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Glia and Glia-Neuron Interaction

開催日 2014/9/12
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

in vitro 炎症モデルにおけるミクログリア活性化に対する抗鬱剤の作用比較
Comparison of the effects of antidepressants on the microglial activation in LPS-inflammation model

  • P2-061
  • 笠原 由佳 / Yuka Kasahara:1,2 藤森 康希 / Koki Fujimori:3 三浦 麻利衣 / Marie Miura:1,2 最上 由香里 / Yukari Mogami:2 関野 祐子 / Yuko Sekino:2 佐藤 薫 / Kaoru Sato:2 鈴木 岳之 / Takeshi Suzuki:1 
  • 1:慶應大・薬 / Div Basic Biol Sci, Fac Pharm, Keio Univ 2:国立医薬品食品衛生研・薬理 / Div Pharmacol, Natl Inst Health Sci 3:慶應大院・医・生理 / Dept Physiol, Keio Univ, Sch Med 

Some antidepressants are reported to have anti-inflammatory effects as well. We therefore studied the effects of various antidepressants, i.e., paroxetine (SSRI), fluvoxamine (SSRI), sertraline (SSRI), milnacipran (SNRI) and amitriptyline (TCA), on microglial activation in the LPS-inflammation model without cell death. Among antidepressants used, only paroxetine suppressed microglial activation as is shown by their morphology, CD11b expression level, and L-Glu release. We thus investigated the mechanisms which restricted the effects to paroxetine. Because we have shown that P2X4 receptor is important for acceleration of microglial activation in this inflammation model, we first examined the interaction between antidepressants described above and P2X4 receptor by comparing the effects of these drugs (0.1nM-10μM) on the P2X4-mediated Ca2+ influx to 1321N1 cells which stably express P2X4 receptors. We also confirmed the cell toxicity of the antidepressants in this concentration range. Unexpectedly, interactions with P2X4 receptors were observed for all antidepressants used here. Further, sertraline showed the most powerful inhibition and paroxetine showed the second-most powerful inhibition in a concentration-dependent manner. Our present results suggest that P2X4 does not restrict the suppressive effects to paroxetine. Currently we are investigating the other possible targets, i.e., ATP release from activated microglia or other subtypes of purinergic receptors.

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