慢性声损伤中毛细胞变性消亡的机理和防护

This project dealth with the process of change in structure of hair cells in chronic acoutic trauma. It was first considered that the intertect of the cuticular plate and the link between the stereocilia was the key point where the temporay threshold shift shifts to permanent threshold shift. The mechanism and causes of dengeration of hair cells in chronic acoustic trauma was investigated. It was found that the elevation of the concentration of glutamate in the perilymph of cochclea was the trig leading the damage of hair cells. Glutamate activated the NMDA and AMPA receptors, that led to accumulation of Free radical, was the primary way by which hair cells were dengerated and lost. This project addressed the prevention of hair cells from dengeration in acoustic trauma. It was found that inhibition of NMDA receptor with its atagnosit MK-801 or admionstration withα-lipoic acid could prevent hair cells from damage caused by noise.

中、低强度噪声长期暴露形成慢性声损伤模型。研究慢性声损伤过程中毛细胞从变性到消亡的病变规律；研究毛细胞内，外微环境中生化特性(钙离子浓度、pH值和内皮素)的变化规律，探讨引起和促进毛细胞变性和消亡的化学因素；研究预防细胞变性消亡的措施和药物。本项目对阐明慢性听力损伤机理工科，防治噪声性耳聋，促进听力恢复具有重要理论和实践意义。