A nerve model of greatly increased energy-efficiency and encoding flexibility over the Hodgkin-Huxley model

A mammalian “RGC model” (retinal ganglion cells) is distinguished from the Hodgkin-Huxley model by the virtual absence of K-current during, and the virtual absence of Na-current after, the regenerative (rising) phase of the action potential. Both Na- and K-currents remain negligible throughout the interspike interval, whose control is therefore relinquished to stimulus currents. These properties yield a highly flexible and energy-efficient nerve impulse encoder. For the Hodgkin-Huxley model, in contrast, only 15% of the Na-ions enter the axon regeneratively during the action potential (squid giant axon); a wasteful 85% enter during the falling phase. Further, early activation of K-current causes the Na- and K-currents of the action potential to dominate over stimulus currents in controlling the sub-threshold membrane potential (interspike interval). This property makes the Hodgkin-Huxley model an intractable high frequency oscillator, which cannot be converted to flexible impulse encoding. The temperature difference between the squid giant axon (6.3 °C) and RGCs (37 °C) is bridged by a Q10 analysis, which suggests that an additional molecular gating mechanism of high Q10 - which is not present in the squid - is active in RGCs.