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The effects of microglial inactivati...

Texas Christian University.

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

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	The effects of microglial inactivation and decreased prostaglandin synthesis on lipopolysaccharide-induced learning deficits./
作者:	Tarr, Andrew Justin.
面頁冊數:	52 p.
附註:	Adviser: Gary W. Boehm.
Contained By:	Masters Abstracts International45-03.
標題:	Biology, Neuroscience. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1440522

The effects of microglial inactivation and decreased prostaglandin synthesis on lipopolysaccharide-induced learning deficits.
Tarr, Andrew Justin.

The effects of microglial inactivation and decreased prostaglandin synthesis on lipopolysaccharide-induced learning deficits. - 52 p.

Adviser: Gary W. Boehm.

Thesis (M.S.)--Texas Christian University, 2007.

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.Subjects--Topical Terms:

1017680
Biology, Neuroscience.

The effects of microglial inactivation and decreased prostaglandin synthesis on lipopolysaccharide-induced learning deficits.
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502 $a Thesis (M.S.)--Texas Christian University, 2007.
520 $a 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.
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