Investigating the Cell-specific Mechanisms That Drive Sex Differences During Neuropathic Pain Development

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dc.contributor.advisorBurton, Michael D
dc.contributor.advisorO'Toole, Alice
dc.contributor.committeeMemberPrice, Theodore
dc.contributor.committeeMemberDussor, Gregory
dc.contributor.committeeMemberRincón-Cortés, Millie
dc.creatorSzabo-Pardi, Thomas Alexander
dc.date.accessioned2023-04-25T19:04:00Z
dc.date.available2023-04-25T19:04:00Z
dc.date.created2022-08
dc.date.issued2022-08-01T05:00:00.000Z
dc.date.submittedAugust 2022
dc.date.updated2023-04-25T19:04:01Z
dc.description.abstractChronic pain patients often suffer from a decline in quality of life due to a lack of efficacious long- term therapeutics. Moreover, the prevalence of chronic pain conditions is on the rise, with an average increase of nearly 10 percent in patients per decade. This, coupled with the devastating impact of the opioid crisis, highlights the need for novel pain therapeutics. An extensive literature has placed microglia, the resident immune cells of the central nervous system, at the forefront of male-specific mechanisms that mediate chronic pain plasticity. Recently, efforts have been made to design studies aimed at dissecting female specific mechanisms in pain plasticity. Evidence suggests that immune-related components of nociceptors are heavily dysregulated following insult and are more directly responsible for changes in female-specific sensitization. Despite advances in the field of pain neurobiology, there remains a clear disconnect between the cellular mechanisms that underlie maladaptive chronic pain in males and females. Moreover, a lack of studies directed towards interventions during early neuropathic pain development make it difficult to assess how functional changes in cellular phenotypes following injury can be manipulated to prevent maladaptive pain plasticity from taking place. The goal of our research was to use an innovative approach to identify nociceptor and immune cell-specific mechanisms in both the peripheral and central nervous systems that mediate sex differences during neuropathic pain development. Our findings suggest that the initial phase of neuropathic development is sexually dimorphic, characterized by nociceptor-specific signaling mechanisms in females and immune cell mediated sensitization in males which may be modulated by genetic and pharmacological manipulation of toll-like receptor 4 signaling.
dc.format.mimetypeapplication/pdf
dc.identifier.uri
dc.identifier.urihttps://hdl.handle.net/10735.1/9669
dc.language.isoen
dc.subjectBiology, Neuroscience
dc.titleInvestigating the Cell-specific Mechanisms That Drive Sex Differences During Neuropathic Pain Development
dc.typeThesis
dc.type.materialtext
thesis.degree.collegeSchool of Behavioral and Brain Sciences
thesis.degree.departmentCognition and Neuroscience
thesis.degree.grantorThe University of Texas at Dallas
thesis.degree.namePHD

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