Pharmacological properties of voltage-gated Na+ currents in motor neurones from a hydrozoan jellyfish Polyorchis penicillatus

The Na+ current of 'swimming motor neurones' in the hydromedusan Polyorchis penicillatus was tetrodotoxin-insensitive. The local anaesthetics lidocaine and procainamide caused partial, non use-dependent blockade of the Na+ channel. Veratridine produced partial blockade of the Na+ channel without affecting inactivation. An order of blocking potency of di- and trivalent cations was established as: La3+ = Zn2+ = Cd2+ > Ni2+ > Mn2+ = Co2+ > Ca2+ > Ba2+ > Mg2+. All these cations, except Ba2+, produced depolarizing shifts in the conductance-voltage curves. Even at relatively high concentrations, the dihydropyridines nicardipine, nitrendipine and (+)Bay K 8644 produced only weak blockade of the Na+ current; while nimodipine, nifedipine and (-)Bay K 8644 were ineffective. Diltiazem and verapamil weakly blocked the Na+ current in a dose-dependent manner with no evidence of use-dependence. The calmodulin inhibitors W7 and calmidazolium were ineffective blockers of Na+ currents. Crude Conus venoms and the Conus peptides, µ-conotoxin GIIA, µO-conotoxin MrVIA, omega-conotoxin GVIA and omega-conotoxin MVIIC, were without effect. Capsaicin produced rapid, reversable blockade of Na+ current. It has been suggested that 'primitive' Na+ channels could be expected to have pharmacological properties that are intermediate between those of Na+ and Ca2+ channels. If such channels exist, the Na+ channel described here is clearly not one of them.