Antimyasthenic action of corticosteroids.
Tests were made in vitro fo the action of prednisolone on nerve backfiring, muscle twitches, tetanus decay rates, miniature end-plate potential amplitude and frequency, and the block induced by curare, hemicholinium, and excess magnesium. At about 0.1 mM concentration, the steroid showed no 'veratrinic' or decurarizing action, and the probability of transmitter release was not increased in 10mM Mg++. Moreover, when acetylcholine stores were depleted in hemicholinium, there was no evidence of repair by steroid. The results are taken to mean that prednisolone and congeners do not owe their therapeutic efficacy in myasthenia to actions at the neuromuscular junction. It is therefore concluded that the clinical benefits from steroids are related to systemic, possibly immunosuppressive effects.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D003472:Curare / Q000494:pharmacology; D003964:Diaphragm; D006426:Hemicholinium 3 / Q000494:pharmacology; D066298:In Vitro Techniques; D008274:Magnesium / Q000494:pharmacology; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009469:Neuromuscular Junction / Q000187:drug effects* / Q000502:physiology; D010791:Phrenic Nerve; D011239:Prednisolone / Q000494:pharmacology*; D051381:Rats; D009435:Synaptic Transmission / Q000187:drug effects
D006426:Hemicholinium 3; D003472:Curare; D011239:Prednisolone; D008274:Magnesium