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Use of geographutoxin II ( u ‐conotoxin) for the study of neuromuscular transmission in mouse
Author(s) -
Hong S.J.,
Chang C.C.
Publication year - 1989
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.1476-5381.1989.tb12034.x
Subject(s) - neuromuscular transmission , neuromuscular junction , depolarization , acetylcholine receptor , acetylcholine , chemistry , neurotransmission , stimulation , biophysics , phrenic nerve , membrane potential , motor nerve , medicine , endocrinology , receptor , anatomy , biology , biochemistry , respiratory system , neuroscience
1 Endplate potentials (e.p.ps) were investigated in the presence of geographutoxin II (GTXII) in the mouse phrenic nerve diaphragm preparation. This toxin preferentially blocks muscle Na + channels which allows the study of e.p.ps in the absence of nicotinic receptor antagonists or substances to depress acetylcholine release. 2 GTXII abolished muscle action potentials and antagonized the depolarization of the muscle membrane produced by the crotamine‐induced opening of Na + channels. 3 E.p.ps as large as 19–25 mV were observed after 2–4 μg ml −1 GTXII. These concentrations of GTXII did not cause discernible changes of resting membrane potential and frequency and amplitude of miniature e.p.ps. 4 Lower concentrations (1–2 μg ml −1 ) of GTXII caused incomplete blockade of the muscle Na + channel resulting in exaggerated ‘e.p.ps’, while higher concentrations of GTXII (8 μg ml −1 ) abolished e.p.ps by a prejunctional effect. 5 Trains of e.p.ps on repetitive stimulation after GTXII neither ran down, as in tubocurarine‐treated preparations, nor facilitated, as in low Ca 2+ and/or high Mg 2+ ‐treated preparations, and were indistinguishable from those of untreated cut muscle preparation. 6 In cut muscle preparations, GTXII did not affect the rise and decay times, amplitude or rundown of e.p.ps. 7 It is concluded that GTXII is a useful agent for studying neuromuscular transmission. This method provides e.p.ps which are neither attenuated nor modified because manipulations that alter transmitter release and postjunctional receptor responses are avoided.