Inhibitory actions of tuberostemonine on the excitatory transmission at the crayfish neuromuscular junction.

At the crayfish neuromuscular junction, tuberostemonine, an alkaloid from Stemona japonica, reduced the amplitude of both the excitatory junctional potential (e.j.p.) and the glutamate response in a dose-dependent manner at concentrations above 0.1 mM. Tuberostemonine acted presynaptically on the crayfish neuromuscular junction to reduce a quantal content of extracellularly recorded e.j.p.s, and postsynaptically to reduce their unit size. The decay of the excitatory synaptic current was accelerated by tuberostemonine. The gradual decline of the successive glutamate currents induced by a train was facilitated by the presence of tuberostemonine even in the muscle fibre pre-treated with concanavalin A. The rate of recovery from the refractory form of the glutamate receptor to the free reactive one was slightly affected by tuberostemonine when it was determined by using a paired pulse method. The inhibitory action of tuberostemonine on glutamate responses was voltage-dependent and hyperpolarization increased the drug action. These results indicate that tuberostemonine acts in part as an open-channel blocker at the crayfish neuromuscular junction.