神経免疫 Neuroimmunology

P1-2-129 Lipopolysaccharide刺激による脳室周囲器官のastrocyte活性化 Lipopolysaccharide-induced astrocytic activation in the circumventricular organs of adult mice ○中野洋輔1, 宮田清司1 ○Yousuke Nakano1, Seiji Miyata1 京都工芸繊維大院・応用生物学1 Dept of Appl Biol, Kyoto Inst of Technol, Kyoto1 The innate immune response is initiated by recognition of bacterial or viral molecules through pathogen-associated molecule receptors called Toll-like receptors on macrophages and other immune tissues. This recognition induces a cascade of events beginning with generation of the proinflammatory cytokines that transported through the capillary vessel to the brain and then results in the generation of fever and sickness behavior. The proinflammatory cytokines is recongnized by the cytokine receptors on the cell membrane and then the intracellular domains of receptors are phosphorylated by JAK and STAT. In the present study, we found that nuclear translocation of STAT3 occurred at astrocytes preferentially in the sensory circumventricular organs (CVOs) including the organum vasculosum of the lamina terminalis, subfornical organ, and area postrema after the intraperitoneal injection of lipopolysaccharide (LPS). The phosphorylation of STAT3 in astrocytes was seen 1 and 2 hr after the intraperitoneal injection of LPS, but it decreased to control levels at 4 hr after the injection. The expression of Fos was observed at both astrocytes and neurons in the sensory CVOs 2 hr after the intraperitoneal injection of LPS. The administration of a microglial inhibitor minocycline slightly decreased the phosphorylation of STAT3 in the sensory CVOs. The present study indicates that activation of astrocytic STAT3 signaling is mediated direct action of cytokines rather than microglia-derived ones.

P1-2-130 感染症に随伴する行動障害の解析 Analysis of the infection-induced behavioral impairment ○近藤誠1, 中村雪子1, 山田貴博1, 石田雄介1, 島田昌一1 ○Makoto Kondo1, Yukiko Nakamura1, Takahiro Yamada1, Yusuke Ishida1, Shoichi Shimada1 大阪大院・医・神経細胞生物1 Dept Neurosci and Cell Biol, Univ of Osaka, Osaka, Japan1 In response to a peripheral infection, immune cells produce pro-inflammatory cytokines, such as IL-1β and TNF-α, that act on the brain to cause behavioral changes. The behavior of sick animals changes dramatically; they often reduce activity levels, ignore food and beverage, and lose interest in their physical and social environments. They tire easily and their sleep is often fragmented. In addition, they feel depressed and can experience mild cognitive disorders. These behavior is called sickness behavior; however, the precise mechanisms of these behavioral changes are not well understood. Meanwhile, the results of infection-induced behavioral changes of mice are often different among mouse strains. C57BL6J mouse strain is most frequently used as a background strain of knockout mice and is known to be suitable for behavioral analyses. Therefore, to analyze the infection-induced behavioral changes, we administerd lipopolysaccharide to C57BL6J mice and performed several behavioral analyses. This time, we present the effects of peripheral lipopolysaccharide administration on behavior of C57BL6J mice.

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