Postsynaptic effects of magnesium and calcium at the mouse neuromuscular junction.

The effects of elevated magnesium and calcium concentrations on height and time course of miniature endplate currents (MEPCs) at the mouse neuromuscular junction were studied. With both ions, MEPC height was decreased; the rate of decay of MEPCs was reduced in high magnesium and was unchanged in high calcium. Raised Mg2+ or Ca2+ both acted to modify the effects on MEPC time course of procaine, scopolamine, atropine, lidocaine, and quinidine, all of which act to cause biphasic decay of MEPCs in a manner consistent with reversible "plugging" of endplate channels, with rate constants for blocking and unblocking that are sensitive to postsynaptic transmembrane potential. Both the blocking and unblocking rate constants were decreased by increasing divalent ion concentration. No such reduction of rate constants was observed using menthol or pentobarbital, which appear to block channels in a voltage-independent manner. It is concluded that the divalent ions act to alter the channel environment via interactions with charged groups in or near the endplate channels.