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Facilitatory effects of 4‐aminopyridine on normal neuromuscular transmission
Author(s) -
Kim Yong I.,
Goldner Marcia M.,
Sanders Donald B.
Publication year - 1980
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.880030202
Subject(s) - neuromuscular transmission , neuromuscular junction , 4 aminopyridine , postsynaptic potential , neurotransmission , acetylcholine , motor endplate , motor nerve , electrophysiology , extracellular , acetylcholine receptor , compound muscle action potential , chemistry , cholinesterase , neuromuscular blockade , neuroscience , anatomy , biophysics , biology , medicine , endocrinology , anesthesia , biochemistry , receptor , potassium channel
The effects of 4‐aminopyridine (4‐AP) on neuromuscular transmission were studied in vitro in the rat flexor digitorum longus muscles. 4‐AP produced dose‐dependent increases in endplate potential (EPP) amplitude, in rise time to peak, and in the average number of acetylcholine quanta released by presynaptic nerve impulses. The neuromuscular blocking effects of d‐tubocurarine or low Ca 2+ /high Mg 2+ concentrations could be completely reversed by 4‐AP, and EPPs developed into muscle action potentials (APs). The drug had minimal effects on the amplitude or frequency of spontaneous miniature endplate potentials, but increased the duration of indirectly elicited muscle APs. The action of 4‐AP required the presence of extracellular Ca 2+ ; thus, its effect may be to promote Ca 2+ entry into the motor nerve terminal, and thereby increase the neurally evoked transmitter release. 4‐AP is effective in overcoming both presynaptic and postsynaptic blockade of neuromuscular transmission, suggesting a potential role for this drug in the treatment of neuromuscular diseases.