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Dalla Porta, L.

Publications and source records attributed to Dalla Porta, L..

9 recordsLinked to original sources

Inferring structural complexity from dynamical measures

Complexity, commonly defined as the coexistence of integration and differentiation, is a fundamental property of thalamocortical networks and is regarded as a prerequisite for adaptive brain function and consciousness. A variety of metrics have been developed to estimate neural complexity from recorded activity and are increasingly employed in both research and clinical settings. Yet, the extent to which these measures reflect specific architectural features of the underlying circuits remains poorly understood. Here, we used Wilson-Cowan mean-field equations to simulate neural dynamics across networks spanning a broad range of architectures. By systematically rewiring connectivity, we generated graded variations in the structural integration-differentiation balance and assessed a panel of complexity measures derived either from spontaneous activity (observational metrics) or from responses to external perturbations (perturbational metrics). Observational measures exhibited markedly heterogeneous behavior: some were primarily sensitive to network integration, others to differentiation, whereas some showed limited sensitivity to architectural manipulations. In contrast, perturbational measures robustly peaked at intermediate rewiring steps and scaled with small-worldness, consistent with architectures that combine local recurrence and distributed communication. Moreover, perturbational metrics proved robust to common-driver confounds and were highest in a wake-like regime near critical instability, declining as sleep-like dynamics became more widespread across the network. Taken together, these findings map widely used empirical complexity measures onto specific network architectures, reveal dynamical factors that can bias observational estimates, and provide guidance for inferring complexity in systems whose internal organization is inaccessible, unconventional, or only partially known, including brain organoids, non-human nervous systems, and synthetic neural networks.

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Intra- and Interhemispheric Signatures of Criticality at the Onset of Synchronization

The cerebral cortex must flexibly alternate between locally segregated activity that supports specialization and long-range interactions that enable integration. How cortical networks balance these competing demands remains unclear. We propose that fluctuations around a critical point between ordered and disordered phases provide a natural framework to understand coordinated neuronal activity across scales. Using simultaneous spiking recordings from the left and right prefrontal cortex (PFC) of freely behaving rats, we found that signatures of criticality emerged at the onset of neuronal synchronization, both locally within individual hemispheres and globally across the combined population. Over time, cortical activity explored a continuum of intra-and inter-hemispheric synchrony levels, including states in which neurons were locally desynchronized yet maintained interhemispheric coupling. A computational model operating near its critical regime reproduced these empirical patterns, capturing the characteristic relationship between local and long-range coordination. These results suggest that cortical networks achieve flexible transitions between local and global computation by fluctuating around a critical regime.

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The Connectome Modulates Critical Brain Dynamics Across Local and Global Scales

Neuronal activity in the brain has been hypothesized to operate near criticality-a dynamical regime poised between order and disorder that maximizes information processing, adaptability, and dynamic range. While criticality has been extensively studied at local scales (within neuronal populations) and at global scales (across interacting brain regions), the interplay between these levels remains poorly understood. Here, we propose a multiscale computational framework that bridges local and global criticality within a single, mechanistic model. At the mesoscopic level, individual brain regions are represented by neural mass models tuned near the transition between asynchronous and synchronous regimes. These regions are then coupled via an empirically derived mouse connectome to investigate how structural connectivity shapes the emergence of large-scale coordination. We show that (i) local near critical dynamics for an isolated brain region can be faithfully reproduced within a mean-field model framework, (ii) local distance to criticality is modulated by long-range coupling, (iii) whole-brain simulations reveal non-linear gradients of timescales and heterogeneous shifts towards/away from local criticality, and (iv) global criticality, manifested in scale-free avalanche distributions and optimal functional connectivity, emerges when local populations are locally tuned near criticality and coupled within an optimal range. These results demonstrate that local and global criticality are dynamically intertwined but not directly aligned, and that their relationship depends on the underlying structural connectivity. Our multiscale modeling framework provides a tractable tool for generating testable hypotheses on how brain criticality co-arises across scales and how it may be modulated in health and disease.

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Slow waves generation and propagation in a model of brain lesions

Slow waves (SWs), the hallmark of non-rapid eye movement (NREM) sleep, reflect the periodic occurrence of transient silent periods in cortical neurons (Down states). During NREM, SWs and Down states physiologically disrupt large-scale network interactions. Since early EEG studies, SWs have also been observed in awake patients after brain injury. Emerging evidence indicates that these intrusions of sleep-like activity interfere with ongoing network activity and contribute to motor and cognitive deficits; yet, the mechanisms governing the generation and spread of post-lesional SWs remain unclear. Here, we extend a neural mass model of EEG to capture transitions between wake-like and sleep-like dynamics and embed it in connectome-based networks with virtual lesions. This model supports that local disfacilitation, topology-dependent propagation, and synchrony-dependent amplification throughout the connectome are sufficient to produce post-lesional SWs. These mechanisms reproduce the spatial gradients of post-lesional SWs seen in patients and identify actionable targets for neuromodulation and rehabilitation.

neuroscience↗

Cholinergic heterogeneity facilitates synchronization and information flow in a whole-brain model

The human brain displays substantial regional variability in molecular, anatomical, and physiological organization. Yet, how this heterogeneity shapes large-scale neuronal dynamics remains poorly understood. To address this question, we employed a biologically informed whole-brain computational model capable of generating distinct brain states, from awake-like to sleep-like regimes. Our model was constrained by empirical human structural connectivity and spatial maps of cholinergic receptor gene expression, thereby embedding regional neuromodulatory variability into a macroscopic framework. We found that incorporating cholinergic heterogeneity had a significant impact on brain dynamics: it not only facilitated network synchronization but also enhanced information flow between brain regions. Furthermore, we addressed a particularly intricate dynamic regime characterized by the coexistence of localized sleep-like activity within otherwise awake-like states. We showed that the emergence of these slow waves was a byproduct of both regional levels of neuronal adaptation and structural connectivity. In summary, our findings highlight the critical role of molecular and anatomical heterogeneity in shaping global brain dynamics, suggesting new avenues for linking microscale diversity to macroscale function.

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H-current modulation of cortical Up and Down states

Understanding the link between cellular processes and brain function remains a key challenge in neuroscience. One crucial aspect is the interplay between specific ion channels and network dynamics. This work reveals a role for h-current, a hyperpolarization-activated cationic current, in shaping cortical slow oscillations. Cortical slow oscillations exhibit rhythmic periods of activity (Up states) alternating with silent periods (Down states). By progressively reducing h-current in both cortical slices and in a computational model, we observed Up states transformed into prolonged plateaus of sustained firing, while Down states were also significantly extended. This transformation led to a five-fold reduction in oscillation frequency. In a biophysical recurrent network model, we identified the cellular mechanisms: an increased input resistance and membrane time constant, increasing neuronal responsiveness to even weak inputs. HCN channels, the molecular basis of h-current, are known neuromodulatory targets, suggesting potential pathways for dynamic control of brain rhythms.

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A mean-field approach to the dynamics of networks of complex neurons, from nonlinear Integrate-and-Fire to Hodgkin-Huxley models

We present a mean-field formalism able to predict the collective dynamics of large networks of conductance-based interacting spiking neurons. We apply this formalism to several neuronal models, from the simplest Adaptive Exponential Integrate-and-Fire model to the more complex Hodgkin-Huxley and Morris-Lecar models. We show that the resulting mean-field models are capable of predicting the correct spontaneous activity of both excitatory and inhibitory neurons in asynchronous irregular regimes, typical of cortical dynamics. Moreover, it is possible to quantitatively predict the populations response to external stimuli in the form of external spike trains. This mean-field formalism therefore provides a paradigm to bridge the scale between population dynamics and the microscopic complexity of the individual cells physiology. NEW & NOTEWORTHYPopulation models are a powerful mathematical tool to study the dynamics of neuronal networks and to simulate the brain at macroscopic scales. We present a mean-field model capable of quantitatively predicting the temporal dynamics of a network of complex spiking neuronal models, from Integrate-and-Fire to Hodgkin-Huxley, thus linking population models to neurons electrophysiology. This opens a perspective on generating biologically realistic mean-field models from electrophysiological recordings.

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Criticality between cortical states

Since the first measurements of neuronal avalanches [1], the critical brain hypothesis has gained traction [2]. However, if the brain is critical, what is the phase transition? For several decades it has been known that the cerebral cortex operates in a diversity of regimes [3], ranging from highly synchronous states (e.g. slow wave sleep [4], with higher spiking variability) to desynchronized states (e.g. alert waking [5], with lower spiking variability). Here, using independent signatures of criticality, we show that a phase transition occurs in an intermediate value of spiking variability. The critical exponents point to a universality class different from mean-field directed percolation (MF-DP). Importantly, as the cortex hovers around this critical point [6], it follows a linear relation between the avalanche exponents that encompasses previous experimental results from different setups [7, 8] and is reproduced by a model.

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Modeling neuronal avalanches and long-range temporal correlations at the emergence of collective oscillations: continuously varying exponents mimic M/EEG results

We revisit the CROS (\"CRitical OScillations\") model which was recently proposed as an attempt to reproduce both scale-invariant neuronal avalanches and long-range time correlations. With excitatory and inhibitory stochastic neurons locally connected in a two-dimensional disordered network, the model exhibits a transition from an active to an oscillating state. Precisely at the transition, the fluctuations of the network activity have detrended fluctuation analysis (DFA) exponents close to one, and avalanches (defined as supra-threshold activity) have power law distributions of size and duration. By simulating larger system sizes, we show that, differently from previous results, the exponents governing the distributions of avalanche size and duration are not necessarily those of the mean-field directed percolation universality class (3/2 and 2, respectively). Instead, exponents obtained via a maximum-likelihood estimator vary continuously in a narrow region of parameter space. Around that critical region, moreover, the values of avalanche and DFA exponents display a spread with negative correlations, in qualitative agreement with the interindividual variability that was experimentally observed in M/EEG data.

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