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Register a new userInferring network connectivity from event timing patterns
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Reconstructing network connectivity from the collective dynamics of a system typically requires access to its complete continuous-time evolution although these are often experimentally inaccessible. Here we propose a theory for revealing physical connectivity of networked systems only from the event time series their intrinsic collective dynamics generate. Representing the patterns of event timings in an event space spanned by inter-event and cross-event intervals, we reveal which other units directly influence the inter-event times of any given unit. For illustration, we linearize an event space mapping constructed from the spiking patterns in model neural circuits to reveal the presence or absence of synapses between any pair of neurons as well as whether the coupling acts in an inhibiting or activating (excitatory) manner. The proposed model-independent reconstruction theory is scalable to larger networks and may thus play an important role in the reconstruction of networks from biology to social science and engineering.
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Functional brain network has been widely studied to understand the relationship between brain organization and behavior. In this paper, we aim to explore the functional connectivity of brain network under a emph{multi-step} cognitive task involving with consecutive behaviors, and further understand the effect of behaviors on the brain organization. The functional brain networks are constructed base on a high spatial and temporal resolution fMRI dataset and analyzed via complex network based approach. We find that at voxel level the functional brain network shows robust small-worldness and scale-free characteristics, while its assortativity and rich-club organization are slightly restricted to order of behaviors performed. More interestingly, the functional connectivity of brain network in activated ROIs strongly correlates with behaviors and behaves obvious differences restricted to order of behaviors performed. These empirical results suggest that the brain organization has the generic properties of small-worldness and scale-free characteristics, and its diverse function connectivity emerging from activated ROIs is strongly driven by these behavioral activities via the plasticity of brain.
Understanding the patterns of mobility of individuals is crucial for a number of reasons, from city planning to disaster management. There are two common ways of quantifying the amount of travel between locations: by direct observations that often involve privacy issues, e.g., tracking mobile phone locations, or by estimations from models. Typically, such models build on accurate knowledge of the population size at each location. However, when this information is not readily available, their applicability is rather limited. As mobile phones are ubiquitous, our aim is to investigate if mobility patterns can be inferred from aggregated mobile phone call data alone. Using data released by Orange for Ivory Coast, we show that human mobility is well predicted by a simple model based on the frequency of mobile phone calls between two locations and their geographical distance. We argue that the strength of the model comes from directly incorporating the social dimension of mobility. Furthermore, as only aggregated call data is required, the model helps to avoid potential privacy problems.
A systematic assessment of global neural network connectivity through direct electrophysiological assays has remained technically unfeasible even in dissociated neuronal cultures. We introduce an improved algorithmic approach based on Transfer Entropy to reconstruct approximations to network structural connectivities from network activity monitored through calcium fluorescence imaging. Based on information theory, our method requires no prior assumptions on the statistics of neuronal firing and neuronal connections. The performance of our algorithm is benchmarked on surrogate time-series of calcium fluorescence generated by the simulated dynamics of a network with known ground-truth topology. We find that the effective network topology revealed by Transfer Entropy depends qualitatively on the time-dependent dynamic state of the network (e.g., bursting or non-bursting). We thus demonstrate how conditioning with respect to the global mean activity improves the performance of our method. [...] Compared to other reconstruction strategies such as cross-correlation or Granger Causality methods, our method based on improved Transfer Entropy is remarkably more accurate. In particular, it provides a good reconstruction of the network clustering coefficient, allowing to discriminate between weakly or strongly clustered topologies, whereas on the other hand an approach based on cross-correlations would invariantly detect artificially high levels of clustering. Finally, we present the applicability of our method to real recordings of in vitro cortical cultures. We demonstrate that these networks are characterized by an elevated level of clustering compared to a random graph (although not extreme) and by a markedly non-local connectivity.
New cells are generated throughout life and integrate into the hippocampus via the process of adult neurogenesis. Epileptogenic brain injury induces many structural changes in the hippocampus, including the death of interneurons and altered connectivity patterns. The pathological neurogenic niche is associated with aberrant neurogenesis, though the role of the network-level changes in development of epilepsy is not well understood. In this paper, we use computational simulations to investigate the effect of network environment on structural and functional outcomes of neurogenesis. We find that small-world networks with external stimulus are able to be augmented by activity-seeking neurons in a manner that enhances activity at the stimulated sites without altering the network as a whole. However, when inhibition is decreased or connectivity patterns are changed, new cells are both less responsive to stimulus and the new cells are more likely to drive the network into bursting dynamics. Our results suggest that network-level changes caused by epileptogenic injury can create an environment where neurogenic reorganization can induce or intensify epileptic dynamics and abnormal integration of new cells.
The thermodynamic definition of entropy can be extended to nonequilibrium systems based on its relation to information. To apply this definition in practice requires access to the physical systems microstates, which may be prohibitively inefficient to sample or difficult to obtain experimentally. It is beneficial, therefore, to relate the entropy to other integrated properties which are accessible out of equilibrium. We focus on the structure factor, which describes the spatial correlations of density fluctuations and can be directly measured by scattering. The information gained by a given structure factor regarding an otherwise unknown system provides an upper bound for the systems entropy. We find that the maximum-entropy model corresponds to an equilibrium system with an effective pair-interaction. Approximate closed-form relations for the effective pair-potential and the resulting entropy in terms of the structure factor are obtained. As examples, the relations are used to estimate the entropy of an exactly solvable model and two simulated systems out of equilibrium. The focus is on low-dimensional examples, where our method, as well as a recently proposed compression-based one, can be tested against a rigorous direct-sampling technique. The entropy inferred from the structure factor is found to be consistent with the other methods, superior for larger system sizes, and accurate in identifying global transitions. Our approach allows for extensions of the theory to more complex systems and to higher-order correlations.
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