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Baud, M. O.

Publications and source records attributed to Baud, M. O..

4 recordsLinked to original sources

REM sleep reconfigures large-scale network dynamics: a link to its suppressive role in epilepsy

Converging evidence suggests that human brain activity operates near a critical-like regime in which balanced excitation and inhibition support efficient large-scale communication. The brains proximity to criticality may be dynamically reset across the sleep-wake cycle and altered by epilepsy, leading to aberrant oscillatory dynamics. Building on recent work demonstrating a tripartite interaction between networks synchronization, oscillatory amplitude bistability, and cross-frequency coupling in the human brain that seems to favour epileptic activity, we examined how this interaction, and its underlying large-scale dynamics are modulated across vigilance states. We analyzed overnight recordings from 20 patients with drug-resistant epilepsy undergoing presurgical evaluation and selected overall 20 minutes of continuous, artifact free stereo-electroencephalography (SEEG) spanning REM sleep, NREM stages N2 and N3, and eyes-closed resting wakefulness. Across states, we quantified phase synchronization, phase-amplitude coupling, bistability and their correlation. REM sleep was consistently associated with a reduction of these dynamics relative to NREM sleep and wakefulness. Importantly, the canonical correlation between these measures -- reflecting the strength of the tripartite interaction -- was significantly weaker during REM sleep. These findings indicate that vigilance states modulate this previously identified multiscale interaction in human brain networks and suggest that the reduced epileptogenicity of REM sleep can be associated with a disruption of coordinated synchronization, coupling, and bistable dynamics at the large-scale network level.

neuroscience↗

Emergent multidien cycles from partial circadian synchrony

Over the past decades, chronobiology has attracted great attention thanks to the elucidation of the molecular mechanisms underpinning the circadian cycle. Now, growing evidence suggests that cycles longer than circadian, so-called multidien cy-cles, are of crucial importance in physiological fluctuations spanning multiple days with repercussions in health and disease. Unlike circadian clocks, multidien cycles may not be genetically encoded, given their heterogeneity within and across individuals and systems. Here, we propose that multidien cycles may be generated by the interaction between partially-coupled circadian oscillators. To demonstrate this possibility theoretically, we use a ring model of coupled circadian oscillators and study how synchrony within this network evolves over time. We found that a free-running, about-weekly period robustly emerges from the networks dynamics. A range of additional multidien cycles resulted from subtle variations in the coupling parameters within the network with periodicities reminiscent of those observed across different species. Thus, our model of emergent multidien cycles from partial circadian synchrony constitutes a credible hypothesis for explaining the timing of a myriad of events on the scale of weeks and months in health and disease.

systems biology↗

Intrinsic neural timescales in the temporal lobe support an auditory processing hierarchy

During rest, intrinsic neural dynamics manifest at multiple timescales, which progressively increase along visual and somatosensory hierarchies. Theoretically, intrinsic timescales are thought to facilitate processing of external stimuli at multiple stages. However, direct links between timescales at rest and sensory processing, as well as translation to the auditory system are lacking. Here, we used intracranial electroencephalography in humans to show that in the auditory network, intrinsic neural timescales progressively increase, while the spectral slope flattens, from temporal to entorhinal cortex, hippocampus, and amygdala. Within the neocortex, intrinsic timescales exhibit spatial gradients that follow the temporal lobe anatomy. Crucially, intrinsic timescales at rest can explain the latency of auditory responses: as intrinsic timescales increase, so do the single-electrode response onset and peak latencies. Our results suggest that the human auditory network exhibits a repertoire of intrinsic neural dynamics, which manifest in cortical gradients with millimeter resolution and may provide a variety of temporal windows to support auditory processing.

neuroscience↗

Probing cortical excitability under GABAergic modulation

Cortical excitability, the variable response to a given cortical input, is widely studied in neuroscience, from slice experiments and in silico modeling work to human clinical settings. However, a unifying definition and a translational approach to the phenomenon are currently lacking. For example, at the onset of epileptic seizures, cortical excitability may impair resilience to perturbations (external or endogenous). In this study, we tested in vivo whether changes in cortical excitability quantified as evoked response to small perturbation corresponded to changes in resilience to larger perturbations. To do so, we used both cell-type circuit specific optogenetic stimulation in mice and direct intracranial stimulation in one human subject and quantified 1) evoked cortical responses to single pulses of varying intensity, and 2) evoked cortical facilitation and suppression to paired pulses at varying intervals. In the presence of a gamma-Aminobutyric acid (GABA) agonist or antagonist, we found that 1) cortical response to single pulses and 2) cortical facilitation decreased and increased, respectively. Additionally, using trains of opto-pulses in mice in the presence of a GABA agonist, we found increased resilience to the induction of seizures. With this study, we provide evidence for a tight correlation between cortical excitability and resilience, exploring a range of cortical dynamics, from physiological excitability, to pathological discharges. Our study carried out with two different stimulation methods in two species suggests that varying cortical excitability can be tracked with simple protocols involving minute short-lived perturbative stimuli.

neuroscience↗