Effects of tiger snake venom on the ultrastructure of motor nerve terminals.

Abstract

FOR several years investigators have been attempting to establish whether or not synaptic vesicles in nerve terminals are the structural basis for the observed quantal release of transmitter1. When neuromuscular junctions are subjected to various procedures, morphological changes are observed which can be correlated with changes in miniature end-plate potential (MEPP) frequency and depletion of transmitter stores: exposure to high potassium or to hyperosmotic solutions results in a reduced population of vesicles2; prolonged tetanic stimulation, combined with inhibition of choline synthesis by hemicholinium, produces a reduction in synaptic vesicle volume3 and a depletion of vesicles1, especially in the presence of a metabolic inhibitor5; nerve section leads to reduction in the number of vesicles6,7; and administration of toxins such as Black Widow spider venom8,9 or beta-bungaro-toxin10 leads to a decrease in the number of synaptic vesicles in the nerve terminals. There is, however, no unequivocal evidence that the synaptic vesicles are directly involved in quantal release9,11, as, for example, massive release of quanta may lead to no immediate detectable reduction in the number of synaptic vesicles12. We describe here a preliminary investigation of a new venom in an attempt to determine whether its effects on nerve terminals accord with the vesicle hypothesis. The elucidation of the activities of such new biotoxins may prove of use in studies on excitable cells, as has been the case with tetrodotoxin13–15.