Effects of Sodium Fluoride on Nerve-Muscle Transmission

Abstract

Anticurare action of NaF at the neuromuscular junction is demonstrated and analyzed for various stages of impulse transmission from nerve to muscle. The e.p.p. of preparations blocked by d-tubocurarine is augmented by 0.5–10 mm NaF. The e.p.p. amplitude is increased about 2.5 times by 0.5–1 mm, nearly three times by 3 mm or higher concentrations, and some prolongation occurs. The e.p.p. of a preparation blocked by tetanization is also augmented promtly by NaF, and transmission is restored. In this case, the threshold voltage for propagated muscle responses is lowered. NaF has no effect on the normal muscle membrane potential, even in the end-plate region —nor has it any effect on the electrical threshold. The end-plate depolarization produced by acetylcholine is considerably increased by NaF; and the curve of NaF concentration against the increase of depolarization is identical with that of the increase of e.p.p. The time course of acetylcholine depolarization, when augmented by small concentrations of NaF produce some prolongation of the falling limb, but the curve is still quite different from one augmented by eserin. NaF has no effect on the frequency of spontaneous e.p.p.s, but it considerably augments the height of each individual miniature e.p.p. The augmentation of the e.p.p. produced by NaF is not explained by an anticholinesterase action; it is mainly due to an increased sensitivity of the end-plate to acetylcholine induced by the fluoride ion.