Lionel Gil | Searcharxiv

arXiv2021

Optimally frequency synchronized networks of non identical Kuramoto oscillators

Based on a local greedy numerical algorithm, we compute the topology of weighted, directed, and of unlimited extension networks of non identical Kuramoto oscillators which simultaneously satisfy 2 criteria: i) global frequency synchronisation and ii) minimal total mass of the connection weights. This problem has been the subject of many previous interesting studies, but from our best knowledge, this is the first time that no a priori constraint is imposed, either on the form or on the dynamics of the connections. The results are surprising: the optimal networks turn out to be strongly symmetric, very economical, to display a strong rich club structure, and next to the already reported strong correlation between natural frequencies and the weight of incoming connections, we also observe a correlation, even more marked, between these same natural frequencies and the weight of outgoing connections. The latter result is at odds with theoretical predictions.

nlin.AO↗

arXiv2018

A biophysical model explains the spontaneous bursting behavior in the developing retina

During early development, waves of activity propagate across the retina and play a key role in the proper wiring of the early visual system. During the stage II these waves are triggered by a transient network of neurons, called Starburst Amacrine Cells (SACs), showing a bursting activity which disappears upon further maturation. While several models have attempted to reproduce retinal waves, none of them is able to mimic the rhythmic autonomous bursting of individual SACs and reveal how these cells change their intrinsic properties during development. Here, we introduce a mathematical model, grounded on biophysics, which enables us to reproduce the bursting activity of SACs and to propose a plausible, generic and robust, mechanism that generates it. The core parameters controlling repetitive firing are fast depolarizing $V$-gated calcium channels and hyperpolarizing $V$-gated potassium channels. The quiescent phase of bursting is controlled by a slow after hyperpolarization (sAHP), mediated by calcium-dependent potassium channels. Based on a bifurcation analysis we show how biophysical parameters, regulating calcium and potassium activity, control the spontaneously occurring fast oscillatory activity followed by long refractory periods in individual SACs. We make a testable experimental prediction on the role of voltage-dependent potassium channels on the excitability properties of SACs and on the evolution of this excitability along development. We also propose an explanation on how SACs can exhibit a large variability in their bursting periods, as observed experimentally within a SACs network as well as across different species, yet based on a simple, unique, mechanism. As we discuss, these observations at the cellular level have a deep impact on the retinal waves description.

q-bio.NC↗