Does the regulation of local excitation–inhibition balance aid in recovery of functional connectivity? A computational account

Computational modeling of the spontaneous dynamics over the whole brain provides critical insight into the spatiotemporal organization of brain dynamics at multiple resolutions and their alteration to changes in brain structure (e.g. in diseased states, aging, across individuals). Recent experimental evidence further suggests that the adverse effect of lesions is visible on spontaneous dynamics characterized by changes in resting state functional connectivity and its graph theoretical properties (e.g. modularity). These changes originate from altered neural dynamics in individual brain areas that are otherwise poised towards a homeostatic equilibrium to maintain a stable excitatory and inhibitory activity. In this work, we employ a homeostatic inhibitory mechanism, balancing excitation and inhibition in the local brain areas of the entire cortex under neurological impairments like lesions to understand global functional recovery (across brain networks and individuals). Previous computational and empirical studies have demonstrated that the resting state functional connectivity varies primarily due to the location and specific topological characteristics of the lesion. We show that local homeostatic balance provides a functional recovery by re-establishing excitation-inhibition balance in all areas that are affected by lesion. We systematically compare the extent of recovery in the primary hub areas (e.g. default mode network (DMN), medial temporal lobe, medial prefrontal cortex) as well as other sensory areas like primary motor area, supplementary motor area, fronto-parietal and temporo-parietal networks. Our findings suggest that stability and richness similar to the normal brain dynamics at rest are achievable by re-establishment of balance.This study was funded by A.B. Ramalingaswami fellowship (BT/RLF/Re-entry/31/2011) and Innovative Young Bio-technologist Award (IYBA) (BT/07/IYBA/2013) from the Department of Biotechnology, Ministry of Science & Technology, Government of India. GD is supported by the ERC Advanced Grant: DYSTRUCTURE (n. 295129), by the Spanish Research ProjectPSI2013-42091-P, and funding from the European Union Seventh Framework Programme (FP7-ICT Human Brain Project (grant no. 60402))