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January 1978

The Effect of Pharmacologic Acetylcholine Receptor on Fibrillation and Myotonia in Rat Skeletal Muscle

Author Affiliations

From the Medical Neurology Branch, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, Md.

Arch Neurol. 1978;35(1):8-10. doi:10.1001/archneur.1978.00500250012002

• 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 α-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 α-bungarotoxin-binding portion of the acetylcholinereceptor molecule and an unblocked atropine-binding site are obligatory only for production of fibrillations.

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