Leduc_2026_Eur.J.Neurosci_64_e70665

Spectral power decay (1/f(beta)) of cortical activity has long been considered of low relevance to the understanding of brain function (e.g., associated with background noise of neuronal activity). However, growing literature suggests that it can reflect optimized spatiotemporal organization of neuronal activity across the cortex serving both cognition and behavior. Thus, clarifying the mechanisms underlying the regulation of this network property could have numerous impacts for the neuroscience field as well as for patients suffering from various neurological disorders with cognitive deficits linked to alterations in brain power decay properties. Using a constitutive knockout mouse and a multifractal wavelet-leaders formalism, we here investigated the involvement of the synaptic adhesion molecule Neuroligin-2, which shapes synaptic inhibition and associates with neurodevelopmental diseases, in modulating spectral power decay properties of the electrocorticographic signal (i.e., the most prominent Hurst exponent "Hm" and its local "Dispersion"). Knockout mice showed increased Hm values across all wake and sleep states together with amplified daily dynamics during wake and paradoxical sleep, and increased Dispersion specifically for slow-wave sleep in comparison with wild-type littermates. Following a 6-h sleep deprivation, Hm daily variations were more altered in knockout mice than controls for wake and paradoxical sleep, but less affected for slow-wave sleep. Importantly, mutant mice display hypersynchronized epileptic-like electrocorticographic events, which were characterized by further increases in Hm and Dispersion. These findings provide support for the involvement of Neuroligin-2 in shaping 1/f(beta) cortical activity properties and bring perspectives, notably, for neurodevelopmental conditions.