Non-equilibrium critical dynamics of bursts in theta and delta Non-equilibrium critical dynamics of bursts in theta and delta rhythms as fundamental characteristic of sleep and wake micro- rhythms as fundamental characteristic of sleep and wake micro-architecture architecture

Origin and functions of intermittent transitions among sleep stages, including short awakenings and arousals, constitute a challenge to the current homeostatic framework for sleep regulation, focusing on factors modulating sleep over large time scales. Here we propose that the complex micro-architecture characterizing the sleep-wake cycle results from an underlying non-equilibrium critical dynamics, bridging collective behaviors across spatio-temporal scales. We investigate θ and δ wave dynamics in control rats and in rats with lesions of sleep-promoting neurons in the parafacial zone. We demonstrate that intermittent bursts in θ and δ rhythms exhibit a complex temporal organization, with long-range power-law correlations and a robust duality of power law ( θ -bursts, active phase) and exponential-like ( δ -bursts, quiescent phase) duration distributions, typical features of non-equilibrium systems self-organizing at criticality. Crucially, such temporal organization relates to anti-correlated coupling between θ - and δ -bursts, and is independent of the dominant physiologic state and lesions, a solid indication of a basic principle in sleep dynamics. cortical activity, and corresponding intermittent transitions in sleep micro-architecture, raise the hypothesis that non-equilibrium critical dynamics underlie sleep regulation at short time scales. We analyze θ and δ cortical rhythms in control rats and rats with lesions in the parafacial zone, which plays a significant role in the regulation of slow-wave sleep. The results demonstrate that critical dynamics underlie cortical activation during sleep and wake, and lay the foundation for a new paradigm, considering sleep micro-architec-ture as result of a non-equilibrium process and self-organization among neuronal assemblies to maintain a critical state, in contrast to the homeostasis paradigm of sleep regulation at large time scales. plotted together. (c) Average Spearman’s cross-correlation coefficient and PZ-lesioned rats in dark, light and 24h periods. Anti-correlations between consecutive - -bursts are stronger during light than during dark periods in each of the two rat groups. Comparing dark vs light periods, the Student’s t-test gives p = 0.651 for control rats and p 0.461 for rats. Importantly, PZ-lesioned rats generally exhibit stronger anti-correlations than the control group, in particular during dark periods, the strength of anti-correlated coupling increases with � 30% compared control rats (control vs t-test : 24h, = 0.158; dark, p = 0.121; light, p = 0.064). All correlation in groups significantly different from the obtained in the (red bars) after randomly reshuffling the original order of - and δ -bursts ( t-test : p < 0.001). All durations are calculated using a window w = 5 s and threshold Th R θ δ (as in Fig 1). This finding of anti-correlated coupling between θ - and δ -bursts durations further supported analysis based