“…The increase in the amplitude of inhibitory postsynaptic potentials induced by dorsal root stimulation (DR-IPSP) in the spinal cord of the frog is comparable with the enhancement in the amplitude of endplate potentials caused by guanidine in nervemuscle preparations (Otsuka and Endo, 1960;Kamenskaya et al, 1975a, b;Terfivfiinen and Larsen, 1975). The small postsynaptic potentials in spinal motoneurons of the frog originate from action potentials of spontaneously active interneurons and, similar to the miniature endplate potentials of neuromuscular transmission, from a spontaneous transmitter release in the nerve terminals (Katz and Miledi, 1963;Colomo and Erulkar, 1968). Guanidine, however, only enhanced the action potential induced transmitter release, since in contrast to the spontaneous transmitter release, which is resistant to high magnesium concentrations (Katz and Miledi, 1963;Erulkar et al, 1974), stimulus induced synaptic activation, as well as the action of guanidine were blocked by addition of magnesium ions (15 mM) into the Ringer solution (see Fig.…”