The short-latency DR-EPSPs resistant to Ca2+-lack and to addition of Mn2+ and Mg2+ result from electrical coupling between primary afferents and spinal motoneurons in frogs and toads. There are two time constants by which the time constant for the decay of the electronic DR-EPSP can be described: 1. the membrane time constant which determines the rate of passive decay of the membrane potential shift produced directly by the presynaptic spike, 2. the rate at which the presynaptic after-depolarization (ADP) declines. The latter value is very large as compared with the postsynaptic membrane time constant. Presynaptic tetanization does not change the magnitude of the initial spike-induced component of the EPSP but its later slowly decaying portion is potentiated markedly as a result of the post-tetanic increase in the amplitude of the ADP. The perfusion with substances blocking potential dependent potassium channels (4-AP and TEA) greatly augments the DR-EPSP due to prolongation of the presynaptic spike and appearance of multiple discharges in the presynaptic fibers. An antidromic electrical coupling between motoneurons and the terminals of primary afferents was demonstrated in the isolated amphibian spinal cord perfused with zero Ca2+, 2 mM Mn2+ solution containing TEA or 4-AP. Under these conditions ventral root volleys may evoke local graded depolarizing potentials in some sensory fibers. Such antidromic coupling potentials can reach the critical level for generating a single or multiple discharge.