The effect of pharmacologic acetylcholine receptor on fibrillation and myotonia in rat skeletal muscle
R. A. Brumback, T. E. Bertorini, W. K. Engel, J. L. Trotter, K. L. Oliver and G. C. Zirzow
Myotonic discharges in rats given 20, 25-diazacholesterol hydrochloride and
fibrillation discharges in denervated rat muscle both were silenced by
procaine hydrochloride, tetrodotoxin or ischemia, or potassium chloride
(after initial activation). They both were activated by succinylcholine,
but only the fibrillations were silenced by alpha-bungarotoxin or atropine
sulfate. It is hypothesized that fibrillations and diazacholesterol-induced
myotonia are mediated through mechanisms involving ionic channels, that
both can be produced by activation of the junctional/nonjunctional
acetylcholine receptors (or some mechanism coupled to the receptors), but
that an unfettered alpha-bungarotoxin-binding portion of the
acetylcholine-receptor molecule and an unblocked atropine-binding site are
obligatory only for production of fibrillations.
