Calcium-dependent inhibition by prostaglandin E1 of spontaneous acetylcholine release from frog motor nerve.
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.
D000109:Acetylcholine / Q000037:antagonists & inhibitors* / Q000378:metabolism; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001001:Anura; D002118:Calcium / Q000494:pharmacology*; D004140:Dinitrophenols / Q000494:pharmacology; D008928:Mitochondria / Q000187:drug effects; D010525:Peripheral Nerves / Q000187:drug effects* / Q000378:metabolism; D011458:Prostaglandins E / Q000494:pharmacology*; D011896:Rana temporaria; D012402:Rotenone / Q000494:pharmacology
D004140:Dinitrophenols; D011458:Prostaglandins E; D012402:Rotenone; D000109:Acetylcholine; D002118:Calcium