Possible mechanisms of action of Gymnodinium breve toxin at the mammalian neuromuscular junction.
1 The mechanism of action of a crude fraction of Gymnodinium breve toxin (GBTX) was investigated by intracellular recording techniques in the rat phrenic nerve diaphragm preparation. 2 GBTX (2 micrograms/ml) decreased the input resistance of the muscle membrane concomitantly with a depolarization of the resting membrane potential. 3 A low sodium solution reversed or prevented a GBTX-induced membrane depolarization. 4 Tetrodotoxin (TTX) antagonized a GBTX-induced increase in miniature endplate potential (m.e.p.p.) frequency and repolarized a GBTX-depolarized membrane. Pretreatment with TTX prevented GBTX effects. 5 GBTX reversibly reduced depolarizations produced by bath applied acetylcholine (ACh). The membrane depolarization was not responsible for the depression of ACh responses. 6 These findings suggest that GBTX increases m.e.p.p. frequency and depolarizes the resting membrane potential by increasing sodium permeability. The reduction of ACh-induced depolarizations suggests that GBTX may be acting at some site on the ACh receptor.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D002463:Cell Membrane Permeability / Q000187:drug effects; D004141:Dinoflagellida / Q000502:physiology*; D066298:In Vitro Techniques; D008297:Male; D008387:Marine Toxins / Q000494:pharmacology*; D008564:Membrane Potentials / Q000187:drug effects; D009045:Motor Endplate / Q000187:drug effects; D009467:Neuromuscular Depolarizing Agents; D009469:Neuromuscular Junction / Q000187:drug effects*; D051381:Rats; D012964:Sodium / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology
D008387:Marine Toxins; D009467:Neuromuscular Depolarizing Agents; D013779:Tetrodotoxin; D012964:Sodium; D000109:Acetylcholine