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Abstract
At frog neuromuscular junctions immersed in solutions containing 0.5 mM Mn2+, verapamil
(40 microM) reduced the increase in miniature end-plate potential (MEPP) frequency
produced by tetanic stimulation (50 Hz, 2 min) of the motor nerve to 5% of that in
the absence of verapamil. In solutions containing 5 mM Mg2+, verapamil reduced the
tetanic increase in MEPP frequency to 8% of that in the absence of verapamil. Verapamil
added to solutions containing 0.15 mM Ca2+ decreased the tetanic rise in MEPP frequency
to 6% of the control value. In low Ca2+ (nominally Ca2(+)-free) solutions, verapamil
decreased the tetanic rise to 70% of the control value. The present results suggest
that Mn2+ and Mg2+, as well as Ca2+, enter the nerve terminal through Ca2+ channels
during nerve stimulation and promote transmitter release. In addition to its effect
on the Ca2+ channel, verapamil at higher concentrations appears to have inhibitory
effects on the acetylcholine-gated end-plate channel and on the Na+ channel as suggested
by its depressive effects on the amplitudes of MEPPs, end-plate potentials and nerve
terminal action potentials.