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dc.contributor.authorMcLinden, Kristina Ashleyen_US
dc.date.accessioned2014-07-22T18:48:18Z
dc.date.available2014-07-22T18:48:18Z
dc.date.created2011en_US
dc.date.issued2011en_US
dc.identifieretd-08102011-122301en_US
dc.identifierumi-10255en_US
dc.identifiercat-001753660en_US
dc.identifier.urihttps://repository.tcu.edu:443/handle/116099117/4333
dc.descriptionTitle from dissertation title page (viewed Aug. 22, 2011).en_US
dc.descriptionIncludes abstract.en_US
dc.descriptionThesis (Ph.D.)--Texas Christian University, 2011.en_US
dc.descriptionDepartment of Psychology; advisors, Gary W. Boehm, Giridhar R. Akkaraju.en_US
dc.descriptionIncludes bibliographical references.en_US
dc.descriptionText (electronic thesis) in PDF.en_US
dc.descriptionA bi-directional relationship exists between the immune system and the central nervous system. A number of in vivo studies have reported that immune stimulation through administration of endotoxin or pro-inflammatory cytokines can lead to cognitive deficits in a variety of paradigms. However, despite a large body of work characterizing the behavioral effects of immune stimulation, the cellular mechanisms that underlie this global cognitive impairment remain unclear. The present study utilized primary hippocampal cell culture to examine the effect of pro-inflammatory cytokines on process extension and expression of relevant proteins. Specifically, we hypothesized that administration of interleukin-1beta (IL-1beta), interleukin-6 (IL-6), or tumor necrosis factor-alpha (TNF-alpha) would lead to morphological alterations (as evidenced by decreased process length, process number, and density of processes), and decreased protein and gene expression of GAP-43 and synapsin-I, two proteins important in synapse formation and process extension. Furthermore, in addition to replicating the prior findings of Neumann et al (2002) with regard to TNF-alpha, our goal was to extend this line of investigation to IL-1beta and IL-6. The observed results were generally inconsistent to our original hypotheses. Rather than decreasing expression, exposure to TNF-alpha led to significantly increased expression of synapsin-I mRNA, and exposure to IL-1beta, IL-6, and TNF-alpha led to significant increases in expression of synapsin-I protein. However, pro-inflammatory cytokine treatment did not significantly impact gene or protein expression of GAP-43. Further, these changes in synapsin-I, though correlated, did not significantly impact cellular morphology, in terms of process number, length, and density. The present study is the first to investigate the effects of IL-1beta or IL-6 on primary hippocampal neurons.en_US
dc.language.isoengen_US
dc.publisher[Fort Worth, Tex.] : Texas Christian University,en_US
dc.relation.ispartofTexas Christian University dissertationen_US
dc.relation.ispartofUMI thesis.en_US
dc.relation.ispartofTexas Christian University dissertation.en_US
dc.relation.requiresMode of access: World Wide Web.en_US
dc.relation.requiresSystem requirements: Adobe Acrobat reader.en_US
dc.subject.lcshCytokines.en_US
dc.subject.lcshHippocampus (Brain) Physiology.en_US
dc.subject.lcshNeurons.en_US
dc.subject.lcshGene expression.en_US
dc.titleEffects of pro-inflammatory cytokines on in vitro measures of gene expression, protein expression, and process extension in primary hippocampal neurons [electronic resource] /en_US
dc.typeTexten_US
etd.degree.departmentDepartment of Psychology
etd.degree.levelDoctoral
local.academicunitDepartment of Psychology


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