Molecular Basis of a Critical Period in Cochlear Nucleus

耳蜗核关键期的分子基础

• 批准号: 6933832
• 负责人: Julie Harris
• 金额: $ 3.2万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 2004
• 资助国家: 美国
• 起止时间: 2004-07-01 至 2006-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6933832
• 关键词: auditory nuclei; auditory pathways; auditory stimulus; brain stem; developmental neurobiology; gene expression; gene induction /repression; genetically modified animals; immunocytochemistry; in situ hybridization; laboratory mouse; microarray technology; molecular biology; neurons; nucleic acid amplification techniques; physiology; polymerase chain reaction; predoctoral investigator; sensory deprivation

DESCRIPTION (provided by applicant): The goal of the present study is to identify the molecular mechanisms that could define a period of dramatic susceptibility to loss of peripheral input in the mouse brainstem cochlear nucleus (CN). The basis of this period and the switch during development to CN neuron survival independent of input is essentially unknown. These studies will use microarrays to identify candidate genes that change in level of expression during and after this critical period as well as to identify genes that are transcriptionally regulated (induced or repressed) following removal of input by cochlear ablation. Genetically altered mice, possibly in combination with other gene manipulation technologies, will be used to study the functional roles of selected candidate genes in death and survival of CN neurons following cochlear ablation. These studies will also examine the role of 8th nerve activity in promoting survival of CN neurons during the critical period, a time before the onset of hearing in mice. With recent advances in cochlear implant technologies, it is of great importance to understand the effects of sensory deprivation and the return of stimulation on central auditory neurons both during development and in adulthood in order to improve rehabilitation of auditory function.

描述（由申请人提供）：本研究的目的是确定可以定义小鼠脑干耳蜗核（CN）中外周血输入丧失的时期的分子机制。这一时期的基础以及与输入无关的CN神经元生存期间的转换基本未知。这些研究将使用微阵列来识别在这个关键时期内和之后改变表达水平的候选基因，以及在通过人工耳蜗消融消除输入后，在转录调节（诱导或抑制）的基因。遗传改变的小鼠可能与其他基因操纵技术结合使用，将用于研究所选候选基因在人工耳蜗后死亡和CN神经元存活中所选候选基因的功能作用。这些研究还将检查第八神经活性在关键时期促进CN神经元存活中的作用，这是小鼠听力发作之前的时期。随着人工耳蜗技术的最新进展，了解感觉剥夺的影响以及刺激在发育和成年期间对中央听觉神经元的恢复至关重要，以改善听觉功能的康复。