The long-term effect of toosendanin on current through nifedipine-sensitive Ca2+ channels in NG108-15 cells

被引:15
作者
Li, MF [1 ]
Shi, YL [1 ]
机构
[1] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Physiol, Key Lab Neurobiol, Shanghai 200031, Peoples R China
基金
中国国家自然科学基金;
关键词
toosendanin; Ca2+ influx; whole-cell recording; L-type; presynaptic blocker; apoptosis;
D O I
10.1016/j.toxicon.2004.09.010
中图分类号
R9 [药学];
学科分类号
1007 [药学];
摘要
Toosendanin is a triterpenoid derivative extracted from Melia toosendan Sieb et Zucc. Previous studies demonstrated that toosendanin could block neurotransmission and stimulate PC12 cell into differentiation and apoptosis. These actions of toosendanin were suggested to result from a continuous increase in Ca2+ influx, which led to intracellular Ca2+ overload. Here, we observed the long-term effect of toosendanin on Ca2+ channels in NG108-15 cells by whole-cell patch-clamp recording. Obtained data showed that a prolonged exposure to toosendanin induced a continuous increase in the Ca2+ influx in a concentration and time-dependent manner while a brief treatment induced an irreversible increase in Ca2+ influx in differentiated NG108-15 cells. The nifedipine-sensitive L-type currents were significantly increased after exposure to TSN while the nifedipine-resistant or omega-conotoxin MVIIC-sensitive currents were not affected. (C) 2004 Elsevier Ltd. All rights reserved.
引用
收藏
页码:53 / 60
页数:8
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