INNER EAR AND CENTRAL AUDITORY DEVELOPMENT

内耳和耳蜗性损伤所致耳聋和听力损失 神经仍然是今天主要的不可治愈的耳科疾病，尽管 人工耳蜗术的新进展。不太常见，但有很多 令人担忧的是，是否存在先天形式的损害，因为由此产生的听力损害 心理障碍对沟通能力的发展有很大的影响。 本提案的目的是阐明这些机制 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。该方法 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中。分离的细胞 确定的组织外植体的培养从耳的原和 鸡或鹌鹑胚胎的声核被用来确定 参与这些相互作用的细胞类型。其目的是确定 在耳蜗神经发生过程中相互作用的特定细胞类型 神经节和细胞核，并描述细胞间的相互作用 在体外发生的，无论是营养的还是热带的，允许的还是有教育意义的， 是否通过扩散因素的接触来调节。实验是 旨在揭示参与这些相互作用的因素和 他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到特定的细胞类型 并在原位扰乱发育过程。最终这些 研究结果应为发展移植提供合理的依据 神经元和耳廓上皮细胞转化为受损的耳蜗组织。

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.