The effects of toxin II (
AaH II) isolated from the scorpion Androctonus australis Hector on
sodium current in
neuroblastoma X
glioma NG 108-15 hybrid cells were analysed under patch clamp conditions in the whole cell configuration.
AaH II (70 nM) induced a maintained
sodium current, as well as increasing both fast and slow inactivation time constants and the amplitude of the peak current. This latter effect occurred via a shift of the activation-voltage curve towards negative voltage values by about 9 mV.
Oleic acid (5 microM), which had no effect on INa under control conditions, decreased the
AaH II-induced maintained current. It also reversed, or prevented the increase of the peak current induced by
AaH II. However, it neither prevented nor modified the
AaH II-induced increase in inactivation time constants. The binding of the toxin to its specific site and the number of binding sites for
AaH II were not significantly modified by
oleic acid. The
oleic acid-induced effects could not be related to the activation of
protein kinase C since PMA, a potent activator of this
enzyme, did not produce
oleic acid-like effects. From these results, it is concluded that
AaH II has several independent effects on
sodium channels, some of which could be modulated by the
lipid environment of
sodium channels in the membrane.