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SH-SY5Y人神经母细胞瘤细胞中去极化和毒蕈碱受体刺激诱导的Ca2+内流的不同机制。

Different mechanisms of Ca2+ entry induced by depolarization and muscarinic receptor stimulation in SH-SY5Y human neuroblastoma cells.

作者信息

Lambert D G, Whitham E M, Baird J G, Nahorski S R

机构信息

Department of Pharmacology and Therapeutics, University of Leicester, U.K.

出版信息

Brain Res Mol Brain Res. 1990 Aug;8(3):263-6. doi: 10.1016/0169-328x(90)90026-a.

Abstract

Depolarization by elevated K+ and stimulation of muscarinic M3 receptors evoke rises in [Ca2+]i in Fura 2-loaded SH-SY5Y human neuroblastoma cells. The response to K+ (30 and 60 mM) could be inhibited by the dihydropyridine L-channel antagonist +PN 200-110 and totally suppressed by Ni2+, the N-channel blocker omega-conotoxin reduced the response to 60 mM K+. Carbachol-stimulated increase in [Ca2+]i was blocked by atropine and Ni2+ but was totally resistant to the L- and N-channel blockers. This study reveals the presence of L- and N-type voltage-sensitive Ca2+ channels on undifferentiated SH-SY5Y cells that are opened by K+ depolarization but not by muscarinic stimulation.

摘要

高钾引起的去极化以及毒蕈碱型M3受体的刺激可使负载Fura 2的SH-SY5Y人神经母细胞瘤细胞中的[Ca2+]i升高。对钾离子(30和60 mM)的反应可被二氢吡啶L型通道拮抗剂+PN 200-110抑制,而被N型通道阻滞剂镍离子完全抑制,ω-芋螺毒素可降低对60 mM钾离子的反应。卡巴胆碱刺激引起的[Ca2+]i增加被阿托品和镍离子阻断,但对L型和N型通道阻滞剂完全耐药。本研究揭示了未分化的SH-SY5Y细胞上存在L型和N型电压敏感型Ca2+通道,这些通道可被钾离子去极化打开,但不能被毒蕈碱刺激打开。

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