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首页> 外文期刊>The European Journal of Neuroscience >Functional importance of Ca2+-activated K+ channels for lysophosphatidic acid-induced microglial migration.
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Functional importance of Ca2+-activated K+ channels for lysophosphatidic acid-induced microglial migration.

机译:Ca2 +激活的K +通道对溶血磷脂酸诱导的小胶质细胞迁移的功能重要性。

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Abstract Migration of microglial cells towards damaged tissue plays a key role in central nervous system regeneration under pathological conditions. Using time lapse video microscopy we show that lysophosphatidic acid (LPA) enhances chemokinetic migration of murine microglial cells. In the presence of 1 micro m LPA, the mean migration rate of microglial cells was increased 3.8-fold. In patch-clamp studies we demonstrate that LPA induces activation of a Ca(2+)-activated K(+) current. Microglial Ca(2+)-activated K(+) currents were abolished by either 50 nm charybdotoxin or 10 micro m clotrimazole. In contrast, 5 micro m paxilline did not have any significant effects on Ca(2+)-activated K(+) currents. The LPA-stimulated migration of microglial cells was inhibited by blockers of IKCa1 Ca(2+)-activated K(+) channels. The mean migration rate of LPA-stimulated cells was decreased by 61% in the presence of 50 nm charybdotoxin or by 51% during exposure to 10 micro m clotrimazole. Microglial migration was not inhibited by 5 micro m paxilline. It is concluded that IKCa1 Ca(2+)-activated K(+) channels are required for LPA-stimulated migration of microglial cells.
机译:摘要小胶质细胞向受损组织的迁移在病理条件下的中枢神经系统再生中起着关键作用。使用延时视频显微镜,我们显示溶血磷脂酸(LPA)增强了小鼠小胶质细胞的化学动力学迁移。在1微米LPA的存在下,小胶质细胞的平均迁移速率增加了3.8倍。在膜片钳研究中,我们证明LPA诱导Ca(2+)激活的K(+)电流的激活。小胶质细胞Ca(2+)激活的K(+)电流被50 nm炭疽毒素或10微米克霉唑废除了。相比之下,5微米的Paxilline对Ca(2+)激活的K(+)电流没有任何显着影响。 LPA刺激的小胶质细胞迁移受到IKCa1 Ca(2+)激活的K(+)通道的阻滞剂抑制。在存在50 nm真菌毒素的情况下,LPA刺激的细胞的平均迁移速率降低了61%,而在暴露于10微米克霉唑的过程中降低了51%。小胶质细胞的迁移不受5微米的Paxilline的抑制。结论是,LPA刺激的小胶质细胞迁移需要IKCa1 Ca(2+)激活的K(+)通道。

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