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The effects of microglial inactivation and decreased prostaglandin synthesis on lipopolysaccharide-induced learning deficits

Posted on:2008-11-04Degree:M.SType:Thesis
University:Texas Christian UniversityCandidate:Tarr, Andrew JustinFull Text:PDF
GTID:2444390005970690Subject:Biology
Abstract/Summary:
Microglial inhibitors and non-selective COX inhibitors maybe possible treatments for neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis by reducing cytokine overexpression. Experiments 1 & 2 attempted to further the understanding of the mechanisms of how proinflammatory cytokines contribute to learning/memory deficits seen after lipopolysaccharide administration and to the extent to which microglial cells play a role in this. Specifically, the present study investigated the role of prostaglandin production and microglial activation in the development of LPS-induced cognitive impairments. Experiment 1 consisted of a co-administration of minocycline and LPS to C57BL/6J male mice. Experiment 2 consisted of a co-administration of indomethacin and LPS also to C57BL/6J male mice. We hypothesized that minocycline and indomethacin would reduce central cytokine levels and reduce or eliminate the effects of LPS-induced anxiety and cognitive deficits in both elevated plus maze and 2-way active avoidance conditioning paradigms.
Keywords/Search Tags:Microglial
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