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POSSIBLE MECHANISMS OF ACTION OF Gymnodinium breve TOXIN AT THE MAMMALIAN NEUROMUSCULAR JUNCTION
Author(s) -
SHINNICKGALLAGHER PATRICIA
Publication year - 1980
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1980.tb07024.x
Subject(s) - toxin , neuromuscular junction , action (physics) , biology , microbiology and biotechnology , neuroscience , physics , quantum mechanics
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 μg/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.