 |
|
The Effect of Pharmacologic Acetylcholine Receptor on Fibrillation and Myotonia in Rat Skeletal Muscle
Roger A. Brumback, MD;
Tulio E. Bertorini, MD;
W. King Engel, MD;
John L. Trotter, MD;
Katherine L. Oliver;
Gregory C. Zirzow
Arch Neurol. 1978;35(1):8-10.
Abstract
• 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  -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 -bungarotoxin-binding portion of the acetylcholinereceptor molecule and an unblocked atropine-binding site are obligatory only for production of fibrillations.
Author Affiliations
From the Medical Neurology Branch, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, Md.
Footnotes
Accepted for publication Aug 16, 1977.
Reprint requests to the Medical Neurology Branch, National Institute of Neurological and Communicative Disorders and Stroke, Bldg 10, Room 10D18, National Institutes of Health, Bethesda, MD (Dr Engel).
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati  Twitter
What's this?
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
Gabapentin for familial paroxysmal dystonic choreoathetosis
Chudnow et al.
Neurology 1997;49:1441-1442.
ABSTRACT
| FULL TEXT
Dagen des Oordeels: Pathokinetic Mechanisms and Molecular Messengers (A Dramatic View)
Engel
Arch Neurol 1979;36:329-339.
ABSTRACT
|
