Nerve stimulation-induced contractions of the chick biventer cervicis muscle were slowly reduced by omega-conotoxin. However, omega-conotoxin had no effect on skeletal muscle function after i.v. injection in mice or on nerve stimulation-induced contractions of focally innervated muscle of the rat diaphragm or the rabbit proximal oesophagus, or the multiply innervated extra-ocular rectus muscle from rabbit. The lack of effect of omega-conotoxin on mammalian neuromuscular junctions was not due to the high safety factor in transmission or to a high local concentration of Ca2+ originating from the muscle, and could not be accounted for in terms of the operation of facilitatory or inhibitory feedback modulation of transmitter release from motoneurone terminals. It is concluded that the Ca2+ channels of mammalian motoneurone terminals differ from those of avian motoneurone terminals and other omega-conotoxin-sensitive nerve terminals.