The effects of oxamniquine on neuromuscular transmission have been investigated in some experimental animals in an effort to unveil some of the unwanted effects of this commonly prescribed schistosomicide. Results obtained show that relatively low concentrations of the drug (oxamniquine, 10-100 micrograms/ml) potentiated acetylcholine-, carbachol- and nicotine-evoked contractions of the toad (Bufo regularis) isolated rectus abdominis muscle. Moderate to high concentrations of the compound (oxamniquine, 500 micrograms/ml and above) contracted rectus abdominis muscle preparations, and depressed indirect electrically-induced twitches of the rat isolated hemidiaphragm and chick isolated biventer muscle preparations. The depression of electrically-evoked twitches of the chick biventer and rat phrenic nerve-hemidiaphragm muscle preparations in vitro induced by moderate to high concentrations of oxamniquine (500 micrograms/ml and above) were resistant to bath-applied physostigmine (1-15 micrograms/ml), but deepened by d-tubocurarine (3-10 micrograms/ml). These findings suggest that the neuromuscular blocking action of oxamniquine is probably post-junctional in origin.