[Mechanism of action of alpha-neurotoxins from snake venom on nicotinic cholinoreceptors of sympathetic ganglion neurons in the rabbit].

Effect of alpha-neurotoxins from snake venoms (alpha-bungarotoxin and alpha-cobratoxin, 10(-6)M) on the ACh-induced current and on the fast excitatory postsynaptic current (EPSC) were studied in voltage-clamped neurons of the isolated rabbit superior cervical ganglion treated with atropine (10(-6)M) alpha-Neurotoxins produced potentiating or inhibitory effects on ACh-induced current and only inhibitory effect on EPSC. alpha-Neurotoxins did not change single channel current and lifetime for short-living nicotinic channels and prolonged the lifetime for long-living channels as well as EPSC decay. It is suggested that the inhibitor effect of alpha-neurotoxins on ACh-induced current and on EPSP is due to partial blockade of nicotinic Ach receptors and that their potentiating effect on ACh-induced current results from the prolonged lifetime for long-living channels.