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Lopez-Sola, E.

Publications and source records attributed to Lopez-Sola, E..

11 recordsLinked to original sources

Whole-Brain Models of Minimal Phenomenal Experience: Approaching Criticality through Jhana Meditation

Advanced meditation offers a powerful lens for investigating consciousness and for understanding how sustained training may contribute to human flourishing. In the spirit of neurophenomenology, we combine first-person reports with model-free empirical analyses and formal whole-brain modeling to investigate the mechanisms underlying advanced meditative states and minimal phenomenal experience (MPE). Specifically, we focus on jh[a]na meditation, a type of advanced concentrative absorption meditation (ACAM-J). Advanced practitioners accessed the eight ACAM-J states during ultra-high-field 7T functional magnetic resonance imaging. For each state, we first characterize empirical functional connectivity and then build a mechanistic whole-brain model that reproduces brain activity by modeling the dynamical regimes of different brain networks. We found that the later ACAM-J states, taken here as candidates for MPE, show increased large-scale functional integration and a shift of functional network dynamics toward near-critical working points. The default mode network (DMN) exhibits the largest shift, from a distant noise-driven regime during the control condition to near-critical dynamics during ACAM-J. We also observed that the trajectory of ACAM-J states is non-linear, with prominent reconfigurations at key meditative milestones. Our results suggest that MPE, as instantiated in later ACAM-J states, corresponds to a globally susceptible state where near-critical dynamics dominate. We interpret this near-critical regime as a form of "openness", in which constrained and differentiated patterns of brain activity give way to greater flexibility. In particular, increased DMN susceptibility is correlated with broader attention and reduced narrative thought, consistent with a more flexible mode of self-related processing. In this context, advanced meditation provides a powerful model for studying how sustained contemplative practice can profoundly shape brain dynamics and provide a window into core aspects of consciousness.

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Personalized whole-brain models of seizure propagation

Objective: Computational modeling has recently emerged as a powerful tool to better understand seizure dynamics and guide new treatment strategies. This work aims to develop and personalize whole-brain computational models in epilepsy using multimodal clinical data to simulate and evaluate individualized therapeutic strategies. Approach: We present a computational framework that constructs patient-specific whole-brain models of seizure propagation by integrating SEEG, MRI, and diffusion MRI data. The pipeline uses neural mass models for each node in the network, simulating whole-brain dynamics. Model personalization involves adjusting global and local parameters representing the excitability of individual brain areas, using an evolutionary algorithm that aims to maximize the correlation between empirical and synthetic functional connectivity matrices derived from SEEG data. Main results: The resulting personalized models successfully reproduce individual seizure propagation patterns and can be used to simulate therapeutic interventions like surgery, stimulation, or pharmacological interventions within a unified physiological framework. Notably, model predictions reveal distinct patient-specific responses across interventions, including variable sensitivity to different pharmacological agents and identification of critical regions whose removal or modulation reduced seizure spread. Significance: This framework provides a mechanistic, interpretable approach to simulate and compare individualized treatment strategies. By integrating multimodal data into a unified whole-brain model, it has the potential to improve clinical decision-making in epilepsy by identifying accessible and functionally relevant targets.

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Fast Interneuron Dysfunction in Laminar Neural Mass Model Reproduces Alzheimer's Oscillatory Biomarkers

Alzheimers disease (AD) is characterized by a progressive cognitive decline underpinned by disruptions in neural circuit dynamics. Early-stage AD is associated with cortical hyperexcitability, whereas later stages exhibit oscillatory slowing and hypoactivity, a progression observable in electrophysiological spectral characteristics. While previous studies have linked these changes to the dysfunction of fast-spiking parvalbumin-positive (PV) interneurons and neuronal loss associated with amyloid-beta (A{beta}) and hyperphos-phorylated tau (hp-{tau}) pathology, the precise mechanistic relationship between cellular and altered electrophysiology remains unclear. To study this relationship, we employed a Laminar Neural Mass Model that integrates excitatory and inhibitory neural populations within a biophysically informed columnar framework. The connectivity constant from PV cells to pyramidal neurons was gradually reduced to simulate the progressive neurotoxic effects of A{beta} oligomers. Other model parameters were systematically varied to compare with existing modeling literature and also to simulate the effects of hp-{tau}. All model predictions were compared to empirical M/EEG findings in the literature. Our simulations of PV interneuron dysfunction successfully reproduced the biphasic electrophysiological progression observed in AD: an early phase of hyperexcitability with increased gamma and alpha power, followed by oscillatory slowing and reduced spectral power. Alternative mechanisms and model parameters, such as increased excitatory drive, failed to replicate the observed biomarker trajectory. Additionally, to reconcile the hypoactivity and decreased firing rates observed in advanced AD stages, we combined the PV dysfunction model with a disruption of the pyramidal cell populations that reflects the neurotoxicity induced by hp-{tau}. Although this additional mechanism is not necessary to reproduce oscillatory changes in the isolated neural mass, it is crucial for aligning the model with evidence of reduced firing rates, metabolic activity, and cell loss and will enhance its applicability in future whole-brain modeling studies. These results support the hypothesis that at the local level, PV interneuron dysfunction is a primary driver of cortical electrophysiological alterations, while pyramidal neuron loss underlies later-stage severe hypoactivity. Our model provides a mechanistic framework for interpreting excitation-inhibition imbalance across AD progression, demonstrating the value of biophysically constrained models for interpreting electrophysiological biomarkers. Author summaryAlzheimers disease (AD) is not just a disorder of memory--it is a disease of brain networks. Before widespread neuronal loss occurs, the brain enters a state of hyperexcitability, which may contribute to disease progression. This hyperactivity is thought to arise from the selective dysfunction of inhibitory interneurons, particularly parvalbumin-positive (PV) interneurons, which play a crucial role in maintaining balanced brain activity. However, as the disease advances, a dramatic shift occurs, with neurons becoming progressively less active, leading to network breakdown. Understanding how this transition unfolds is essential for identifying new targets for early intervention. In this study, we developed a computational model of AD that represents the effects of amyloid-beta (A{beta}) oligomers and hyperphosphorylated tau (hp-{tau}) on neural circuits in a biologically meaningful way. Our model reproduces key features of M/EEG biomarkers, demonstrating that PV interneuron dysfunction leads to early hyperexcitability and the electrophysiological oscillatory changes characteristic of AD, while pyramidal cell pathology is necessary to drive later hypoactivity and network failure. By bridging molecular pathology mechanisms with mesoscale neural activity, our model provides a powerful tool for studying AD-related circuit dysfunction. It also highlights the importance of PV interneurons as a potential therapeutic target, paving the way for biologically informed interventions that could alter the course of the disease.

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Cross-Frequency Coupling as a Neural Substrate for Prediction Error Evaluation: A Laminar Neural Mass Modeling Approach

Predictive coding frameworks suggest that neural computations rely on hierarchical error minimization, where sensory signals are evaluated against internal model predictions. However, the neural implementation of this inference process remains unclear. We propose that cross-frequency coupling (CFC) furnishes a fundamental mechanism for this form of inference. We first demonstrate that our previously described Laminar Neural Mass Model (LaNMM) supports two key forms of CFC: (i) Signal-Envelope Coupling (SEC), where lowfrequency rhythms modulate the amplitude envelope of higher-frequency oscillations and (ii) Envelope-Envelope Coupling (EEC), where the envelopes of slower oscillations modulate the envelopes of higher-frequency rhythms. Then, we propose that, by encoding information in signals and their envelopes, these processes instantiate a hierarchical "Comparator" mechanism at the columnar level. Specifically, SEC generates fast prediction-error signals by subtracting top-down predictions from bottom-up oscillatory envelopes, while EEC operates at slower timescales to instantiate gating--a critical computational mechanism for precision-weighting and selective information routing. To establish the face validity and clinical implications of this proposal, we model perturbations of these CFC mechanisms to investigate their roles in pathophysiological and altered neuronal function. We illustrate how, in disorders such as Alzheimers disease, disruptions in gamma oscillations following dysfunction in fast-spiking inhibitory interneurons impact Comparator function with an aberrant amplification of prediction errors in the early stages and a drastic attenuation in late phases of the disease. In contrast, by increasing excitatory gain, serotonergic psychedelics diminish the modulatory effect of predictions, resulting in a failure to attenuate prediction error signals (c.f., a failure of sensory attenuation). Collectively, these findings implicate cross-frequency coupling across multiple temporal scales as a key computational mechanism supporting predictive coding and suggest that disruptions in these processes play a central role in disease. HighlightsO_LIUsing an encoding scheme where information is encoded in signals, their envelopes, and envelopes of envelopes, we show how to implement prediction error and precision modulation in a neural mass model through cross-frequency coupling (CFC). C_LIO_LIWe use the laminar neural mass model (LaNMM), which integrates Jansen-Rit and pyramidal interneuron gamma (PING) submodels to display fast and slow rhythms and provides mechanisms for a) Signal-Envelope Coupling (SEC), where slow-wave activity modulates the amplitude envelope of fast oscillations (analogous to phase-amplitude coupling), and b) Envelope-Envelope Coupling (EEC), where the envelopes of slower oscillations modulate the envelopes of higher-frequency rhythms. C_LIO_LIWe show how to use the LaNMM to implement information-based prediction-error evaluation (as used in Active Inference and Kolmogorov Theory), computing the approximate precision-weighted difference between incoming sensory data (envelopes) and internal model predictions (signals or envelopes). C_LIO_LIWe show that using these mechanisms, the Comparator mechanism can operate at multiple levels and timescales, generating fast prediction-error signals (via SEC) and slower gating signals that encode context (e.g., precision) (via EEC). C_LIO_LIOur model provides insights into the physiological and cognitive consequences of mesoscale circuital alterations in the context of predictive coding. First, we study disorders of fast-spiking interneurons, such as Alzheimers Disease (AD). In the early stages of AD, error evaluation and precision are disrupted (inflated error and reduced gating/weight of predictions), leading to higher prediction errors. In later stages, prediction errors are suppressed regardless of predictions or their precision. C_LIO_LIThen, we show how serotonergic psychedelics increase the effective weight of inputs and diminish that of predictions, resulting in higher prediction error signals. C_LIO_LIThese observations link oscillatory mechanisms and predictive coding alterations, and potentially with the subjective phenomena in each condition--including cognitive decline in AD and hallucinatory states under psychedelics. C_LI

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Collapse of directed functional hierarchy under classical serotonergic psychedelics

Despite divergent behavioral and phenomenological profiles, both psychedelic states and reduced states of consciousness have been associated with a flattening of the brains functional hierarchy. To address this apparent paradox, we developed a more specific definition of hierarchy based on the proximity of the brain to thermodynamic equilibrium and then applied it to investigate the changes to the functional hierarchy elicited by three classical serotonergic psychedelics - psilocybin, lysergic acid diethylamide, and dimethyltryptamine. We found that all three psychedelics consistently induced a global reduction in the functional hierarchy. In contrast to the flattening of the functional hierarchy observed during loss of consciousness, psychedelics displaced the brain towards equilibrium while simultaneously increasing the complexity of neural activity, indicating a unique mechanism linked to specific changes in the configuration and differentiation of resting-state networks. This work showcases how metrics based on statistical mechanics can be used for the specific characterization of different global brain states, contributing to the understanding of consciousness as a collective process emerging from complex neural interactions.

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Restoring Oscillatory Dynamics in Alzheimer's Disease: A Laminar Whole-Brain Model of Serotonergic Psychedelic Effects

Classical serotonergic psychedelics show promise in addressing neurodegenerative disorders such as Alzheimers disease by modulating pathological brain dynamics. However, the precise neurobiological mechanisms underlying their effects remain elusive. This study introduces a personalized whole-brain model built upon a laminar neural mass framework to elucidate these effects. Using multimodal neuroimaging data from thirty subjects diagnosed with mild to moderate Alzheimers disease, we simulate the impact of serotonin 2A receptor activation, characteristic of psychedelics, on cortical dynamics. By modulating the excitability of layer 5 pyramidal neurons, our models reproduce hallmark changes in EEG power spectra observed under psychedelics, including alpha power suppression and gamma power enhancement. These spectral shifts are shown to correlate strongly with the regional distribution of serotonin 2A receptors. Furthermore, simulated EEG reveals increased complexity and entropy, suggesting restored network function. These findings underscore the potential of serotonergic psychedelics to reestablish healthy oscillatory dynamics in the prodromal and early phases of Alzheimers disease and offer mechanistic insights into their potential therapeutic effects in neurodegenerative disorders.

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Neural geometrodynamics: a psychedelic perspective

We explore the intersection of neural dynamics and the effects of psychedelics in light of distinct timescales in a framework integrating concepts from dynamics, complexity, and plasticity. We call this framework neural geometrodynamics for its parallels with general relativitys description of the interplay of spacetime and matter. The geometry of trajectories within the dynamical landscape of "fast time" dynamics are shaped by the structure of a differential equation and its connectivity parameters, which themselves evolve over "slow time" driven by state-dependent and state-independent plasticity mechanisms. Finally, the adjustment of plasticity processes (metaplasticity) takes place in an "ultraslow" time scale. Psychedelics flatten the neural landscape, leading to heightened entropy and complexity of neural dynamics, as observed in neuroimaging and modeling studies linking increases in complexity with a disruption of functional integration. We highlight the relationship between criticality, the complexity of fast neural dynamics, and synaptic plasticity. Pathological, rigid, or "canalized" neural dynamics result in an ultrastable confined repertoire, allowing slower plastic changes to consolidate them further. However, under the influence of psychedelics, the destabilizing emergence of complex dynamics leads to a more fluid and adaptable neural state in a process that is amplified by the plasticity-enhancing effects of psychedelics. This shift manifests as an acute systemic increase of disorder and a possibly longer-lasting increase in complexity affecting both short-term dynamics and long-term plastic processes. Our framework offers a holistic perspective of the acute effects of these substances and their potential long-term impacts on neural structure and function.

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A physical neural mass model framework for the analysis of oscillatory generators from laminar electrophysiological recordings

Cortical function emerges from the interactions of multi-scale networks that may be studied at a high level using neural mass models (NMM), representing the mean activity of large numbers of neurons. In order to properly reproduce experimental data, these models require the addition of further elements. Here we provide a framework integrating conduction physics that can be used to simulate cortical electrophysiology measurements, particularly those obtained from multi-contact laminar electrodes. This is achieved by endowing NMMs with basic physical properties, such as the average laminar location of the apical and basal dendrites of pyramidal cell populations. We call this framework laminar NMM, or LaNMM for short. We then employ this framework to infer the location of oscillatory generators from laminar-resolved data collected from the prefrontal cortex in the macaque monkey. Based on the literature on columnar connectivity, we define a minimal neural mass model capable of generating amplitude and phase coupled slow (alpha/beta, 4-22 Hz) and fast (gamma, 30-250 Hz) oscillations. The synapse layer locations of the two pyramidal cell populations are treated as optimization parameters, together with two more LaNMM-specific parameters, to compare the models with the multi-contact recordings. We rank the candidate models using an optimization function that evaluates the match between the functional connectivity (FC) of the model and data, where the FC is defined by the covariance between bipolar voltage measurements at different cortical depths. The family of best solutions reproduces the FC of the observed electrophysiology while selecting locations of pyramidal cells and their synapses that result in the generation of fast activity at superficial layers and slow activity across most depths, in line with recent literature proposals. HighlightsO_LIWe provide a neural mass modeling formalism that includes a physical layer to simulate electrophysiology measurements. C_LIO_LITo analyze in-vivo data collected in the macaque monkey during a memory task, we propose a specific model with two coupled main circuits that can generate realistic electrophysiological signals in two important oscillatory regimes--the alpha/beta and the gamma bands. C_LIO_LIPhysical elements in the model shed light on the generation of oscillations in the two regimes and on the relative power distribution of fast and slow oscillatory signals across cortical depth, which we show can be altered by the choice of the reference location or method. C_LIO_LIThe model is contrasted with in-vivo data, with parameters adjusted by matching voltage statistics in the alpha/beta and gamma bands, leading to a solution with slow frequency components generated by synapses spanning most cortical layers and fast oscillations in superficial layers. C_LIO_LIThe resulting formalism provides useful tools and concepts to analyze and model data, with implications for understanding altered oscillatory EEG activity in dementia, Alzheimers disease and other disorders with oscillatory features. C_LI

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Towards a mesoscale physical modeling framework for stereotactic-EEG recordings

ObjectiveStereotactic-EEG (SEEG) and scalp EEG recordings can be modeled using mesoscale neural mass population models (NMM). However, the relationship between those mathematical models and the physics of the measurements is unclear. In addition, it is challenging to represent SEEG data by combining NMMs and volume conductor models due to the intermediate spatial scale represented by these measurements. ApproachWe provide a framework combining the multicompartmental modeling formalism and a detailed geometrical model to simulate the transmembrane currents that appear in layer 3, 5 and 6 pyramidal cells due to a synaptic input. With this approach, it is possible to realistically simulate the current source density (CSD) depth profile inside a cortical patch due to inputs localized into a single cortical layer and the induced voltage measured by two SEEG contacts using a volume conductor model. Based on this approach, we built a framework to connect the activity of a NMM with a volume conductor model and we simulated an example of SEEG signal as a proof of concept. Main resultsCSD depends strongly on the distribution of the synaptic inputs onto the different cortical layers and the equivalent current dipole strengths display substantial differences (of up to a factor of four in magnitude in our example). Thus, the inputs coming from different neural populations do not contribute equally to the electrophysiological recordings. A direct consequence of this is that the raw output of neural mass models is not a good proxy for electrical recordings. We also show that the simplest CSD model that can accurately reproduce SEEG measurements can be constructed from discrete monopolar sources (one per cortical layer). SignificanceOur results highlight the importance of including a physical model in NMMs to represent measurements. We provide a framework connecting microscale neuron models with the neural mass formalism and with physical models of the measurement process that can improve the accuracy of predicted electrophysiological recordings.

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A personalizable autonomous neural mass model of epileptic seizures

Work in the last two decades has shown that neural mass models (NMM) can realistically reproduce and explain epileptic seizure transitions as recorded by electrophysiological methods (EEG, SEEG). In previous work, advances were achieved by increasing excitation and heuristically varying network inhibitory coupling parameters in the models. Based on these early studies, we provide a laminar NMM capable of realistically reproducing the electrical activity recorded by SEEG in the epileptogenic zone during interictal to ictal states. With the exception of the external noise input into the pyramidal cell population, the model dynamics are autonomous. By setting the system at a point close to bifurcation, seizure-like transitions are generated, including pre-ictal spikes, low voltage fast activity, and ictal rhythmic activity. A novel element in the model is a physiologically motivated algorithm for chloride dynamics: the gain of GABAergic post-synaptic potentials is modulated by the pathological accumulation of chloride in pyramidal cells due to high inhibitory input and/or dysfunctional chloride transport. In addition, in order to simulate SEEG signals for comparison with real seizure recordings, the NMM is embedded first in a layered model of the neocortex and then in a realistic physical model. We compare modeling results with data from four epilepsy patient cases. By including key pathophysiological mechanisms, the proposed framework captures succinctly the electrophysiological phenomenology observed in ictal states, paving the way for robust personalization methods based on NMMs.

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Sense of Agency for Mental Actions: Insights from a Belief-Based Action-Effect Paradigm

A substantial body of research in the past few decades has converged on the idea that the so-called "sense of agency", the feeling of being in control of our own actions, arises from the integration of multiple sources of information at different levels. In this study, we investigated whether a measurable sense of agency can be detected for mental actions, without the contribution of motor components. We used a fake action-effect paradigm, where participants were led to think that a motor action or a particular thought could trigger a sound. Results showed that the high-level sense of agency, measured through explicit reports, was of comparable strength for motor and mental actions. The intentional binding effect, a phenomenon typically associated with the experience of agency, was also observed for both motor and mental actions, with the only exception of short action-effect delays. Furthermore, a consistent relationship between explicit reports of agency and intentional binding was found. Taken together, our results provide novel insights into the specific role of intentional cues in instantiating a sense of agency, even in the absence of motor signals. These results may have important implications for future brain-computer interfaces as well as for the study of pathological disruptions of agency.

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