Using an electrically coupled chain of Hindmarsh-Rose neural models, we analytically derived the nonlinearly coupled complex Ginzburg-Landau equations. This is realized by superimposing the lower and upper cutoff modes of wave propagation and by employing the multiple scale expansions in the semidiscrete approximation. We explore the modified Hirota method to analytically obtain the bright-bright pulse soliton solutions of our nonlinearly coupled equations. With these bright solitons as initial conditions of our numerical scheme, and knowing that electrical signals are the basis of information transfer in the nervous system, it is found that prior to collisions at the boundaries of the network, neural information is purely conveyed by bisolitons at lower cutoff mode. After collision, the bisolitons are completely annihilated and neural information is now relayed by the upper cutoff mode via the propagation of plane waves. It is also shown that the linear gain of the system is inextricably linked to the complex physiological mechanisms of ion mobility, since the speeds and spatial profiles of the coupled nerve impulses vary with the gain. A linear stability analysis performed on the coupled system mainly confirms the instability of plane waves in the neural network, with a glaring example of the transition of weak plane waves into a dark soliton and then static kinks. Numerical simulations have confirmed the annihilation phenomenon subsequent to collision in neural systems. They equally showed that the symmetry breaking of the pulse solution of the system leaves in the network static internal modes, sometime referred to as Goldstone modes.

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In this paper, we report the propensity to excitability of the internal structure of cellular microtubules, modelled as a relatively large one-dimensional spatial array of electrical units with nonlinear resistive features. We propose a model mimicking the dynamics of a large set of such intracellular dynamical entities as an excitable medium. We show that the behavior of such lattices can be described by a complex Ginzburg-Landau equation, which admits several wave solutions, including the plane waves paradigm. A stability analysis of the plane waves solutions of our dynamical system is conducted both analytically and numerically. It is observed that perturbed plane waves will always evolve toward promoting the generation of localized periodic waves trains. These modes include both stationary and travelling spatial excitations. They encompass, on one hand, localized structures such as solitary waves embracing bright solitons, dark solitons, and bisolitonic impulses with head-on collisions phenomena, and on the other hand, the appearance of both spatially homogeneous and spatially inhomogeneous stationary patterns. This ability exhibited by our array of proteinic elements to display several states of excitability exposes their stunning biological and physical complexity and is of high relevance in the description of the developmental and informative processes occurring on the subcellular scale.

We systematically study the evolution of modulated nerve impulses in a myelinated nerve fiber, where both the ionic current and membrane capacitance provides the necessary nonlinear feedbacks. This is achieved by using a perturbation technique, in which the Liénard form of the modified discrete Fitzhugh-Nagumo equation is reduced to the complex Ginzburg-Landau amplitude equation. Three distinct values of the capacitive feedback parameter are considered. At the critical value of the capacitive feedback parameter, it is shown that the dynamics of the system is governed by the dissipative nonlinear Schrödinger equation. Linear stability analysis of the system depicts the instability of plane waves, which is manifested as burst of modulated nerve impulses that fulfills the Benjamin-Feir criteria. Variations of the capacitive feedback parameter generally influences the plane wave stability and hence the type of wave profile identified in the neural network. Results of numerical simulations mainly confirms the propagation, collision, and annihilation of nerve impulses in the myelinated axon.