Effects of crude brevetoxin on membrane potential and spontaneous or evoked end-plate potentials in rat hemidiaphragm

The principal effects of crude brevetoxins on the neuromuscular junction of rat phrenic--diaphragm preparations are to: preferentially depress indirectly induced muscle contractions at concentrations lower than those required to affect directly induced muscle contractions; depolarize muscle membrane at both synaptic and extra-synaptic areas; increase MEPP frequency and eventually block end-plate potential generation; induce a concentration dependent biphasic effect on MEPP amplitude; depress acetylcholine-induced depolarizations. The mechanism of muscle membrane depolarization appears to involve an increase in membrane permeability, as shown by a decrease in input resistance at both synaptic and non-synaptic areas. That the major change is in sodium ion permeability is indicated by the observations that depolarizations do not occur in the absence of extracellular sodium or in the presence of tetrodotoxin, a sodium channel blocker.