Protection of the auditory nerve from traumatic stress experimental studies

本研究利用2000年建立的大鼠实验模型，对创伤性听神经变性的病理生理机制及预防措施进行了实验研究（Sekiya T等，Exp Neurol 161：490- 502，2000）这些实验研究的结果公开如下：1）研究了创伤性听神经变性的时间模式，并揭示了其相对快速的进展; 2）第二个发现是我们的研究首次揭示了创伤性听神经变性是由坏死和凋亡机制引起的。这些结果对于制定听神经损伤的神经保护措施具有重要意义。3）我们继续研究了类固醇、钙离子阻滞剂和碱性成纤维细胞生长因子等药物的神经保护作用。我们发现它们对改善创伤后听神经退行性变有一定的效果，但效果有限。4）我们未来的计划，以防止创伤性听神经退行性变和促进其再生的创伤后应包括神经干细胞或ES细胞的神经细胞移植的方法。

We performed the experimental studies to clarify the Pathophysiological mechanisms responsible for traumatic auditory nerve degeneration and the countermeasures to prevent this pathological process using the rat experimental model that we had established in 2000(Sekiya T, et al. Exp Neurol 161:490-502,2000)The results of these experimental studies disclosed as follows ;1)The temporal pattern of traumatic auditory nerve degeneration was investigated and its relatively rapid progression was revealed ; within one week postcompression, auditory nerve degeneration was completed.2)The second findings that has been disclosed from our studies for the first time was that traumatic auditory nerve degeneration was caused both by necrotic and apoptotic mechanisms. These results are crucial to plan the neuroprotective measures to traumatized auditory nerve.3)We continued to investigate the neuroprotective effectiveness of several pharmacological agents such as steroid, calcium blocker, and basic fibroblast growth factor. We found that they had some effectiveness to ameliorate posttraumatic auditory nerve degeneration but their effects were limited.4)Our future plan to prevent traumatic auditory nerve degeneration and to foster its regeneration after trauma should include neurocelluar transplantation approach using neural stem cells or ES cells.