Trachynilysin, a protein neurotoxin isolated from stonefish (Synanceia trachynis) venom, increases spontaneous quantal acetylcholine release from Torpedo marmorata neuromuscular junctions

Trachynilysin, a neurotoxin isolated from the venom of the stonefish (Synan ceia trachynis, Scorpaenidae), produced a marked increase in the frequency of spontaneous miniature endplate potentials (MEPPs) at Torpedo neuromuscul ar junctions. The periods of high frequency MEPP discharges were of variabl e duration and were followed by periods of rest. In addition, trachynilysin increased as a function of time the proportion of larger than normal MEPPs , the so-called "giant" MEPPs. Trachynilysin did not affect the junctions w hen applied in Ca2+-free medium supplemented with EGTA, but the subsequent addition of Ca2+ caused a rapid increase in MEPP frequency, even when the t oxin was washed out of the Ca2+-free medium. Thus, trachynilysin binding to nerve terminals is not dependent on external Ca2+, but the cation is requi red for trachynilysin-elicited quantal transmitter release. The effect of t rachynilysin on MEPP frequency was unaffected by the Ca2+ channel blockers omega -conotoxin GVIA, omega -agatoxin IVA and Gd3+, which indicates that t he toxin's action involves Ca2+ entry via a pathway independent of voltage- sensitive Ca2+ channels. Pre-treatment of the junctions with concanavalin-A prevented the trachynilysin-induced enhancement of quantal transmitter rel ease, which suggests that the toxin interacts with or binds to a glycoprote in on the surface of motor nerve terminals.