de Palma Aristides, R. | Search bioRxiv

bioRxiv2026

Structure-Constrained Intrinsic Timescales Across Tasks

Intrinsic neural timescale (INT) quantifies the persistence of spontaneous neural dynamics and offers a principled metric for characterizing brain-wide temporal organization. Although a hierarchy of INTs has been established during rest, how task engagement reconfigures this organization and how it is constrained by the structural connectome (SC) remain poorly understood. Here, we systematically mapped whole-brain INT using high-resolution fMRI data from the Human Connectome Project during rest and seven tasks spanning working memory, gambling, motor, language, social, relational, and emotion domains. Task engagement induced robust, regionally heterogeneous changes in INT while largely preserving the brain-wide temporal hierarchy across cognitive states. SC-INT coupling remained strong but consistently decreased during tasks, indicating that anatomical architecture continues to constrain INT, although its influence is attenuated under task demands. To investigate these findings mechanistically, we employed a multiscale, whole-brain neuronal-network model, which revealed that INT increase and peak within a broad critical-like regime. Strong SC-INT coupling, as observed empirically, emerged in the subcritical regime, weakened progressively with increasing network excitability, and reversed in the supercritical regime. These results demonstrate that task engagement reconfigures INTs while maintaining their hierarchical organization, suggesting that both resting and task states operate largely within a common subcritical dynamical regime.

neuroscience↗

bioRxiv2025

Emergence of multifrequency activity in a laminar neural mass model

Neural mass models (NMMs) aim to capture the principles underlying mesoscopic neural activity representing the average behavior of large neural populations in the brain. Recently, a biophysically grounded laminar NMM (LaNMM) has been proposed, capable of generating coupled slow and fast oscillations resulting from interactions between different cortical layers. This concurrent oscillatory activity provides a mechanistic framework for studying information processing mechanisms and various disease-related oscillatory dysfunctions. We show that this model can exhibit periodic, quasiperiodic, and chaotic oscillations. Additionally we demonstrate, through bifurcation analysis and numerical simulations, the emergence of rhythmic activity and various frequency couplings in the model, including delta-gamma, theta-gamma, and alpha-gamma couplings. We also examine how alterations linked with Alzheimers disease impair the models ability to display multifrequency activity. Furthermore, we show that the model remains robust when coupled to another neural mass. Together, our results offer a dynamical systems perspective of the laminar NMM model, thereby providing a foundation for future modeling studies and investigations into cognitive processes that depend on cross-frequency coupling. Author SummaryUnderstanding how the brain generates and coordinates rhythms across different layers is essential for uncovering the mechanisms underlying perception, memory, and cognition. In this work, we analyze a previously developed model of mesoscopic brain activity that simulates the layered structure of the cortex and its ability to produce coupled slow and fast neural oscillations. Using tools from dynamical systems theory, we reveal how the model gives rise to a rich repertoire of dynamical patterns--including periodic, quasiperiodic, and chaotic activity--through the coexistence of multiple oscillatory modes. We also investigate how pathological changes, such as those linked to Alzheimers disease, alter the models dynamics and impair its capacity to sustain complex cross-frequency interactions. Finally, we show that the model remains stable when connected to another brain region, highlighting its robustness. Our findings provide a deeper understanding of how multifrequency neural rhythms may emerge, how they might break down in disease, and how this modeling framework can inform both future theoretical studies and the development of new brain models.

neuroscience↗