SPECIFIC BLOCKAGE OF SQUID AXON RESTING POTASSIUM PERMEABILITY BY HALICLONA-VIRIDIS (PORIFERA, HALICLONIDAE) TOXIN (HVTX)

The action of partially purified HvTX, toxin of the marine sponge H. v iridis, was explored on the giant axon of the tropical squids Doryteut his plei and Sepioteuthis sepioidea. HvTX depolarizes the nerves dose dependently. The effect occurs after blocking sodium channels with tet rodotoxin (1 mu M), removing external Na+, blocking electrically excit able K+ channels with 3,4-diamino-pyridine (10 mM) or internal and ext ernal application of tetraethylammonium (40 mM). Ouabain (up to 10 mM) does not modify HvTX effect. The action of HvTX occurs only when it i s applied to the outer phase of the nerve membrane; microinjection of the toxin into the axons lacks depolarizing effects. HvTX reduces the dependence of membrane potential on external potassium concentration. The apparent Rb-86(+) permeability (pi') was measured in axons of S. s epioidea. The value of pi' in normal artificial sea water was 80 (61, 96) nm/sec (median and its 95% confidence interval, n = 8) and raised to 1030 (588, 2113) nm/sec (n = 7) when the axons were depolarized to 0 mV raising external K+ to 300 mM. In axons depolarized with HvTX (10 mM external K+) to 0 mV, pi' was 88 (55, 97) nm/sec (n = 8). HvTX cou ld not prevent (P>>0.05) the increase in pi' induced by 300 mM K+ when the ion concentration was raised before toxin application [pi' = 660 (354, 1876) nm/sec, n = 7]. Most of the Rb-86(+) permeability increase in high K+ was prevented if HvTX was added before external K+ was rai sed [pi' = 298 (264, 337) nm/sec, n = 8]. All the measures of pi' were carried out in solutions containing 1 mu M tetrodotoxin, 1 mM 3,4-dia minopyridine and 2 mM ouabain.