ArticleIllés P, Vyskocil F.
Eur J Pharmacol. 1978 Apr 15;48(4):455-7.
PGE1 (10(-7) M) in the absence of Ca2+ or at low external Ca2+ concentrations (0.2-0.5 mM) depressed the frequency of miniature end-plate potentials (m.e.p.p.s) in frog sartorius muscle, but m.e.p.p. amplitudes were unchanged. Both an increase in Ca2+ concentration to 2 mM or a blockade of Ca2+ uptake into mitochondria by metabolic inhibitors (5 X 10(-5) M 2,4-dinitrophenol or 2 X 10(-5) M rotenone) prevented the inhibitory action of PGE1 on m.e.p.p. frequency. We suggest that PGE1 may inhibit acetylcholine release from motor nerve terminals by promoting the active uptake of Ca2+ by mitochondria, or by facilitating the efflux of Ca2+ from the axoplasm into the extracellular medium.