Effect of uncouplers of oxidative phosphorylation on transmitter release in dystrophic mice.

Intracellular recording was used to study the effect of uncouplers of oxidative phosphorylation on miniature endplate potentials (m.e.p.p.s) in skeletal muscles from dystrophic mice and their clinically normal littermates. Control m.e.p.p. frequency in muscles from dystrophic mice was not significantly different from normal. In the presence of the inhibitors 2,4-dinitrophenol (10(-4) M) or guanidine (5 X 10(-3) M) m.e.p.p. frequency was increased less in muscles from dystrophic mice than that in muscles from normal littermates. In contrast, raising the extracellular calcium concentration, depolarising nerve terminals with potassium or motor nerve stimulation all caused a similar increase in m.e.p.p. frequency in normal and dystrophic muscles. It is suggested that there is a difference in the way in which calcium is stored in dystrophic nerve terminals but that their ability to regulate free calcium is normal.