Postsynaptic inhibition of the frog neuromuscular transmission by prostaglandin E1.
Intracellular recordings were made from the frog sartorius muscle end plate. Prostaglandin (PG) E1 (100 nM-10 microM) decreased the amplitude of the end plate potential (EPP). PGE1 decreased the quantal size of EPPs, while it rather increased the quantum content. The frequency of miniature (m) EPPs was not affected by PGE1. PGE1 depressed the acetylcholine (ACh)-induced depolarization, as well as the amplitude of mEPPs. These results suggest that PGE1 decreases the sensitivity of nicotinic ACh receptors at the end plate membrane, resulting in postsynaptic depressions of neuromuscular transmission.
D000818:Animals; D003864:Depression, Chemical; D004553:Electric Conductivity; D008564:Membrane Potentials / Q000187:drug effects; D009045:Motor Endplate / Q000187:drug effects; D009469:Neuromuscular Junction / Q000187:drug effects*; D011458:Prostaglandins E / Q000494:pharmacology*; D011898:Ranidae; D009435:Synaptic Transmission / Q000187:drug effects*
D011458:Prostaglandins E