Mechanism of action of gallamine.
The mechanisms of action of gallamine on nerve terminals, cholinergic receptors, and the threshold for propagation of end-plate potentials to the muscle fiber were investigated in rat phrenic nerve-diaphragm preparations. Intracellular studies were made with glass microelectrodes to determine changes in end-plate potentials and miniature end-plate potentials produced by gallamine at concentrations between 10(-7) M to 10(-4) M. Gallamine excited and then depressed the release of transmitter from nerve terminals. This effect was clearly seen at rapid rate of stimulation and during studies of refractoriness using paried stimulation tests. Gallamine had no significant effects on the electrogenic properties of the excitable membranes of motor nerve terminals and muscle fibers; this compound depressed the response of postsynaptic receptors to action of acetylcholine as seen by the reduction in miniature end-plate potentials amplitude. Reduction in muscle twitch was caused solely by failure of propagation of end-plate potentials as muscle action potentials.
D000818:Animals; D005703:Gallamine Triethiodide / Q000494:pharmacology*; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009045:Motor Endplate / Q000187:drug effects; D009119:Muscle Contraction / Q000187:drug effects; D009469:Neuromuscular Junction / Q000187:drug effects*; D051381:Rats; D011950:Receptors, Cholinergic / Q000187:drug effects; D012032:Refractory Period, Electrophysiological / Q000187:drug effects
D011950:Receptors, Cholinergic; D005703:Gallamine Triethiodide