ROLE OF MACROPHAGES IN NOISE-INDUCED COCHLEAR SYNAPTOPATHY AND NEUROPATHY

巨噬细胞在噪声引起的耳蜗突触病和神经病中的作用

基本信息

  • 批准号:
    9098921
  • 负责人:
  • 金额:
    $ 15.25万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2016
  • 资助国家:
    美国
  • 起止时间:
    2016-04-01 至 2019-03-31
  • 项目状态:
    已结题

项目摘要

 DESCRIPTION (provided by applicant): Noise exposures that cause both permanent threshold shift (with accompanying hair cell loss) and temporary threshold shifts (no evident hair cell loss) also result in rapid and permanent loss of synaptic elements and cochlear nerve terminals. Such injury also leads to degeneration of spiral ganglion (SG) cell bodies, but this occurs over a period of months to years. Neuronal survival is a key determinant of the success of cochlear implants, so it is of great interest to understand the mechanisms that promote neuronal survival after cochlear insults. We have recently discovered that hair cell loss is sufficient to recruit macrophages into the spiral ganglion, and that disruption of signaling between macrophages and afferent neurons (by genetic deletion of fractalkine receptor CX3CR1), leads to reduced macrophage recruitment into the spiral ganglion, and also results in diminished survival of afferent neurons. Here we propose to investigate the role of fractalkine signaling after noise induced hearing loss. We hypothesize that: 1) fractalkine regulates macrophage recruitment into the noise-damaged cochlea, and 2) fractalkine promotes the survival of afferent synapses and neurons after noise injury. Aim 1 will examine the role of fractalkine signaling in neuropathy caused by permanent threshold shift. Specific experiments will assess the effects of genetic disruption of fractalkine signaling on macrophage infiltration, spiral ganglion cell pathology, and auditory function over short (weeks) and long (months) survival periods. Aim 2 will test the hypothesis that macrophages also serve a critical role after noise exposure that causes temporary threshold shift (TTS). We will characterize any migration of macrophages towards inner hair cell-afferent nerve fiber synapse, and determine whether disruption of fractalkine signaling can influence the severity of, or recovery from, noise-induced cochlear synaptopathy and neuropathy. For both aims, we will monitor changes in cochlear function via ABRs, and cochleae will be collected for histological analysis of macrophages, hair cells and afferent neurons, as well as inner hair cell- cochlear nerve terminal synapse number and morphology.


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)
专利数量(0)

数据更新时间:{{ journalArticles.updateTime }}

{{ item.title }}
{{ item.translation_title }}
  • DOI:
    {{ item.doi }}
  • 发表时间:
    {{ item.publish_year }}
  • 期刊:
  • 影响因子:
    {{ item.factor }}
  • 作者:
    {{ item.authors }}
  • 通讯作者:
    {{ item.author }}

数据更新时间:{{ journalArticles.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ monograph.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ sciAawards.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ conferencePapers.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ patent.updateTime }}

Tejbeer Kaur其他文献

Tejbeer Kaur的其他文献

{{ item.title }}
{{ item.translation_title }}
  • DOI:
    {{ item.doi }}
  • 发表时间:
    {{ item.publish_year }}
  • 期刊:
  • 影响因子:
    {{ item.factor }}
  • 作者:
    {{ item.authors }}
  • 通讯作者:
    {{ item.author }}

{{ truncateString('Tejbeer Kaur', 18)}}的其他基金

Innate Immunity to Spiral Ganglion Neuron Degeneration
对螺旋神经节神经元变性的先天免疫
  • 批准号:
    10640178
  • 财政年份:
    2022
  • 资助金额:
    $ 15.25万
  • 项目类别:
Innate Immunity to Spiral Ganglion Neuron Degeneration
对螺旋神经节神经元变性的先天免疫
  • 批准号:
    10880051
  • 财政年份:
    2022
  • 资助金额:
    $ 15.25万
  • 项目类别:
Contribution of Macrophages and Fractalkine Towards Degeneration and Repair of Cochlear Synapses
巨噬细胞和分形蛋白对耳蜗突触退化和修复的贡献
  • 批准号:
    10090991
  • 财政年份:
    2021
  • 资助金额:
    $ 15.25万
  • 项目类别:
Contribution of Macrophages and Fractalkine Towards Degeneration and Repair of Cochlear Synapses
巨噬细胞和分形蛋白对耳蜗突触退化和修复的贡献
  • 批准号:
    10579968
  • 财政年份:
    2021
  • 资助金额:
    $ 15.25万
  • 项目类别:

相似海外基金

How Spinal Afferent Neurons Control Appetite and Thirst
脊髓传入神经元如何控制食欲和口渴
  • 批准号:
    DP220100070
  • 财政年份:
    2023
  • 资助金额:
    $ 15.25万
  • 项目类别:
    Discovery Projects
The mechanisms of the signal transduction from brown adipocytes to afferent neurons and its significance.
棕色脂肪细胞向传入神经元的信号转导机制及其意义。
  • 批准号:
    23K05594
  • 财政年份:
    2023
  • 资助金额:
    $ 15.25万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
GPR35 on Vagal Afferent Neurons as a Peripheral Drug Target for Treating Diet-Induced Obesity
迷走神经传入神经元上的 GPR35 作为治疗饮食引起的肥胖的外周药物靶点
  • 批准号:
    10315571
  • 财政年份:
    2021
  • 资助金额:
    $ 15.25万
  • 项目类别:
Neurobiology of Intrinsic Primary Afferent Neurons
内在初级传入神经元的神经生物学
  • 批准号:
    10477437
  • 财政年份:
    2021
  • 资助金额:
    $ 15.25万
  • 项目类别:
Neurobiology of Intrinsic Primary Afferent Neurons
内在初级传入神经元的神经生物学
  • 批准号:
    10680037
  • 财政年份:
    2021
  • 资助金额:
    $ 15.25万
  • 项目类别:
Neurobiology of Intrinsic Primary Afferent Neurons
内在初级传入神经元的神经生物学
  • 批准号:
    10654779
  • 财政年份:
    2021
  • 资助金额:
    $ 15.25万
  • 项目类别:
Neurobiology of Intrinsic Primary Afferent Neurons
内在初级传入神经元的神经生物学
  • 批准号:
    10275133
  • 财政年份:
    2021
  • 资助金额:
    $ 15.25万
  • 项目类别:
GPR35 on Vagal Afferent Neurons as a Peripheral Drug Target for Treating Diet-Induced Obesity
迷走神经传入神经元上的 GPR35 作为治疗饮食引起的肥胖的外周药物靶点
  • 批准号:
    10470747
  • 财政年份:
    2021
  • 资助金额:
    $ 15.25万
  • 项目类别:
Roles of mechanosensory ion channels in myenteric intrinsic primary afferent neurons
机械感觉离子通道在肌间固有初级传入神经元中的作用
  • 批准号:
    RGPIN-2014-05517
  • 财政年份:
    2018
  • 资助金额:
    $ 15.25万
  • 项目类别:
    Discovery Grants Program - Individual
Roles of mechanosensory ion channels in myenteric intrinsic primary afferent neurons
机械感觉离子通道在肌间固有初级传入神经元中的作用
  • 批准号:
    RGPIN-2014-05517
  • 财政年份:
    2017
  • 资助金额:
    $ 15.25万
  • 项目类别:
    Discovery Grants Program - Individual
{{ showInfoDetail.title }}

作者:{{ showInfoDetail.author }}

知道了