Abstract :
[en] For more than 20 years, a growing body of evidence indicates that the brain functions near a critical point, where neural activity is balanced between damping and amplification. One of the appealing benefits of criticality is its optimal information processing [1, 2]. In addition, deviations from criticality are associated with age and disease [3] but also physiological state [4]. Yet the neural mechanisms involved in maintaining and/or altering this criticality remain unclear. To investigate how cellular mechanisms can influence criticality, we analyze a model of neuronal network [5] and quantify criticality as we vary the neuronal excitability properties at the cellular level.
This poster highlights the role of a positive feedback gating mechanism at the cellular level in the robustness and modulation properties of criticality in neural activities both at the cellular and circuit levels. We observed that by varying a simple slow feedback gain, the width of the bistability region varies as well. Then, the avalanche-like behavior appears more explicitly in the bistable rather than in the monostable regime (Fig. 1A,C,E,G). Also, for a fixed and sufficiently large noise amplitude, the firing rate (FR) showed variable fluctuations depending on the window size over which FR is computed (Fig. 1D,H). Using the detrended fluctuation analysis (DFA; [6]), these fluctuations exhibited power laws for all window sizes (Fig. 1I). However, the scaling exponent obtained from DFA, used as an indication of criticality, showed stronger closeness to criticality for increasing window size (Fig. 1I green versus orange). More importantly, by varying the slow feedback gain (Fig.1 left versus right), the criticality properties already change at the cellular level. Finally, the criticality is stronger in a bistable rather than a monostable regime for all window sizes (Fig. 1I circles versus crosses). In conclusion, the regulation of neuronal excitability at the cellular level has an influence on criticality both at the cellular and circuit levels. This mechanism will need to be considered in future studies of neurodegenerative diseases.
