly influences human life. Effective treatment for SHL is unavailable in nowadays since the underlying mechanism is still unclear. In the process of the occurrence of SHL, alteration of neural plasticity are always accompanied with SHL in central auditory pathway, especially in cochlear nucleus, where neuron and glial cell interact with each other. Our pilot study indicated that as a key molecule in the oxidative stress, acrolein could modulate neuron-glial network which may subsequently cause pathogenesis of SHL induced by noise. Based on behavioral, electrophysiological and morphological methods, we first plan to investigate the relationship between acrolein, signaling molecules released from neurons and astrocytes in SHL animal model. After that, molecular mechanism of neuron-glial interaction underlying SHL will be studied. We will also evaluate the effects of inhibiting acrolein activity on hearing ability and intercellular interactions. Our proposed study may be helpful for further disclose the mechanism of SHL and provide new strategies for related prevention and treatment.