Action of the presynaptic neurotoxin notechis II-5 from the venom of Notechis scutatus scutatus on mouse motor nerve endings

Abstract

The neurotoxin notechis II-5 (N-II-5) from the venom of the Australian tiger snake (Viperidae family) gave rise to changes in the frequency of miniature end-plate potentials (MEPP) in the mouse diaphragm in three distinct phases: An initial decrease in frequency, then an increase, and finally a decrease in the frequency of MEPP or even a complete block. The effect of N-II-5 was enhanced with a rise in the temperature of the solution from 20 to 30 and 35°C. There was no effect if Ca⁺⁺ was removed from the solution. Addition of Ca⁺⁺ to the solution after washing the muscle to remove N-II-5 effect. In the presence of N-II-5, an increase in the K⁺ concentration in the solution to 20 mM did not lead to a sharp increase in the frequency of MEPP typical of depolarized nerve endings. Agents which increased the intracellular Ca⁺⁺ concentration, not through depolarization of the nerve endings (hypertonic solution, ionophore A 23187), preserved the ability to increase the frequency of MEPP. It is suggested that the presynaptic effect of N-II-5 is connected with its phosphorylase activity and can be explained by the disturbance of the activity of the liberation sites and not by exhaustion of mediator reserves.