EFFECT OF PHARMACOLOGIC ACETYLCHOLINE-RECEPTOR ON FIBRILLATION AND MYOTONIA IN RAT SKELETAL-MUSCLE

被引：15

作者：

BRUMBACK, RA ^{[1
]}

BERTORINI, TE ^{[1
]}

ENGEL, WK ^{[1
]}

TROTTER, JL ^{[1
]}

OLIVER, KL ^{[1
]}

ZIRZOW, GC ^{[1
]}

机构：

[1] NINCDS, MED NEUROL BRANCH, BETHESDA, MD 20014 USA

来源：

ARCHIVES OF NEUROLOGY | 1978年 / 35卷 / 01期

关键词：

D O I：

10.1001/archneur.1978.00500250012002

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

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. © 1978, American Medical Association. All rights reserved.

引用

页码：8 / 10

页数：3

共 19 条

[11] A STUDY OF INDIVIDUAL NEURO-MUSCULAR JUNCTIONS IN MYOTONIA [J].