Abstract
The effect of neurotoxin (JSTX) separated from spider venom on the lobster neuromuscular junction was studied. JSTX selectively suppressed excitatory postsynaptic potentials (epsp) without affecting the inhibitory postsynaptic potentials (ipsp). The effect of JSTX was dose-dependent. The threshold dose for suppressing epsp corresponded to a small fraction of the toxin amount in a venom gland. At high concentration, JSTX irreversibly blocked epsp. The reduction in amplitude of extracellularly recorded epsp after JSTX application followed an exponential time course. The rate of suppression increased proportionally with toxin concentration. JSTX blocked the glutamate potential in the postsynaptic membrane but it failed to affect the aspartate-induced depolarization. Kainic acid potentiated the glutamate-induced depolarization but it was without effect in the presence of JSTX. Depolarization produced by quisqualic acid was suppressed by the toxin. The spider venom contained specific blockers of glutamate receptors in crustacean neuromuscular junctions.