A further study on the kinetics of the subcellular current events at the mouse end-plate in the presence of cimetidine and ranitidine.
The cholinomimetic activity of Cimetidine and Ranitidine has been demonstrated by several authors. In the aim to better understand the phenomenon, we analyse the miniature end-plate current decay time. The prolongation of the decay phase of the synaptic current induced by the "selective" H2-antagonist Ranitidine, and to a lesser extent and at higher concentrations by Cimetidine, resembles that of the cholinesterase inhibitors. These agents usually prolong the quantal conductance change having little or no effect on the channel lifetime. The results of our previous experiments, which data were obtained by analyzing the "voltage" events, either spontaneous or evoked, of a classic frog preparation, showed a marked alteration of the temporal parameters. These effects, obtained at higher drug concentrations than those used in the present work, are now better defined by deriving extracellularly the "current" events. The results are also compared with those obtained by assaying the cholinesterase inhibitor Eserine, under the same experimental conditions.
D000818:Animals; D002800:Cholinesterase Inhibitors / Q000494:pharmacology; D002927:Cimetidine / Q000494:pharmacology*; D004553:Electric Conductivity; D007473:Ion Channels / Q000187:drug effects; D051379:Mice; D009045:Motor Endplate / Q000502:physiology*; D009469:Neuromuscular Junction / Q000502:physiology*; D011899:Ranitidine / Q000494:pharmacology*; D011978:Receptors, Nicotinic / Q000187:drug effects; D009435:Synaptic Transmission / Q000187:drug effects*
D002800:Cholinesterase Inhibitors; D007473:Ion Channels; D011978:Receptors, Nicotinic; D002927:Cimetidine; D011899:Ranitidine