tetrodotoxin and Muscle-Spasticity

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.

Topics: Acetylcholine; Animals; Atropine; Azacosterol; Bungarotoxins; Evoked Potentials; Ischemia; Male; Muscle Denervation; Muscle Spasticity; Muscles; Myotonia; Potassium Chloride; Procaine; Pyridostigmine Bromide; Rats; Receptors, Cholinergic; Succinylcholine; Tetrodotoxin; Tubocurarine