INNER EAR AND CENTRAL AUDITORY DEVELOPMENT

内耳和耳蜗损伤导致的耳聋和听力损失 神经仍然是主要的不可治愈的耳科疾病的今天，尽管 人工耳蜗的最新进展 不太常见，但很多 关注，是先天性的损害形式，因为由此产生的听力 这种障碍严重妨碍了交流技能的发展。 本提案的目的是阐明 控制内耳感觉神经结构的组装 以及它们与中枢听觉通路的联系。 的方法 使用体外方法分析感觉神经相互作用的作用 在这些听觉结构的发展过程中。 游离细胞 来自耳原基的确定的组织外植体的培养物， 鸡或鹌鹑胚胎的声核被用于确定 参与这些相互作用的细胞类型。 目的是确定 在耳蜗神经发生过程中相互作用的特定细胞类型 神经节和核，并表征细胞相互作用 在体外发生的，无论是营养性的还是热带性的，许可性的还是指导性的， 无论是通过接触扩散因子介导的。 实验 旨在揭示参与这些相互作用的因素以及 它们在分子水平上的行为。 抗体将用于 在关键阶段将这些分子定位于特定的细胞类型 并扰乱原位的发育过程。 最终这些 研究结果应为开展移植提供了合理的依据 神经元和耳上皮细胞进入受损的耳蜗。

Deafness and hearing loss due to damage of the inner ear and cochlear nerve remain as the major incurable otological disorders today, despite recent advances with cochlear prostheses. Less common, but of much concern, are congenital forms of damage, since the resulting hearing impairment profoundly disturbs the development of communication skills. The goal of the present proposal is to elucidate the mechanisms controlling the assembly of the sensorineural structures of the Inner ear and their connections with the central auditory pathways. The approach uses in vitro methods to analyze the role of sensorineural interactions in the development of these auditory structures. Dissociated cell cultures of defined tissue explants from the anlagen of the ear and acoustic nuclei of chicken or quail embryos are used to determine the cell types Involved in these interactions. The aim is to identify the specific cell types that interact during neurogenesis of the cochlear ganglion and nucleus and to characterize the cellular Interactions occurring In vitro, whether trophic or tropic, permissive or instructive, whether mediated by contact of diffusible factors. Experiments are designed to reveal factors involved in these interactions and the loci of their actions at the molecular level. Antibodies will be used for localizing such molecules to specific cell types at the critical stages and to perturb the developmental process in situ. Ultimately these findings should provide a rational basis for developing transplantation of neuronal and otic epithelial cells into damaged cochleas.