Activation of Microglia Induced Learning and Memory Deficits

被引:0
|
作者
Tanaka, Sachko [1 ]
Ohtaki, Hirokazu [2 ]
Nakamachi, Tomoya [2 ]
Numazawa, Satoshi [1 ]
Shioda, Seiji [2 ]
Yoshida, Takemi [1 ]
机构
[1] Showa Univ, Sch Pharmaceut Sci, Dept Biochem Toxicol, Shinagawa Ku, 1 5 8 Hatanodai, Tokyo 1428555, Japan
[2] Showa Univ, Sch Med, Dept Anat, Tokyo 1428555, Japan
关键词
Lipopolysaccharide; Learning and memory; Microglia; NMDA receptors; LONG-TERM POTENTIATION; NEURONAL CELL-DEATH; CHRONIC NEUROINFLAMMATION; NITRIC-OXIDE; RAT-BRAIN; LIPOPOLYSACCHARIDE; DISEASE;
D O I
10.1007/978-4-431-99039-0_17
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We used lipopolysaccharide (LPS) to activate microglia which play an important role in the brain immune system. LPS injected into the rat hippocampus CA1 region activated microglial cells resulting in an increased production of interleukin (IL)-1 beta and tumor necrosis factor (TNF) alpha in the hippocampus during the early stage of its treatment. Subacute treatment with LPS for 5 days caused activation of microglia and induced learning and memory deficits in animals when examined with a step-through passive avoidance test. And then we had found the decreased [H-3]MK801 binding in the hippocampus CA1, CA3 and DG. The gene expression of NMDA receptor NR1 subunits was also decreased by the LPS treatment. These results suggest that activation of microglia induced by LPS results in a decrease of glutamatergic transmission which leads to learning and memory deficits.
引用
收藏
页码:191 / +
页数:3
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