Interactions of maitotoxin with voltage-sensitive calcium channels in cultured neuronal cells

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 on 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.