Diphenylhydantoin reduces veratridine-induced sodium permeability in frog skeletal muscle.
The effect of the anti-epileptic drug 5,5'-diphenylhydantoin (Dilantin) on Na permeability (PNa) in frog skeletal muscle was studied. Because there is no detectable tetrodotoxin-sensitive Na permeability in resting frog muscle, PNa was induced using the alkaloid 'neurotoxin' veratridine. Veratridine has been previously characterized as a useful 'tool' for producing a population of open Na channels in frog muscle. The amount of sodium permeability produced by veratridine was quantified in two ways: by measuring (a) membrane potential (Vm) and (b) 22Na influx. Dilantin was shown to reverse veratridine-induced depolarization by approximately one-third and to inhibit veratridine-induced Na influx in a dose-dependent manner, with an apparent Km of 78 +/- 8 microM.
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D000818:Animals; D002463:Cell Membrane Permeability / Q000187:drug effects*; D007473:Ion Channels / Q000187:drug effects; D008274:Magnesium / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects; D009132:Muscles / Q000187:drug effects*; D010672:Phenytoin / Q000494:pharmacology*; D011894:Rana pipiens; D012964:Sodium / Q000378:metabolism*; D013779:Tetrodotoxin / Q000494:pharmacology; D014701:Veratridine / Q000037:antagonists & inhibitors*; D014702:Veratrine / Q000031:analogs & derivatives*
D007473:Ion Channels; D013779:Tetrodotoxin; D010672:Phenytoin; D014701:Veratridine; D012964:Sodium; D014702:Veratrine; D008274:Magnesium