MANY polyvalent cations have been used in studies of synaptic transmission either as tools for gaining a better understanding of synaptic processes or, in their own right, as potentially toxic substances1–7. Inorganic lead although long known to have neurotoxic effects, has not been studied extensively at the synaptic level until recently. Kostial and Vouk8 found that lead blocked transmission in the perfused superior cervical ganglion of the cat in vitro by reducing the amount of acetylcholine released from presynaptic nerve terminals without affecting the response of ganglion cells to applied acetylcholine. The addition of excess calcium to the perfusion solution restored acetylcholine output and relieved the lead block. Manalis and Cooper9, working with the frog sciatic nerve-sartorius muscle preparation in vitro, showed that lead depresses phasic transmitter release evoked by nerve stimulation and increases spontaneous release as evidenced by an increase in frequency of miniature endplate potentials. Lead had only a weak, curare-like effect on the postsynaptic response to applied acetylcholine. In this paper we show, using electrophysiological techniques, that PbCl2 blocks synaptic transmission pre-synaptically by competitive inhibition of calcium. In support of this data, we further show, using 45Ca, that lead in fact does reduce the uptake of calcium by preganglionic nerve terminals.
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