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Effects of network topology, transmission delays, and refractoriness on the response of coupled excitable systems to a stochastic stimulus.

ABSTRACT: We study the effects of network topology on the response of networks of coupled discrete excitable systems to an external stochastic stimulus. We extend recent results that characterize the response in terms of spectral properties of the adjacency matrix by allowing distributions in the transmission delays and in the number of refractory states and by developing a nonperturbative approximation to the steady state network response. We confirm our theoretical results with numerical simulations. We find that the steady state response amplitude is inversely proportional to the duration of refractoriness, which reduces the maximum attainable dynamic range. We also find that transmission delays alter the time required to reach steady state. Importantly, neither delays nor refractoriness impact the general prediction that criticality and maximum dynamic range occur when the largest eigenvalue of the adjacency matrix is unity.

SUBMITTER: Larremore DB

PROVIDER: S-EPMC3183795 | biostudies-other | 2011 Jun

REPOSITORIES: biostudies-other

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Project description:Directed random graph models frequently are used successfully in modeling the population dynamics of networks of cortical neurons connected by chemical synapses. Experimental results consistently reveal that neuronal network topology is complex, however, in the sense that it differs statistically from a random network, and differs for classes of neurons that are physiologically different. This suggests that complex network models whose subnetworks have distinct topological structure may be a useful, and more biologically realistic, alternative to random networks. Here we demonstrate that the balanced excitation and inhibition frequently observed in small cortical regions can transiently disappear in otherwise standard neuronal-scale models of fluctuation-driven dynamics, solely because the random network topology was replaced by a complex clustered one, whilst not changing the in-degree of any neurons. In this network, a small subset of cells whose inhibition comes only from outside their local cluster are the cause of bistable population dynamics, where different clusters of these cells irregularly switch back and forth from a sparsely firing state to a highly active state. Transitions to the highly active state occur when a cluster of these cells spikes sufficiently often to cause strong unbalanced positive feedback to each other. Transitions back to the sparsely firing state rely on occasional large fluctuations in the amount of non-local inhibition received. Neurons in the model are homogeneous in their intrinsic dynamics and in-degrees, but differ in the abundance of various directed feedback motifs in which they participate. Our findings suggest that (i) models and simulations should take into account complex structure that varies for neuron and synapse classes; (ii) differences in the dynamics of neurons with similar intrinsic properties may be caused by their membership in distinctive local networks; (iii) it is important to identify neurons that share physiological properties and location, but differ in their connectivity.

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Effects of network topology, transmission delays, and refractoriness on the response of coupled excitable systems to a stochastic stimulus.

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