Effect of Cardiac Glycosides on Neuromuscular Transmission

Abstract

BIRKS has recently suggested that raised intracellular sodium concentrations increase transmitter release from pre-synaptic nerve terminals¹. This hypothesis is based on measurements of the amount of acetylcholine which was released from the perfused cat superior cervical ganglion and from cholinergic nerve terminals in frog sartorii when active sodium transport had been inhibited with the cardiac glycosides digoxin or ouabain. In the neuromuscular preparation an increased acetylcholine release was signalled by increases both in the quantal content of the endplate potentials (e.p.p.s) and in the frequency of spontaneous miniature endplate potentials (m.e.p.p.s.). These drugs have been tested at a mammalian neuromuscular junction in the present investigation in an attempt to demonstrate the phenomena at this synapse.