A fractional-order Wilson-Cowan formulation of cortical disinhibition.

This work presents a fractional-order Wilson-Cowan model derivation under Caputo's formalism, considering an order of 0 < α ≤ 1 . To that end, we propose memory-dependent response functions and average neuronal excitation functions that permit us to naturally arrive at a fractional-order model that incorporates past dynamics into the description of synaptically coupled neuronal populations' activity. We then shift our focus on a particular example, aiming to analyze the fractional-order dynamics of the disinhibited cortex. This system mimics cortical activity observed during neurological disorders such as epileptic seizures, where an imbalance between excitation and inhibition is present, which allows brain dynamics to transition to a hyperexcited activity state. In the context of the first-order mathematical model, we recover traditional results showing a transition from a low-level activity state to a potentially pathological high-level activity state as an external factor modifies cortical inhibition. On the other hand, under the fractional-order formulation, we establish novel results showing that the system resists such transition as the order is decreased, permitting the possibility of staying in the low-activity state even with increased disinhibition. Furthermore, considering the memory index interpretation of the fractional-order model motivation here developed, our results establish that by increasing the memory index, the system becomes more resistant to transitioning towards the high-level activity state. That is, one possible effect of the memory index is to stabilize neuronal activity. Noticeably, this neuronal stabilizing effect is similar to homeostatic plasticity mechanisms. To summarize our results, we present a two-parameter structural portrait describing the system's dynamics dependent on a proposed disinhibition parameter and the order. We also explore numerical model simulations to validate our results.

The effect of inhibition on the existence of traveling wave solutions for a neural field model of human seizure termination.

In this paper we study the influence of inhibition on an activity-based neural field model consisting of an excitatory population with a linear adaptation term that directly regulates the activity of the excitatory population. Such a model has been used to replicate traveling wave data as observed in high density local field potential recordings (González-Ramírez et al. PLoS Computational Biology, 11(2), e1004065, 2015). In this work, we show that by adding an inhibitory population to this model we can still replicate wave properties as observed in human clinical data preceding seizure termination, but the parameter range over which such waves exist becomes more restricted. This restriction depends on the strength of the inhibition and the timescale at which the inhibition acts. In particular, if inhibition acts on a slower timescale relative to excitation then it is possible to still replicate traveling wave patterns as observed in the clinical data even with a relatively strong effect of inhibition. However, if inhibition acts on the same timescale as the excitation, or faster, then traveling wave patterns with the desired characteristics cease to exist when the inhibition becomes sufficiently strong.