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    Mechanisms Underlying Noise-Induced PV+ Neuron Loss

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    Author
    Hossainy, Nadia Nahal
    Issue Date
    2021
    Keywords
    Apoptosis
    Inflammation
    Necroptosis
    Noise induced hearing loss
    Parvalbumin
    Tinnitus
    Advisor
    Bao, Shaowen
    
    Metadata
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    Publisher
    The University of Arizona.
    Rights
    Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction, presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
    Abstract
    There is a decrease of PV+ neurons in the primary auditory cortex of noise-exposed C57BL/6 mice. However, the mechanism behind this decrease was not clear. Therefore, the primary purpose of this study was to assess the possible cell death mechanisms involved in PV+ reduction. To help us identify potential cell death mechanisms to further look into, we first compared PV+ neuron reduction in noise-exposed C57BL/6 mice to noise-exposed FVB mice. C57BL/6 and FVB strains have different immune response profiles. Therefore, differences in PV+ neuron reduction in the primary auditory cortex of these two mouse strains can imply that pro-inflammatory cytokines might have a role in PV+ neuron density reduction. We observed different gap detection patterns and differences in PV+ neuron loss in the primary auditory cortex between noise-exposed C57BL/6 and FVB mice. Noise-exposed C57BL/6 mice displayed impairments in gap detection and reduction in PV+ neuron density in the primary auditory cortex. However, noise-exposed FVB mice did not show impairments in gap detection, and there was no change in their PV+ neuron density. Based on this finding, as well as previous studies linking tinnitus to pro-inflammatory cytokines, we examined PV+ neurons of noise-exposed C57BL/6 mice for signs of apoptosis and necroptosis. Both of these cell death mechanisms can be triggered by pro-inflammatory cytokines. TUNEL staining was used to identify apoptosis. Immunohistochemistry staining with the RIP3 primary antibody was used as a marker for necroptosis. We did not observe apoptosis in PV+ neurons in the primary auditory cortex of noise-exposed mice. Necroptosis was observed in PV+ neurons in the primary auditory cortex of noise-exposed mice (p < 0.05). Therefore, necroptosis might play a role in the observed PV+ loss in the primary auditory cortex of noise-exposed mice.
    Type
    text
    Electronic Thesis
    Degree Name
    M.S.
    Degree Level
    masters
    Degree Program
    Graduate College
    Physiological Sciences
    Degree Grantor
    University of Arizona
    Collections
    Master's Theses

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