With the simulated second-order reaction, both excitatory and inhibitory synapses exhibit facilitation. In this case, two facilitory mechanisms are present—one in the postsynaptic membrane and one in the nonconstant transmitter inactivation reaction. The active membrane currents can, in fact, be removed; and this system will still exhibit facilitation. With the second-order auxiliary network, the presence of excitatory facilitation, antifacilitation, or neither depends on the initial, or resting, transmitter inactivation rate. The synaptic behavior also depends parametrically on the simulated enzyme reactivation rate. Inhibitory antifacilitation can be introduced with either type of auxiliary network by limiting the simulated presynaptic transmitter supply. Certain classes of aftereffects are inherent in the mechanisms of the Ionic Hypothesis. In the electronic model, aftereffects are observed following presynaptic volleys with either type of auxiliary network. Following a volley of spikes into the simulated excitatory synapse, for example, rebound hyperpolarization may or may not occur depending on the simulated transmitter inactivation rate. If the inactivation rate is sufficiently high, rebound will occur. This rebound can be monophasic (inhibitory phase only) or polyphasic (successive cycles of excitation and inhibition). Following a volley of spikes into the simulated inhibitory synapse, rebound depolarization may or may not occur depending on the simulated transmitter inactivation rate. This rebound can also be monophasic or polyphasic. Sustained postexcitatory depolarization and sustained postinhibitory hyperpolarization (2) have been achieved in the model by making the transmitter inactivation rate sufficiently low. The general forms of the postsynaptic potentials simulated with the electronic model are strikingly similar to those published in the literature for real neurons. The first-order auxiliary network produces facilitation of a form almost identical to that shown by Otani and Bullock (8) while the second-order auxiliary network produces facilitation of the type shown by Chalazonitis and Arvanitake (2). The excitatory antifacilitation is almost identical to that shown by Hagiwara and Bullock (1) in both form and dependence on presynaptic spike frequency. In every case, the synaptic behavior is determined by the effective rate of transmitter inactivation, which in real neurons would presumably be directly proportional to the effective concentration of inactivating enzyme at the synapse.