No Arabic abstract
Cortical neural circuits display highly irregular spiking in individual neurons but variably sized collective firing, oscillations and critical avalanches at the population level, all of which have functional importance for information processing. Theoretically, the balance of excitation and inhibition inputs is thought to account for spiking irregularity and critical avalanches may originate from an underlying phase transition. However, the theoretical reconciliation of these multilevel dynamic aspects in neural circuits remains an open question. Herein, we study excitation-inhibition (E-I) balanced neuronal network with biologically realistic synaptic kinetics. It can maintain irregular spiking dynamics with different levels of synchrony and critical avalanches emerge near the synchronous transition point. We propose a novel semi-analytical mean-field theory to derive the field equations governing the network macroscopic dynamics. It reveals that the E-I balanced state of the network manifesting irregular individual spiking is characterized by a macroscopic stable state, which can be either a fixed point or a periodic motion and the transition is predicted by a Hopf bifurcation in the macroscopic field. Furthermore, by analyzing public data, we find the coexistence of irregular spiking and critical avalanches in the spontaneous spiking activities of mouse cortical slice in vitro, indicating the universality of the observed phenomena. Our theory unveils the mechanism that permits complex neural activities in different spatiotemporal scales to coexist and elucidates a possible origin of the criticality of neural systems. It also provides a novel tool for analyzing the macroscopic dynamics of E-I balanced networks and its relationship to the microscopic counterparts, which can be useful for large-scale modeling and computation of cortical dynamics.
Characterizing the in uence of network properties on the global emerging behavior of interacting elements constitutes a central question in many areas, from physical to social sciences. In this article we study a primary model of disordered neuronal networks with excitatory-inhibitory structure and balance constraints. We show how the interplay between structure and disorder in the connectivity leads to a universal transition from trivial to synchronized stationary or periodic states. This transition cannot be explained only through the analysis of the spectral density of the connectivity matrix. We provide a low dimensional approximation that shows the role of both the structure and disorder in the dynamics.
We investigate the dynamics of two models of biological networks with purely suppressive interactions between the units; species interacting via niche competition and neurons via inhibitory synaptic coupling. In both of these cases, power-law scaling of the density of states with probability arises without any fine-tuning of the model parameters. These results argue against the increasingly popular notion that non-equilibrium living systems operate at special critical points, driven by there by evolution so as to enable adaptive processing of input data.
We investigated the influence of efficacy of synaptic interaction on firing synchronization in excitatory neuronal networks. We found spike death phenomena, namely, the state of neurons transits from limit cycle to fixed point or transient state. The phenomena occur under the perturbation of excitatory synaptic interaction that has a high efficacy. We showed that the decrease of synaptic current results in spike death through depressing the feedback of sodium ionic current. In the networks with spike death property the degree of synchronization is lower and unsensitive to the heterogeneity of neurons. The mechanism of the influence is that the transition of neuron state disrupts the adjustment of the rhythm of neuron oscillation and prevents further increase of firing synchronization.
We study the dynamics of networks with inhibitory and excitatory leaky-integrate-and-fire neurons with short-term synaptic plasticity in the presence of depressive and facilitating mechanisms. The dynamics is analyzed by a Heterogeneous Mean-Field approximation, that allows to keep track of the effects of structural disorder in the network. We describe the complex behavior of different classes of excitatory and inhibitory components, that give rise to a rich dynamical phase-diagram as a function of the fraction of inhibitory neurons. By the same mean field approach, we study and solve a global inverse problem: reconstructing the degree probability distributions of the inhibitory and excitatory components and the fraction of inhibitory neurons from the knowledge of the average synaptic activity field. This approach unveils new perspectives in the numerical study of neural network dynamics and in the possibility of using these models as testbed for the analysis of experimental data.
This report is concerned with the relevance of the microscopic rules, that implement individual neuronal activation, in determining the collective dynamics, under variations of the network topology. To fix ideas we study the dynamics of two cellular automaton models, commonly used, rather in-distinctively, as the building blocks of large scale neuronal networks. One model, due to Greenberg & Hastings, (GH) can be described by evolution equations mimicking an integrate-and-fire process, while the other model, due to Kinouchi & Copelli, (KC) represents an abstract branching process, where a single active neuron activates a given number of postsynaptic neurons according to a prescribed activity branching ratio. Despite the apparent similarity between the local neuronal dynamics of the two models, it is shown that they exhibit very different collective dynamics as a function of the network topology. The GH model shows qualitatively different dynamical regimes as the network topology is varied, including transients to a ground (inactive) state, continuous and discontinuous dynamical phase transitions. In contrast, the KC model only exhibits a continuous phase transition, independently of the network topology. These results highlight the importance of paying attention to the microscopic rules chosen to model the inter-neuronal interactions in large scale numerical simulations, in particular when the network topology is far from a mean field description. One such case is the extensive work being done in the context of the Human Connectome, where a wide variety of types of models are being used to understand the brain collective dynamics.