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The decay of end‐plate currents in neostigmine‐treated frog muscle blocked by acetylcholine or tubocurarine.
Author(s) -
Guinan J J
Publication year - 1980
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1980.sp013368
Subject(s) - acetylcholine , chemistry , d tubocurarine , neostigmine , acetylcholine receptor , population , neuromuscular junction , biophysics , receptor , medicine , endocrinology , pharmacology , biochemistry , neuroscience , biology , environmental health
1. The decay times of e.p.c.s. (with acetylcholinesterase inhibited by neostigmine) were measured with a view to inferring the extent of acetylcholine (ACh) binding. 2. E.p.c.s from muscles blocked by ACh decayed at less than half the rate of e.p.c.s. from muscles blocked by tubocurarine, and slightly more slowly than m.e.p.c.s. from unblocked muscles. 3. ACh prolonged e.p.c.s and reduced their amplitudes when added to muscles blocked by tubocurarine. 4. After treatment with alpha‐bungarotoxin, some e.p.c.s. from muscles blocked by ACh were prolonged relative to e.p.c.s from muscles blocked by tubocurarine. 5. These phenomena are interpreted as indicating that either (a) desensitized receptors bind ACh and prolong e.p.c.s by buffered diffusion or (b) in highly desensitized muscles there is a population of active receptors which bind ACh for many milliseconds.