Block of locust muscle glutamate receptors by δ-philathotoxin occurs after receptor activations

One component (δ-philathottoxin (δ-PTX)) of the venom from the wasp (Philanthus triangulum blocks transmission postsynaptically at excitatory synapses on locust muscle. δ-PTX depresses both the iontophoretic glutamate potential and the excitatory junctional current (e.j.c.) in a glutamate receptor activation-dependent manner. The rate of recovery from the effects of the toxin is reduced following either prolonged application of l-glutamate or repetitive iontophoretic application of this amino acid or high frequency neural stimulation of the muscle in the presence of δ-PTX. The decay phase of the e.j.c. is shortened by δ-PTX. The effects of δ-PTX on the e.j.c. are not voltage dependent. The open-close kinetics of glutamate channels in extrajunctional muscle membrane are modified by δ-PTX as shown by patch clamp analysis. The mean life time of the glutamate channel is reduced, whilst the mean interval between single opening events is increased with the events often occurring in bursts. These data are consistent with glutamate channel blocking by this toxin. It is proposed that the toxin blocks open channels gated by both junctional and extrajunctional glutamate receptors on locust muscle. It is further proposed that δ-PTX enters a compartment of the muscle through the glutamate open channels and that it can also block the open channels from this site.