ABSTRACT
The neurotoxin notechis II-5 (N-II-5) from tiger snake venom (Notechis scutatus) induces three-phasic changes in miniature end-plate potential (MEPP) frequency recorded in the mouse diaphragm muscle: an initial fall of frequency followed by increase and decrease in MEPP frequency up to complete blockade. The effect of N-II-5 was enhanced with rising of the solution temperature from 20 to 30 and 35 degrees C. Removal of Ca2+ from the solution prevented the presynaptic effect of N-II-5. After washing out of the muscle from N-II-5 with Ca-free solution, addition of Ca2+ to the solution provoked the development of the effect typical of the effect of typical of the toxin. In the presence of N-II-5 an increase in K+ concentration in the solution up to 20 mM did not result in a sharp rise of MEPP frequency characteristic of depolarized nerve terminals. The agents that raise Ca2+ axoplasmic concentration not on account of depolarization of nerve terminals (hypertonic solution, ionofor A23187) preserved the capacity for increasing MEPP frequecy. It is suggested that the presynaptic effect of N-II-5 is related to its phospholipase activity and can be explained by disturbance of the activity of release sites rather than by depletion of transmitter stores.
