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dc.contributor.advisorPrice, Theodore J.
dc.creatorMoy, Jamie K.
dc.date.accessioned2018-05-31T21:59:39Z
dc.date.available2018-05-31T21:59:39Z
dc.date.created2017-05
dc.date.issued2017-05
dc.date.submittedMay 2017
dc.identifier.urihttp://hdl.handle.net/10735.1/5792
dc.description.abstractPain under normal circumstances serves as a protective mechanism allowing recovery and survival. However, when pain becomes chronic, it no longer provides preservation but rather debilitation. Chronic pain is an important medical problem affecting greater than 33% of the population in America and current treatment options are only effective in a small percentage of the population and often accompanied with side effects. Determining the underlying molecular mechanisms of the maintenance and transition to chronic pain would lead us to developing new therapeutic treatments. Many studies suggest that translational control of gene expression is a key process for the regulation of plasticity in the nervous system. Multiple lines of evidence indicate that translation control plays a critical role in pathological pain plasticity, but precise gene targets have thus far not been elucidated. Brain-derived neurotrophic factor (BDNF) signaling through its cognate receptor, TrkB, is a well-known promoter of synaptic plasticity at nociceptive synapses in the dorsal horn of the spinal cord. However, the downstream effects contributing to the maintenance of a chronic pain state remain elusive. The goal of our research is to further understand the biochemical mechanisms driving chronic pain using pharmacological techniques and transgenic mice. Our work provides novel insight into mechanisms driving pain chronification and defines MNK regulation of eIF4E phosphorylation as a key target for pain therapeutics.
dc.format.mimetypeapplication/pdf
dc.language.isoen
dc.rights©2018 The Author. Digital access to this material is made possible by the Eugene McDermott Library. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
dc.subjectNeuroplasticity
dc.subjectChronic pain
dc.subjectPain—Treatment
dc.subjectGene expression
dc.subjectEukaryotic cells
dc.subjectPhosphorylation
dc.titleTranslation Regulation in Central and Peripheral Pain Plasticity
dc.typeDissertation
dc.date.updated2018-05-31T21:59:39Z
dc.type.materialtext
thesis.degree.grantorThe University of Texas at Dallas
thesis.degree.departmentCognition and Neuroscience
thesis.degree.levelDoctoral
thesis.degree.namePHD


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