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 a particular phase of the retina development (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. The underlying mechanisms of the spontaneous bursting and the transient excitability of immature SACs are not completely clear yet. While several models have tried to reproduce retinal waves, none of them is able to mimic the rhythmic autonomous bursting of individual SACs and understand 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. Based on a bifurcation analysis we exhibit a few biophysical parameters, especially regulating calcium and potassium activity, controlling bursting. 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 across different species can exhibit a large variability in their bursting periods, as observed experimentally, 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.