The actions of presynaptic snake toxins on membrane currents of mouse motor nerve terminals.

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Abstract
1. The m. triangularis sterni of the mouse was used to investigate the actions of dendrotoxin, .beta.-bungarotoxin, crotoxin, taipoxin, bee venom phospholipase A2, aprotinin and apamin on presynaptic currents which flow inside the perineural sheath of nerve bundles upon nerve stimulation. 2. Neither the fast K+ current (IK,f) for the Ca2+-dependent K+ current IK(CA) (unmasked after blockade of IK,f by 3,4-diaminopyridine) was affected by the neurotoxins and drugs mentioned. 3. Inhibition of both IK,f and IK(Ca) by tetraethylammonium (30 mM) prolonged presynaptic depolariztion owing to Ca2+ influx through fast and slow Ca2+ channels. Additional application of dendrotoxin, .beta.-bungarotoxin, crotoxin or taipoxin in the nanomolar range caused further prolongation of Ca2+ influx, presumably due to blockade of slowly activating K+ current (IK,s). Onset of toxin effects was immediate and could not be reversed by washing for 60 min. 4. Similar prolongation of slow Ca2+ current was effected by 3,4-diaminopyridine, whereas addition of apamin, aprotinin or phospholipase A2 left the signals unchanged. 5. These data indicate that facilitatory actions of dendrotoxin, .beta.-bungarotoxin, taipoxin and crotoxin are mediated by an increase of Ca2+ entry into nerve terminals. The actions of these toxins are discussed in terms of a blockade of presynaptic K+ channels with slow activation kinetics.