In addition to the axon properties, however, the electronic model is able to reproduce all of the somatic and dendritic activity outlined in the section on subthreshold activity. Simulation of the pacemaker and graded-response potentials is accomplished without additional circuitry. In the case of synaptically induced potentials, however, auxiliary networks are required. These networks provide additive terms to the variable conductances in accordance with current notions on synaptic transmission (19). Two types of networks have been used. In both, the inputs are simulated presynaptic spikes, and in both the outputs are the resulting simulated chemical transmitter concentration. In both, the transmitter substance was assumed to be injected at a constant rate during a presynaptic spike and subsequently inactivated in the presence of an enzyme. One network simulates a first-order chemical reaction, where the enzyme concentration is effectively constant. The other simulates a second-order chemical reaction, where the enzyme concentration is assumed to be reduced during the inactivation process. For simulation of an excitatory synapse, the output of the auxiliary network is added directly to G_{Na} in the electronic model. For inhibition, it is added to G_{K}. With the parameters of the electronic membrane model set at the values measured by Hodgkin and Huxley, we have attempted to simulate synaptic activity with the aid of the two types of auxiliary networks. In the case of the simulated first-order reaction, the excitatory synapse exhibits facilitation, antifacilitation, or neither—depending on the setting of a single parameter, the transmitter inactivation rate (_i.e._, the effective enzyme concentration). This parameter would appear, in passing, to be one of the most probable synaptic variables. In this case, the mechanisms for facilitation and antifacilitation are contained in the simulated postsynaptic membrane. Facilitation is due to the nonlinear dependence of G_{Na} on membrane potential, while antifacilitation is due to inactivation of G_{Na}. The occurrence of one form of response or the other is determined by the relative importance of the two mechanisms (18). Grundfest (20) has mentioned both of these mechanisms as potentially facilitory and antifacilitory, respectively. The simulated inhibitory synapse with the first order input is capable of facilitation (18), but no antifacilitation has been observed. Again, the presence or absence of facilitation is determined by the inactivation rate.