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Some factors affecting spontaneous transmitter release in dystrophic mice
Author(s) -
Shalton Penny M.,
Wareham Anthony C.
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.880030204
Subject(s) - calcium , muscular dystrophy , ruthenium red , extracellular , neuromuscular junction , chemistry , endocrinology , ionophore , motor nerve , intracellular , medicine , calcium in biology , dystrophy , free nerve ending , motor endplate , biophysics , anatomy , biology , biochemistry , neuroscience , genetics
Neuromuscular junctions of slow‐ and fast‐twitch skeletal muscles from dystrophic (dy 2J /dy 2J ) and control mice of the C57BL/6J strain were used to investigate the effect of muscular dystrophy on nerve‐terminal regulation of their intracellular concentration of free calcium ions. The frequency of spontaneous miniature endplate potentials (MEPPs) was taken as an indicator of the intraterminal free calcium ion concentration. Dicoumarol, 2,4‐dinitrophenol, ruthenium red, and the calcium ionophore A‐23187 all potentiated the MEPP frequency in dystrophic muscles at concentrations which had negligible effects on normal muscles. Dystrophic muscle preparations were also more sensitive to an increased extracellular calcium concentration. Usually, these manipulations had more effect on the nerve terminals of dystrophic slow muscle than on those of dystrophic fast muscle. We conclude that muscular dystrophy alters the nerve terminal's ability to regulate the concentration of intracellular free calcium ions.