Generalized cable equation model for myelinated nerve fiber

Herein, the well-known cable equation for nonmyelinated axon model is extended analytically for myelinated axon formulation. The myelinated membrane conductivity is represented via the Fourier series expansion. The classical cable equation is thereby modified into a linear second order ordinary differential equation with periodic coefficients, known as Hill's equation. The general internal source response, expressed via repeated convolutions, uniformly converges provided that the entire periodic membrane is passive. The solution can be interpreted as an extended source response in an equivalent nonmyelinated axon (i.e., the response is governed by the classical cable equation). The extended source consists of the original source and a novel activation function, replacing the periodic membrane in the myelinated axon model. Hill's equation is explicitly integrated for the specific choice of piecewise constant membrane conductivity profile, thereby resulting in an explicit closed form expression for the transmembrane potential in terms of trigonometric functions. The Floquet's modes are recognized as the nerve fiber activation modes, which are conventionally associated with the nonlinear Hodgkin-Huxley formulation. They can also be incorporated in our linear model, provided that the periodic membrane point-wise passivity constraint is properly modified. Indeed, the modified condition, enforcing the periodic membrane passivity constraint on the average conductivity only leads, for the first time, to the inclusion of the nerve fiber activation modes in our novel model. The validity of the generalized transmission-line and cable equation models for a myelinated nerve fiber, is verified herein through a rigorous Green's function formulation and numerical simulations for transmembrane potential induced in three-dimensional myelinated cylindrical cell. It is shown that the dominant pole contribution of the exact modal expansion is the transmembrane potential solution of our generalized model.