Modulation of signal transmission in myelinated axons by feedback conduction currents

In the nervous system, action potentials (APs) that propagate along axons are the primary carriers of encoded information. On the basis of the Hodgkin-Huxley model, this study constructs a model of a myelinated cortical axon to investigate the conduction dynamics of action potentials under sinusoidal and synaptic-like random current stimulation. The results demonstrated that under sinusoidal input, the stimulation frequency ((f_mathrmin)) and amplitude ((A_mathrmin)) jointly regulated the frequency-locked mode ((r = f_mathrmout/f_mathrmin)) at the proximal axon. AP transmission was modulated by the internodal conductance ((κ)) and feedback conduction current ((I^←i,textrminter)). The feedback conduction current suppressed proximal depolarization, thereby reducing the frequency-locked ratio (r). In contrast, increasing (κ) ((>0.2) mS/cm$^2$) synchronized frequency-locked behaviors of distal nodes with that of the proximal node. Under synaptic-like stochastic input, high-frequency truncation (ISI $<~20$ ms) at the proximal axon and AP loss during propagation caused a progressive decrease in information entropy ((H)) along the axon. However, the feedback conduction current attenuated proximal high-frequency truncation and achieved entropy conservation between input entropy and axonal conduction entropy ((H_mathrmaxon= H_mathrmin= 4.3) bit) at a specific parameter ((λ = 22) ms), enhancing transmission fidelity. Moreover, under certain conditions, the temperature maximizes the locking frequency within (27.25)$^\circ$C–(30.75)$^\circ$C while simultaneously intensifying high-frequency truncation. This work reveals that the feedback conduction current optimizes axonal information transmission efficiency through a dual mechanism: suppressing proximal firing and maintaining entropy conservation.