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DESCRIPTION (provided by applicant): The goal of this proposal is to identify sensory- and motor-driven genes activated by learned vocal communication in normal and deafened subjects. The animal model we will utilize is a songbird. Songbirds are one of the only accessible non-human animals where learned vocal communication, the substrate for human language, can be studied. Non-human primates, rodents, and other commonly studied animals do not have; this ability. In songbirds, hearing species-specific vocalizations (sensory activity) induces large increases of gene expression throughout the auditory pathway. This sensory-driven expression is experience-dependent, as induction requires that the birds be raised with adult conspecifics and induction is highest when the birds hear novel species-specific songs. The expression is blocked by deafening. The act of producing imitated vocalizations (motor activity) induces large increases of gene expression throughout the cerebral vocal pathway, and this motor-driven expression is not blocked by deafening. However, when birds are deafened, like humans, their learned vocalizations deteriorate. This deterioration, in songbirds, is an active process that requires the basal ganglia cortical-like vocal pathway, in which vocalizing-driven gene expression is found. To date, few genes have been identified with such sensory- and motor-driven regulation during behavior and none have yet been identified that change with deafening-induced deterioration of learned vocalizations. It is believed that an entire gene regulatory network is activated in these behavioral processes. We will use behavioral, neuroanatomical, and high throughput molecular biological approaches to identify and characterize sensory and motor-driven genes activated by normal vocal communication and by deafened-induced deterioration of learned vocalizations. Since most songbird genes have significant homology to known mammalian genes our experiments will enable us to identify avian brain genes with humain/mammalian homologues amenable to experimental characterization in the songbird system.
期刊论文(8)
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会议论文
DOI: 10.1093/molbev/msr047
发表时间: 2011-08
期刊: Molecular biology and evolution
影响因子: 10.7
作者: [B. Nabholz;Axel Künstner;Rui Wang;E. Jarvis;H. Ellegren]
通讯作者: B. Nabholz;Axel Künstner;Rui Wang;E. Jarvis;H. Ellegren
DOI: 10.1371/journal.pone.0042173
发表时间: 2012
期刊: PloS one
影响因子: 3.7
作者: [Horita H, Kobayashi M, Liu WC, Oka K, Jarvis ED, Wada K]
通讯作者: Wada K
DOI: 10.1002/cne.22370
发表时间: 2010-07-15
期刊: The Journal of comparative neurology
影响因子: --
作者: [Horita H, Wada K, Rivas MV, Hara E, Jarvis ED]
通讯作者: Jarvis ED
DOI: 10.1111/j.1460-9568.2008.06535.x
发表时间: 2008-12
期刊: The European journal of neuroscience
影响因子: --
作者: [Horita H, Wada K, Jarvis ED]
通讯作者: Jarvis ED
6
    Neuroengineering a Robust Vocal Learning Phenotype in Mice as a Model for Treating Communication Disorders
    • 批准号:
      10685974
    • 项目类别:
    • 资助金额:
      $109.98万
    • 财政年份:
      2019
    • 负责人:
      Erich D Jarvis
    • 依托单位:
    Neuroengineering a Robust Vocal Learning Phenotype in Mice as a Model for Treating Communication Disorders
    • 批准号:
      10002032
    • 项目类别:
    • 资助金额:
      $102.6万
    • 财政年份:
      2019
    • 负责人:
      Erich D Jarvis
    • 依托单位:
    Neuroengineering a Robust Vocal Learning Phenotype in Mice as a Model for Treating Communication Disorders
    • 批准号:
      10472693
    • 项目类别:
    • 资助金额:
      $108.02万
    • 财政年份:
      2019
    • 负责人:
      Erich D Jarvis
    • 依托单位:
    Neuroengineering a Robust Vocal Learning Phenotype in Mice as a Model for Treating Communication Disorders
    • 批准号:
      10241317
    • 项目类别:
    • 资助金额:
      $106.12万
    • 财政年份:
      2019
    • 负责人:
      Erich D Jarvis
    • 依托单位:
    海外基金