The effect of the oxime reactivator obidoxime chloride (obidoxime) on single frog neuromuscular junctions has been studied in order to clarify its action on the acetylcholine receptor (AChR) and on the acetylcholine esterase (AChE), both before and after blocking its enzymatic activity with the organophosphorus compound sarin. Experiments iontophoretic application of obidoxime to end-plates demonstrated that it has a weak direct depolarizing effect. Furtheron, the drug is shown to possess a potentiating effect on the ACh-induced depolarization. After the AChE activity had been inhibited with sarin, obidoxime on the contrary decreases the depolarization induced by ACh. Both effects are fully reversible. It is concluded that obidoxime acts as an inhibitor of the AChE and as a partial antagonist of the AChR. The antagonistic effect on the receptor is usually masked by the predominating anticholinesterase effect. The effect of obidoxime on miniature end-plate potentials in long-time experiments on sarin-poisoned muscles, showed only weak signs of recovery from the action of the AChE inhibitor. Only focally higher concentration of the drug produced a more marked but short term recovery of the mepps, which is, however, supposed to be dependent on the AChR antagonism. It is still unclear how much of the varying therapeutic usefulness of obidoxime in clinical cases is due to its AChE reactivation and how much to the antagonistic effect on the AChR.