Use of geographutoxin II (u‐conotoxin) for the study of neuromuscular transmission in mouse

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Abstract
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 Ca2+ and/or high Mg2+-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.

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