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

Abstract

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.