COMPUTATIONAL INVESTIGATION OF SLOW WAVE PROPAGATION IN A DESYNCHRONIZED CORTICAL NETWORK AND DEPENDENCE ON EXCITATORY/INHIBITORY BALANCE

Following brain injury, dysfunction arises not only around the lesion area but also in structurally intact regions connected to it. Among the electrophysiological changes observed in the perilesional cortex, the emergence of slow oscillations (SO) is a recurrent phenomenon (Massimini, et al. 2024). The presence of local SO may reduce the precision required for information processing in the awake brain, and their propagation into unaffected cortical networks can lead to selective impairments in perception, motor function, and cognition. A central factor identified in both human and animal studies of brain injury is the disruption of the excitatory/inhibitory (E/I) balance, particularly involving GABAergic inhibition. Although recent studies have described this phenomenon (Frankowski, et al. 2022, Guerriero, et al. 2015), the role of inhibition in promoting SO emergence in perilesional cortex and its spread into desynchronized cortical areas remains poorly understood.
To address this question, we employed a biophysically realistic two-dimensional computational model that reproduces the desynchronized activity characteristic of awake states (Barbero-Castillo, et al. 2021). By locally manipulating the E/I balance, we investigated the contribution of inhibition to the emergence of SO and how it propagates throughout the network. Propagation was quantified using multiple percolation-based metrics applied to spontaneous network activity. Our results show that reduced inhibition in a localized cortical region enhances synchronization, facilitating SO emergence and their spread into desynchronized areas. These findings indicate that E/I balance plays a key role in perilesional SO generation and represents a first step toward understanding the dynamic changes occurring after brain lesions. ​