Effects of a spider toxin on the glutaminergic synapse of lobster muscle.
We studied the effect of neurotoxin (JSTX) separated from spider venom on the lobster neuromuscular junction. JSTX selectively suppressed excitatory post-synaptic potentials (e.p.s.p.s) without affecting the inhibitory post-synaptic potentials (i.p.s.p.s). The effect of JSTX was dose-dependent. The threshold dose for suppressing e.p.s.p.s corresponded to a small fraction of the toxin amount in a venom gland. At high concentration, JSTX irreversibly blocked e.p.s.p.s. The reduction in amplitude of extracellularly recorded e.p.s.p.s after JSTX application followed an exponential time course. The rate of suppression increased proportionally with the toxin concentration. JSTX blocked the glutamate potential in the post-synaptic 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 is suppressed by the toxin. Our results suggest that the spider venom contains specific blockers of glutamate receptors in crustacean neuromuscular junctions.
D000818:Animals; D001224:Aspartic Acid / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005971:Glutamates / Q000494:pharmacology; D007608:Kainic Acid / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects; D008121:Nephropidae; D009469:Neuromuscular Junction / Q000187:drug effects*; D009498:Neurotoxins / Q000494:pharmacology*; D011956:Receptors, Cell Surface / Q000187:drug effects; D017470:Receptors, Glutamate; D017981:Receptors, Neurotransmitter / Q000187:drug effects; D013111:Spider Venoms; D013997:Time Factors
D005971:Glutamates; D009498:Neurotoxins; D011956:Receptors, Cell Surface; D017470:Receptors, Glutamate; D017981:Receptors, Neurotransmitter; D013111:Spider Venoms; D001224:Aspartic Acid; D007608:Kainic Acid