Development of Inhibition in the Avian Cochlear Nucleus

禽耳蜗核抑制的发展

基本信息

  • 批准号:
    7198079
  • 负责人:
  • 金额:
    $ 3.24万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2006
  • 资助国家:
    美国
  • 起止时间:
    2006-01-09 至 2009-07-23
  • 项目状态:
    已结题

项目摘要

DESCRIPTION (provided by applicant): The auditory system localizes sound in azimuth by computing interaural time delays. In the avian auditory brainstem, nucleus magnocellularis (NM) is the first central nucleus in this temporal coding pathway. NM contains highly specialized anatomic, synaptic, and intrinsic properties that play key roles in shaping inhibitory responses and maintaining temporal fidelity in NM. The development of these specializations is poorly understood. The first aim is to describe the time-course of the development of inhibition in chick NM using in vitro electrophysiological techniques.. The second aim is to understand the developmental importance of afferent excitatory inputs in the development of inhibition using otocyst removal followed by physiological recordings. The third aim will examine role of Kv1.1 in developing the normal NM phenotype using RNA interference techniques. Plasmids encoding RNAs designed to interfere with the Kcnal, the Kv1.1 gene, and an EGFP reporter gene will be electroporated in ovo in early embryos. The physiology of transfected cells will be examined through development. These manipulations are hypothesized to alter the normal development of NM anatomy and physiological responses to excitatory and inhibitory inputs.
描述(由申请人提供):听觉系统通过计算耳间时间延迟来定位方位角上的声音。在鸟类听觉脑干中,大细胞核(NM)是这条时间编码通路的第一个中枢核团。NM包含高度专业化的解剖,突触和内在的属性,在塑造抑制反应和维持NM的时间保真度中发挥关键作用。对这些专业化的发展知之甚少。第一个目的是使用体外电生理技术描述鸡NM抑制发展的时间过程。第二个目的是了解发展的重要性,传入兴奋性输入的抑制使用耳囊去除生理记录。第三个目标是利用RNA干扰技术研究Kv1.1在正常NM表型形成中的作用。编码旨在干扰Kcnal、Kv1.1基因和EGFP报告基因的RNA的质粒将在早期胚胎的卵内电穿孔。将通过发育检查转染细胞的生理学。这些操作被假设为改变NM解剖学的正常发育和对兴奋性和抑制性输入的生理反应。

项目成果

期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
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MacKenzie A Howard其他文献

MacKenzie A Howard的其他文献

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{{ truncateString('MacKenzie A Howard', 18)}}的其他基金

Mechanisms of altered synaptic integration and plasticity underlying cellular and circuit dysfunction in genetic epilepsy disorders
遗传性癫痫病中细胞和回路功能障碍的突触整合和可塑性改变的机制
  • 批准号:
    10586117
  • 财政年份:
    2020
  • 资助金额:
    $ 3.24万
  • 项目类别:
Mechanisms of altered synaptic integration and plasticity underlying cellular and circuit dysfunction in genetic epilepsy disorders
遗传性癫痫病中细胞和回路功能障碍的突触整合和可塑性改变的机制
  • 批准号:
    10376364
  • 财政年份:
    2020
  • 资助金额:
    $ 3.24万
  • 项目类别:
Mechanisms of altered synaptic integration and plasticity underlying cellular and circuit dysfunction in genetic epilepsy disorders
遗传性癫痫病中细胞和回路功能障碍的突触整合和可塑性改变的机制
  • 批准号:
    10179505
  • 财政年份:
    2020
  • 资助金额:
    $ 3.24万
  • 项目类别:
Mechanisms of altered synaptic integration and plasticity underlying cellular and circuit dysfunction in genetic epilepsy disorders
遗传性癫痫病中细胞和回路功能障碍的突触整合和可塑性改变的机制
  • 批准号:
    9973980
  • 财政年份:
    2020
  • 资助金额:
    $ 3.24万
  • 项目类别:
Molecular Mechanisms Underlying PSD-MAGUK/NMDA Receptor Interactions
PSD-MAGUK/NMDA 受体相互作用的分子机制
  • 批准号:
    8061587
  • 财政年份:
    2010
  • 资助金额:
    $ 3.24万
  • 项目类别:
Molecular Mechanisms Underlying PSD-MAGUK/NMDA Receptor Interactions
PSD-MAGUK/NMDA 受体相互作用的分子机制
  • 批准号:
    7910286
  • 财政年份:
    2010
  • 资助金额:
    $ 3.24万
  • 项目类别:
Molecular Mechanisms Underlying PSD-MAGUK/NMDA Receptor Interactions
PSD-MAGUK/NMDA 受体相互作用的分子机制
  • 批准号:
    8245101
  • 财政年份:
    2010
  • 资助金额:
    $ 3.24万
  • 项目类别:
Development of Inhibition in the Avian Cochlear Nucleus
禽耳蜗核抑制的发展
  • 批准号:
    7113269
  • 财政年份:
    2006
  • 资助金额:
    $ 3.24万
  • 项目类别:
Development of Inhibition in the Avian Cochlear Nucleus
禽耳蜗核抑制的发展
  • 批准号:
    7338006
  • 财政年份:
    2006
  • 资助金额:
    $ 3.24万
  • 项目类别:

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