Pacemaker potentials are easily simulated with the electronic model without the use of auxiliary networks. This is achieved either by inserting a large, variable shunt resistor across the simulated membrane (see Figure 5) or by allowing a small sodium current leakage at the resting potential. With the remaining parameters of the model set as close as possible to the values determined by Hodgkin and Huxley, the leakage current induces low-frequency, spontaneous spiking. The spike frequency increases monotonically with increasing leakage current. In addition, if the sodium conductance inactivation is allowed to accumulate over several spikes, periodic spike pairs and spike bursts will result. Subthreshold pacemaker potentials have also been observed in the model, but with parameter values set close to the Hodgkin-Huxley data these are generally higher in frequency than pacemaker potentials in real neurons. It is interesting that a pacemaker mode may exist in the absence of the simulated sodium conductance. It is a very high-frequency mode (50 cps or more) and results from the alternating dominance of potassium current and chloride (or leakage ion) current in determining the membrane potential. The significance of this mode cannot be assessed until better data is available for the potassium conductance at low levels of depolarization in real neurons. In general, as far as the model is concerned, pacemaker potentials are possible because the potassium conductance is delayed in both its rise with depolarization and its fall with repolarization. Rate sensitive graded response has also been observed in the electronic model. The rate sensitivity—or accommodation—is due to the sodium conductance inactivation. The response of the model to an imposed ramp depolarization was discussed in Reference 18. At this time, several alternative model parameters could be altered to bring about reduced electrical excitability. None of the parameter changes was very satisfying, however, because none of them was in any way justified by physiological data. We have since found that the membrane capacitance, a plausible parameter in view of recent physiological findings, can completely determine the electrical excitability. Thus, with the capacitance determined by Hodgkin and Huxley (1 microfarad per cm²), the model exhibits excitability characteristic of the axon. As the capacitance is increased, the model becomes less excitable until, with 10 or 12 μμf, it is effectively inexcitable. Thus, with an increased capacitance—but with all the remaining parameters set as close as possible to the Hodgkin-Huxley values—the electronic model exhibits the characteristics of Bullock’s graded-response regions.