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缓激肽刺激和注射肌醇1,4,5-三磷酸诱导大鼠胶质瘤细胞中钙依赖性钾通道活性。

Ca(2+)-dependent K+ channel activity in rat glioma cells induced by bradykinin stimulation and by inositol 1,4,5-trisphosphate injection.

作者信息

Binmöller F J, Reiser G

机构信息

Physiologisch-chemisches Institut, Universität Tübingen, Germany.

出版信息

Cell Mol Neurobiol. 1993 Dec;13(6):615-24. doi: 10.1007/BF00711561.

Abstract
  1. A glial cell line derived from C6 rat glioma cells has been shown previously to respond to extracellular pulses of bradykinin or intracellular injection of inositol 1,4,5-trisphosphate (Ins-P3) with a slow hyperpolarizing response due to activation of a K+ current (G. Reiser et al., Brain Res. 506, 205-214; 1990). 2. We determined the ensuing single-channel activity, which is most likely caused by Ca2+ released from internal stores after bradykinin stimulation. Bradykinin-activated channels were selectively permeable to K+, but not to Na+ or to Cl-, and exhibited conductances of mainly 40 and 50 pS. In glioma cells the same type of channel was activated by intracellular injection of Ins-P3 and by extracellular bradykinin pulses.
摘要
  1. 先前已表明,源自C6大鼠胶质瘤细胞的神经胶质细胞系会因钾离子电流激活而对缓激肽的细胞外脉冲或肌醇1,4,5 -三磷酸(Ins - P3)的细胞内注射产生缓慢的超极化反应(G. 赖泽尔等人,《脑研究》506, 205 - 214;1990年)。2. 我们确定了随后的单通道活性,这很可能是缓激肽刺激后从内部储存库释放的钙离子所致。缓激肽激活的通道对钾离子有选择性通透性,对钠离子或氯离子则无通透性,且主要表现出40和50皮西门子的电导。在胶质瘤细胞中,相同类型的通道可通过细胞内注射Ins - P3和细胞外缓激肽脉冲激活。

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本文引用的文献

2
Bradykinin induces hyperpolarizations in rat glioma cells and in neuroblastoma X glioma hybrid cells.
Brain Res. 1982 May 6;239(1):191-9. doi: 10.1016/0006-8993(82)90841-1.
7
Bradykinin causes a transient rise of intracellular Ca2+-activity in cultured neural cells.
Pflugers Arch. 1985 Oct;405(3):260-4. doi: 10.1007/BF00582570.

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