We introduce a free boundary model to study the effect of vesicle transport onto neurite growth. It consists of systems of drift-diffusion equations describing the evolution of the density of antero- and retrograde vesicles in each neurite coupled to reservoirs located at the soma and the growth cones of the neurites, respectively. The model allows for a change of neurite length as a function of the vesicle concentration in the growth cones. After establishing existence and uniqueness for the time-dependent problem, we briefly comment on possible types of stationary solutions. Finally, we provide numerical studies on biologically relevant scales using a finite volume scheme. We illustrate the capability of the model to reproduce cycles of extension and retraction.

We prove the existence of a solution for a class of activator–inhibitor system of type $- \Delta u +u = f(u) -v$ , $-\Delta v+ v=u$ in $\mathbb{R}^{N}$ . The function f is a general nonlinearity which can grow polynomially in dimension $N\geq 3$ or exponentiallly if $N=2$ . We are able to treat f when it has critical growth corresponding to the Sobolev space we work with. We transform the system into an equation with a nonlocal term. We find a critical point of the corresponding energy functional defined in the space of functions with norm endowed by a scalar product that takes into account such nonlocal term. For that matter, and due to the lack of compactness, we deal with weak convergent minimizing sequences and sequences of Lagrange multipliers of an action minima problem.

The paper presents a conceptual mathematical model for Alzheimer’s disease (AD). According to the so-called amyloid cascade hypothesis, we assume that the progression of AD is associated with the presence of soluble toxic oligomers of beta-amyloid. Monomers of this protein are produced normally throughout life, but a change in the metabolism may increase their total production and, through aggregation, ultimately results in a large quantity of highly toxic polymers. The evolution from monomeric amyloid produced by the neurons to senile plaques (long and insoluble polymeric amyloid chains) is modelled by a system of ordinary differential equations (ODEs), in the spirit of the Smoluchowski equation. The basic assumptions of the model are that, at the scale of suitably small representative elementary volumes (REVs) of the brain, the production of monomers depends on the average degradation of the neurons and in turn, at a much slower timescale, the degradation is caused by the number of toxic oligomers. To mimic prion-like diffusion of the disease in the brain, we introduce an interaction among adjacent REVs that can be assumed to be isotropic or to follow given preferential patterns. We display the results of numerical simulations which are obtained under some simplifying assumptions. For instance, the amyloid cascade is modelled by just three ordinary differential equations (ODEs), and the simulations refer to abstract 2D domains, simplifications which can be easily avoided at the price of some additional computational costs. Since the model is suitably flexible to incorporate other mechanisms and geometries, we believe that it can be generalised to describe more realistic situations.

In 1992 Ermentrout and McLeod published in this journal a landmark study of travelling wavefronts for a differential–integral equation model of a neural network. Since then a number of authors have extended the model by adding an additional equation for a ‘recovery variable’, thus allowing the possibility of travelling-pulse-type solutions. In a recent paper, Faye gave perhaps the first rigorous proof of the existence (and stability) of a travelling-pulse solution for a model of this type, treating a simplified version of equations originally developed by Kilpatrick and Bressloff. The excitatory weight function J used in this work allowed the system to be reduced to a set of four coupled ordinary differential equations (ODEs), and a specific firing-rate function S, with parameters, was considered. The method of geometric singular perturbation was employed, together with blow-ups. In this paper we extend Faye's results on existence by dropping one of his key hypotheses, proving the existence of pulses at least two different speeds, and, in a sense, allowing a wider range of the small parameter in the problem. The proofs are classical and self-contained aside from standard ODE material.

In this paper we consider the generalized Hodgkin-Huxley model introduced in Austin (2008). This model describes the propagation of an action potential along the axon of a neuron at the scale of ion channels. Mathematically, this model is a fully coupled piecewise-deterministic Markov process (PDMP) in infinite dimensions. We introduce two time scales in this model in considering that some ion channels open and close at faster jump rates than others. We perform a slow-fast analysis of this model and prove that, asymptotically, this ‘two-time-scale’ model reduces to the so-called averaged model, which is still a PDMP in infinite dimensions, for which we provide effective evolution equations and jump rates.

In this paper, we construct a simplified neuronal model that is capable of simulating the instigation of cortical spreading depression (CSD) and propagation of a CSD wave. Our model is a simplification and extension of a single neuron model proposed in the literature for studying the instigation of CSD. Using the simplified neuronal model, we construct a network of these simplified neurons. This network model shows that the propagation of a CSD wave occurs naturally after it is instigated electrically or chemically. Although the model is simple, the speed of the CSD wave predicted by our model is consistent with experimentally observed values. Finally, our model allows us to investigate the effects of specific ion channels on the spread of a CSD wave.

We prove that the first passage time density ρ(t) for an Ornstein-Uhlenbeck process X(t) obeying dX = -β Xdt + σdW to reach a fixed threshold θ from a suprathreshold initial condition x0 > θ > 0 has a lower bound of the form ρ(t) > kexp[-pe6βt] for positive constants k and p for times t exceeding some positive value u. We obtain explicit expressions for k, p, and u in terms of β, σ, x0, and θ, and discuss the application of the results to the synchronization of periodically forced stochastic leaky integrate-and-fire model neurons.

In this paper we establish limit theorems for a class of stochastic hybrid systems (continuous deterministic dynamics coupled with jump Markov processes) in the fluid limit (small jumps at high frequency), thus extending known results for jump Markov processes. We prove a functional law of large numbers with exponential convergence speed, derive a diffusion approximation, and establish a functional central limit theorem. We apply these results to neuron models with stochastic ion channels, as the number of channels goes to infinity, estimating the convergence to the deterministic model. In terms of neural coding, we apply our central limit theorems to numerically estimate the impact of channel noise both on frequency and spike timing coding.