Kongsamut S, Freedman S B, Simon B E, Miller R J
Life Sci. 1985 Apr 15;36(15):1493-501. doi: 10.1016/0024-3205(85)90058-x.
Depolarization with 50 mM K+ increased 45Ca2+ uptake into neuronal clonal cell lines NG108-15, N1E-115 and NH15-CA2. In each cell line this depolarization-induced uptake was blocked by inorganic and organic blockers of voltage sensitive calcium channels. However, tetrodotoxin (10(-6) M) was ineffective. Moreover, in the presence of tetrodotoxin, neither batrachotoxin nor veratridine inhibited the depolarization-induced uptake. The novel dihydropyridine BAY K8644 enhanced depolarization-induced 45Ca2+ uptake into each cell line in a nitrendipine reversible fashion. In the presence of tetrodotoxin, the BAY K8644/50 mM K+ stimulated uptake could be partially inhibited by batrachotoxin (10(-6) M) and veratridine (5 X 10(-5) M). These effects were not altered by the presence of scorpion venom (1 microgram/ml). The results indicate that both batrachotoxin and veratridine can modulate the effects of dihydropyridines on the gating properties of voltage sensitive calcium channels.
50 mM钾离子引起的去极化增加了神经母细胞瘤克隆细胞系NG108 - 15、N1E - 115和NH15 - CA2对45Ca2 +的摄取。在每个细胞系中,这种去极化诱导的摄取被电压敏感钙通道的无机和有机阻滞剂所阻断。然而,河豚毒素(10(-6) M)无效。此外,在存在河豚毒素的情况下,无论是蟾毒素还是藜芦碱都不能抑制去极化诱导的摄取。新型二氢吡啶BAY K8644以尼群地平可逆的方式增强了去极化诱导的45Ca2 +向每个细胞系的摄取。在存在河豚毒素的情况下,BAY K8644 / 50 mM钾离子刺激的摄取可被蟾毒素(10(-6) M)和藜芦碱(5×10(-5) M)部分抑制。蝎毒(1微克/毫升)的存在并未改变这些效应。结果表明,蟾毒素和藜芦碱均可调节二氢吡啶对电压敏感钙通道门控特性的影响。