刺尾鱼毒素与培养神经元细胞中电压敏感性钙通道的相互作用。
Interactions of maitotoxin with voltage-sensitive calcium channels in cultured neuronal cells.
作者信息
Freedman S B, Miller R J, Miller D M, Tindall D R
出版信息
Proc Natl Acad Sci U S A. 1984 Jul;81(14):4582-5. doi: 10.1073/pnas.81.14.4582.
The dinoflagellate toxin maitotoxin (MTX) stimulated 45Ca2+ uptake in cultured NG108-15 neuroblastoma X glioma cells. Depolarizing stimuli (e.g., 50 mM K+) produced an immediate stimulation in Ca2+ uptake, whereas that produced by MTX occurred only after a lag period of about 2 min. MTX did not stimulate Ca2+ uptake into fibroblasts. Both 50 mM K+- and MTX-stimulated Ca2+ uptake was blocked by organic calcium channel antagonists (nitrendipine, D-600, diltiazem) at very low concentrations. Cd2+ was also a potent blocker. The novel dihydropyridine BAY K8644 enhanced Ca2+ uptake in the presence of 50 mM K+ but had no effect in 5 mM Ca2+. However, in the presence of MTX, BAY K8644 stimulated Ca2+ uptake in 5 mM K+. The effects of MTX were not blocked by tetrodotoxin but were decreased in Na+-free medium. MTX did not stimulate Na+ uptake into NG108-15 cells and did not alter [3H]nitrendipine binding to rat brain cortical synaptosomes. It is concluded that MTX may alter the voltage dependence of calcium-channel activation.
双鞭甲藻毒素刺尾鱼毒素（MTX）刺激培养的NG108 - 15神经母细胞瘤X胶质瘤细胞摄取45Ca2+。去极化刺激（如50 mM K+）能立即刺激Ca2+摄取，而MTX产生的刺激仅在约2分钟的延迟期后出现。MTX不会刺激成纤维细胞摄取Ca2+。50 mM K+和MTX刺激的Ca2+摄取在极低浓度下均被有机钙通道拮抗剂（尼群地平、D - 600、地尔硫䓬）阻断。Cd2+也是一种有效的阻断剂。新型二氢吡啶BAY K8644在50 mM K+存在时增强Ca2+摄取，但在5 mM Ca2+时无作用。然而，在MTX存在时，BAY K8644在5 mM K+中刺激Ca2+摄取。MTX的作用不被河豚毒素阻断，但在无钠培养基中作用减弱。MTX不会刺激NG108 - 15细胞摄取Na+，也不会改变[3H]尼群地平与大鼠脑皮质突触体的结合。结论是MTX可能改变钙通道激活的电压依赖性。
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