Bistable Firing Pattern in a Neural Network Model

Excessively high, neural synchronization has been associated with epileptic seizures, one of the most common brain diseases worldwide. A better understanding of neural synchronization mechanisms can thus help control or even treat epilepsy. In this paper, we study neural synchronization in a random network where nodes are neurons with excitatory and inhibitory synapses, and neural activity for each node is provided by the adaptive exponential integrate-and-fire model. In this framework, we verify that the decrease in the influence of inhibition can generate synchronization originating from a pattern of desynchronized spikes. The transition from desynchronous spikes to synchronous bursts of activity, induced by varying the synaptic coupling, emerges in a hysteresis loop due to bistability where abnormal (excessively high synchronous) regimes exist. We verify that, for parameters in the bistability regime, a square current pulse can trigger excessively high (abnormal) synchronization, a process that can reproduce features of epileptic seizures. Then, we show that it is possible to suppress such abnormal synchronization by applying a small-amplitude external current on > 10% of the neurons in the network. Our results demonstrate that external electrical stimulation not only can trigger synchronous behavior, but more importantly, it can be used as a means to reduce abnormal synchronization and thus, control or treat effectively epileptic seizures.Peer Reviewe

Bistable firing pattern in a neural network model

Excessively high, neural synchronization has been associated with epileptic seizures, one of the most common brain diseases worldwide. A better understanding of neural synchronization mechanisms can thus help control or even treat epilepsy. In this paper, we study neural synchronization in a random network where nodes are neurons with excitatory and inhibitory synapses, and neural activity for each node is provided by the adaptive exponential integrate-and-fire model. In this framework, we verify that the decrease in the influence of inhibition can generate synchronization originating from a pattern of desynchronized spikes. The transition from desynchronous spikes to synchronous bursts of activity, induced by varying the synaptic coupling, emerges in a hysteresis loop due to bistability where abnormal (excessively high synchronous) regimes exist. We verify that, for parameters in the bistability regime, a square current pulse can trigger excessively high (abnormal) synchronization, a process that can reproduce features of epileptic seizures. Then, we show that it is possible to suppress such abnormal synchronization by applying a small-amplitude external current on > 10% of the neurons in the network. Our results demonstrate that external electrical stimulation not only can trigger synchronous behavior, but more importantly, it can be used as a means to reduce abnormal synchronization and thus, control or treat effectively epileptic seizures. © 2019 Protachevicz, Borges, Lameu, Ji, Iarosz, Kihara, Caldas, Szezech, Baptista, Macau, Antonopoulos, Batista and Kurths

Macroscopic equations governing noisy spiking neuronal populations

At functional scales, cortical behavior results from the complex interplay of a large number of excitable cells operating in noisy environments. Such systems resist to mathematical analysis, and computational neurosciences have largely relied on heuristic partial (and partially justified) macroscopic models, which successfully reproduced a number of relevant phenomena. The relationship between these macroscopic models and the spiking noisy dynamics of the underlying cells has since then been a great endeavor. Based on recent mean-field reductions for such spiking neurons, we present here {a principled reduction of large biologically plausible neuronal networks to firing-rate models, providing a rigorous} relationship between the macroscopic activity of populations of spiking neurons and popular macroscopic models, under a few assumptions (mainly linearity of the synapses). {The reduced model we derive consists of simple, low-dimensional ordinary differential equations with} parameters and {nonlinearities derived from} the underlying properties of the cells, and in particular the noise level. {These simple reduced models are shown to reproduce accurately the dynamics of large networks in numerical simulations}. Appropriate parameters and functions are made available {online} for different models of neurons: McKean, Fitzhugh-Nagumo and Hodgkin-Huxley models

Fundamental activity constraints lead to specific interpretations of the connectome

The continuous integration of experimental data into coherent models of the brain is an increasing challenge of modern neuroscience. Such models provide a bridge between structure and activity, and identify the mechanisms giving rise to experimental observations. Nevertheless, structurally realistic network models of spiking neurons are necessarily underconstrained even if experimental data on brain connectivity are incorporated to the best of our knowledge. Guided by physiological observations, any model must therefore explore the parameter ranges within the uncertainty of the data. Based on simulation results alone, however, the mechanisms underlying stable and physiologically realistic activity often remain obscure. We here employ a mean-field reduction of the dynamics, which allows us to include activity constraints into the process of model construction. We shape the phase space of a multi-scale network model of the vision-related areas of macaque cortex by systematically refining its connectivity. Fundamental constraints on the activity, i.e., prohibiting quiescence and requiring global stability, prove sufficient to obtain realistic layer- and area-specific activity. Only small adaptations of the structure are required, showing that the network operates close to an instability. The procedure identifies components of the network critical to its collective dynamics and creates hypotheses for structural data and future experiments. The method can be applied to networks involving any neuron model with a known gain function.Comment: J. Schuecker and M. Schmidt contributed equally to this wor