Divisive Normalization from Wilson-Cowan Dynamics

Divisive Normalization and the Wilson-Cowan equations are influential models of neural interaction and saturation [Carandini and Heeger Nat.Rev.Neurosci. 2012; Wilson and Cowan Kybernetik 1973]. However, they have not been analytically related yet. In this work we show that Divisive Normalization can be obtained from the Wilson-Cowan model. Specifically, assuming that Divisive Normalization is the steady state solution of the Wilson-Cowan differential equation, we find that the kernel that controls neural interactions in Divisive Normalization depends on the Wilson-Cowan kernel but also has a signal-dependent contribution. A standard stability analysis of a Wilson-Cowan model with the parameters obtained from our relation shows that the Divisive Normalization solution is a stable node. This stability demonstrates the consistency of our steady state assumption, and is in line with the straightforward use of Divisive Normalization with time-varying stimuli. The proposed theory provides a physiological foundation (a relation to a dynamical network with fixed wiring among neurons) for the functional suggestions that have been done on the need of signal-dependent Divisive Normalization [e.g. in Coen-Cagli et al., PLoS Comp.Biol. 2012]. Moreover, this theory explains the modifications that had to be introduced ad-hoc in Gaussian kernels of Divisive Normalization in [Martinez et al. Front. Neurosci. 2019] to reproduce contrast responses. The proposed relation implies that the Wilson-Cowan dynamics also reproduces visual masking and subjective image distortion metrics, which up to now had been mainly explained via Divisive Normalization. Finally, this relation allows to apply to Divisive Normalization the methods which up to now had been developed for dynamical systems such as Wilson-Cowan networks

Physiologically motivated multiplex Kuramoto model describes phase diagram of cortical activity

We derive a two-layer multiplex Kuramoto model from weakly coupled Wilson-Cowan oscillators on a cortical network with inhibitory synaptic time delays. Depending on the coupling strength and a phase shift parameter, related to cerebral blood flow and GABA concentration, respectively, we numerically identify three macroscopic phases: unsynchronized, synchronized, and chaotic dynamics. These correspond to physiological background-, epileptic seizure-, and resting-state cortical activity, respectively. We also observe frequency suppression at the transition from resting-state to seizure activity.Comment: 8 pages, 3 figure

Critical behaviour of the stochastic Wilson-Cowan model

Spontaneous brain activity is characterized by bursts and avalanche-like dynamics, with scale-free features typical of critical behaviour. The stochastic version of the celebrated Wilson- Cowan model has been widely studied as a system of spiking neurons reproducing non-trivial features of the neural activity, from avalanche dynamics to oscillatory behaviours. However, to what extent such phenomena are related to the presence of a genuine critical point remains elusive. Here we address this central issue, providing analytical results in the linear approximation and extensive numerical analysis. In particular, we present results supporting the existence of a bona fide critical point, where a second-order-like phase transition occurs, characterized by scale-free avalanche dynamics, scaling with the system size and a diverging relaxation time-scale. Moreover, our study shows that the observed critical behaviour falls within the universality class of the mean-field branching process, where the exponents of the avalanche size and duration distributions are, respectively, 3/2 and 2. We also provide an accurate analysis of the system behaviour as a function of the total number of neurons, focusing on the time correlation functions of the firing rate in a wide range of the parameter space

Modeling focal epileptic activity in the Wilson-Cowan model with depolarization block

Measurements of neuronal signals during human seizure activity and evoked epileptic activity in experimental models suggest that, in these pathological states, the individual nerve cells experience an activity driven depolarization block, i.e. they saturate. We examined the effect of such a saturation in the Wilson–Cowan formalism by adapting the nonlinear activation function; we substituted the commonly applied sigmoid for a Gaussian function. We discuss experimental recordings during a seizure that support this substitution. Next we perform a bifurcation analysis on the Wilson–Cowan model with a Gaussian activation function. The main effect is an additional stable equilibrium with high excitatory and low inhibitory activity. Analysis of coupled local networks then shows that such high activity can stay localized or spread. Specifically, in a spatial continuum we show a wavefront with inhibition leading followed by excitatory activity. We relate our model simulations to observations of spreading activity during seizures

Beyond Wilson-Cowan dynamics: oscillations and chaos without inhibition

Fifty years ago, Wilson and Cowan developed a mathematical model to describe the activity of neural populations. In this seminal work, they divided the cells in three groups: active, sensitive and refractory, and obtained a dynamical system to describe the evolution of the average firing rates of the populations. In the present work, we investigate the impact of the often neglected refractory state and show that taking it into account can introduce new dynamics. Starting from a continuous-time Markov chain, we perform a rigorous derivation of a mean-field model that includes the refractory fractions of populations as dynamical variables. Then, we perform bifurcation analysis to explain the occurance of periodic solutions in cases where the classical Wilson-Cowan does not predict oscillations. We also show that our mean-field model is able to predict chaotic behavior in the dynamics of networks with as little as two populations.Comment: 14 pages, 14 figure