The generation and propagation of physical signals in living biosystems are continuous issues. Traditional Hodgkin-Huxley model based on ionic current conduction could not explain the fast transmission of action potential in myelinated axons and factors influencing action potential velocity. We propose that the ion flow induced by Nav channel generates near field quasi-static electric field at extracellular space, termed as an ephaptic field which is able to excite nearby passive axons. Our simulation indicates that the static electric field produced by sodium ion channels in one node of Ranvier is improbable to stimulate the ion channels in the adjacent neighboring node. However, the ion channel ring in one node of Ranvier could induce the shift of membrane potential (0.01 mV) on the node at nearby axons (100 μm) in a bundle of axon synchronously, suggesting zig-zag propagation of action potential. Together with the superposition effect of ephaptic feedback field generated by the synchronized movement of adjacent parallel axons stimulate the adjacent node of the original axon, strengthen the action potential to travel in a zig-zag pattern. Our model also provides an explanation for the rapid velocity of action potential propagation reported in experimental studies. We propose that the ion flow induced by N a v channel generates near field quasi-static electric field at extracellular space, termed as an ephaptic field which is able to excite nearby passive axons. Our simulation indicates that the static electric field produced by sodium ion channels in one node of Ranvier is improbable to stimulate the ion channels in the adjacent neighboring node. However, the ion channel ring in one node of Ranvier could induce the shift of membrane potential (0.01 mV) on the node at nearby axons (100 μm) in a bundle of axon synchronously, suggesting zig-zag propagation of action potential. Together with the superposition effect of ephaptic feedback field generated by the synchronized movement of adjacent parallel axons stimulate the adjacent node of the original axon, strengthen the action potential to travel in a zig-zag pattern. Our model also provides an explanation for the rapid velocity of action potential propagation reported in experimental studies. AP will occur in the axon and will be further elaborated upon at a later point. Figure 1 (a) The schematic graph of a motor neuron shows that it can be divided into dendrites, axons, and synapses. The nerve signal is transmitted from the dendrites through the axon and reaches the synapses. (b) Myelinated axons are mainly divided into three sections, including the nodes of Ranvier (Black), paranodes (Dark grey), juxtaparanodes (Light grey), and internodes. Each contains different specific domains. The Na v s mainly distributed in the node of Ranvier, K v s in juxtaparanodes and Caspr protein in paranodes. Recent research has focused on ephaptic interactions in spike propagation among a group of axons. This research has discovered that the extracellular potential also significantly influences the propagation of AP. It has been observed that the extracellular potential alters the speed of conduction [10] and contributes in synchronized firing [11] . The impact of the extracellular electrical characteristics can also be examined using modified cable theory, which elucidates the increase in conduction velocity through ephaptic coupling and the enhancement of energy efficiency in propagation. Additionally, other factors can influence propagation [12] . We suggest a signaling transmission method facilitated by the ephaptic field through adjacent passive parallel axons in the extracellular region. The opening and shutting of voltage-gated ion channels create dipole oscillations that produce an ephaptic field. This field depolarizes passive axons in the vicinity through the extracellular region and triggers the activation of channels in those axons. The adjacent axons will replicate and produce the ephaptic field, so stimulating the subsequent node in the original axons through a feedback mechanism. 2 Result The abbreviation of the parameters concerned is listed in Table 1 . Table 1 List of abbreviation. Table 1 Notation Meaning r Radius of axon d Inter-nodal distance l Length of the node of Ranvier ρ N a v Number density of voltage-controlled Na v channel I Na The ion current inflow cross membrane through a Na v channel ϵ r Relative dielectric constant p ( t ) Dipole moment of single Na v channel Δ q The accumulation charge in a dipole N Number of the ion channel in Sodium channel zone 2.1 Collective electric field from dipoles generated by ion channels The influx of sodium ions from the extracellular fluid to the intracellular fluid through the opening N a v channels, driven by chemical potential, causes localized potential variation across the membrane. The transmembrane electric potential difference and chemical potential cross-membrane influence the flow of sodium ions simultaneously. The electric field drives sodium ions to flow out through the ion channel, and the diffusion chemical potential force inhibits the flow of sodium ions. The balance between membrane electric potential difference and chemical potential will arise after 2 ms, determined by the experiment [19] . The extracellular fluid has the relative dielectric constant of ε r = 60 [20] . For example, if we consider there are 10 axons in the firing channel, the accumulation time required for the AP to excite the next node would be 500 μ s / 10 = 50 μ s , which is in the order of relay time reported [6] . 3 Discussion AP propagation through ephaptic field cannot be established in unmyelinated axon. The ion channel, both the N a v channel and the K v channel, is distributed uniformly on the surface of the unmyelinated axon instead of being distributed in rings as in myelinated neurons. The density of the ion channel [33] is 5 − 50 μ m − 2 , lower than that in myelinated axons. Fig.