Résumé
Maitotoxin (3 ng/mol) induced a massive uptake of 45 Ca 2+ into BC 3 H 1 cells. This effect exhibits a lag phase of 3 min. Inositol diphosphate formation occurred concomittantly with the 45 Ca 2+ uptake but inositol monophosphate formation was found only after a 5‐min delay following toxin addition. Maitotoxin‐induced 45 Ca 2+ influxes could not be blocked by either 1 μM verapamil, 1 μM nifedipine or 1 mM La 3+ but was blocked by Zn 2+ (IC 50 = 41 μM). In addition to inositol phosphate formation and 45 Ca 2+ uptake, maitotoxin stimulated a large uptake of Na + and a great loss of K + in BC 3 H 1 cells. In the absence of Ca 2+ (1 mM EGTA) none of the four maitotoxin effects could be detected. After restoration of Ca 2+ the maitotoxin effects reappeared even when the toxin itself was no longer present. The divalent cation, Co 2+ (1 mM), inhibited ion movements induced by maitotoxin and also digitonin (8.1 μM). The toxin action showed a very pronounced pH dependence. At low pH, maitotoxin was inactive. The dose‐response curves for H + ion inhibition of maitotoxin‐induced Ca 2+ uptake showed a shift to the right when determined in the absence of HCO 3 ‐ and HCO 3 ‐ /Cl ‐ ions. It was concluded that the primary action of maitotoxin in BC 3 H 1 cells was a pore‐forming or channel‐forming activity of a non‐classical type. Some properties of maitotoxin resemble those of α‐latrotoxin, others those of pore‐forming agents such as melittin or α‐toxin of Staphylococcus aureus.