毒蕈碱受体激活NlE - 115神经母细胞瘤细胞中的钙通道和钙依赖性钾通道。

Muscarinic receptors activate calcium channels and calcium dependent potassium channels in NlE-115 neuroblastoma cells.

作者信息

Hedlund B, Lorentz M, Arhem P

出版信息

Pharmacol Toxicol. 1987 Feb;60(2):156-60. doi: 10.1111/j.1600-0773.1987.tb01516.x.

DOI:10.1111/j.1600-0773.1987.tb01516.x

Abstract

Responses of NlE-115 neuroblastoma cells to application of carbachol were studied using intracellular recording techniques. Activation of muscarinic cholinergic receptors by carbachol resulted in a depolarization of the cells. The response was blocked by pirenzepine (1 microM) and by CoCl2 (5 mM), verapamil (10 microM) and gallopamil (10 microM), and prolonged by quinine (5 mM). It is suggested that muscarinic receptors increase the membrane calcium permeability, and that the influx of calcium activates calcium dependent potassium channels.

摘要

利用细胞内记录技术研究了NlE - 115神经母细胞瘤细胞对卡巴胆碱应用的反应。卡巴胆碱激活毒蕈碱胆碱能受体导致细胞去极化。该反应被哌仑西平（1微摩尔）、氯化钴（5毫摩尔）、维拉帕米（10微摩尔）和加洛帕米（10微摩尔）阻断，并被奎宁（5毫摩尔）延长。提示毒蕈碱受体增加膜钙通透性，且钙内流激活钙依赖性钾通道。

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