The effect of lanthanum on nerve terminals in goldfish muscle after paralysis with tetanus toxin.

Lanthanum (1.9 mM) has previously been shown to produce a massive increase in the frequency of spontaneous miniature junction potentials at the neuromuscular junctions of goldfish fin muscles. In fins where transmission has been blocked by previous injection of tetanus toxin and where there are few (if any) spontaneous miniature potentials, lanthanum treatment is able to restore a modest frequency. The results of parallel experiments in which the ultrastructure of the nerve endings has been investigated by electron microscopy are reported. In normal goldfish muscles, the lanthanum-induced increase in frequency is accompanied by depletion of synaptic vesicles. In contrast, there is no depletion in tetanus toxin-paralysed nerve endings subjected to lanthanum treatment, which parallels the relative insensitivity of the endings to activation by lanthanum. Of particular interest is the finding that the lanthanum treatment of the toxin muscles apparently causes accumulation of vesicles in a row just inside the terminal membrane, both at synaptic and non-synaptic positions. The results are discussed with respect to the mechanisms of transmitter release and to the actions of tetanus toxin and lanthanum.