title: Effects of gallamine triethiodide on membrane currents in amphibian and mammalian peripheral nerve.
abstract: Gallamine triethiodide ("Flaxedil") is in common clinical and experimental use specifically to block neuromuscular transmission. Voltage-clamp studies show that gallamine also has direct effects on amphibian and mammalian nerve fibers, whether applied externally or internally. With external application, gallamine (0.1-10.0 mM) is about 5 times more potent than tetraethylammonium chloride in blocking the delayed potassium conductance (gk), where this is present. The sodium conductance is completely unaffected by external gallamine in both species. Internal application of gallamine to myelinated nerve fibers slows sodium inactivation. In addition, at positive potentials, gallamine can enter Na+ channels and occlude them, thereby almost eliminating outward sodium currents. In rat fibers, a significant fraction of the sodium channels fail to inactivate and thus large inward sodium tail currents occur upon repolarization. The general consequences of these findings with regard to possible "side-effects: in gallamine-paralyzed preparations is discussed.
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D005703:Gallamine Triethiodide / Q000494:pharmacology*; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009413:Nerve Fibers, Myelinated / Q000187:drug effects; D010525:Peripheral Nerves / Q000187:drug effects*; D011188:Potassium / Q000502:physiology; D011894:Rana pipiens; D051381:Rats; D012964:Sodium / Q000502:physiology; D013757:Tetraethylammonium Compounds / Q000494:pharmacology
chemical_list: D013757:Tetraethylammonium Compounds; D012964:Sodium; D005703:Gallamine Triethiodide; D011188:Potassium