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Register a new userInhibition causes ceaseless dynamics in networks of excitable nodes
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The collective dynamics of a network of excitable nodes changes dramatically when inhibitory nodes are introduced. We consider inhibitory nodes which may be activated just like excitatory nodes but, upon activating, decrease the probability of activation of network neighbors. We show that, although the direct effect of inhibitory nodes is to decrease activity, the collective dynamics becomes self-sustaining. We explain this counterintuitive result by defining and analyzing a branching function which may be thought of as an activity-dependent branching ratio. The shape of the branching function implies that for a range of global coupling parameters dynamics are self-sustaining. Within the self-sustaining region of parameter space lies a critical line along which dynamics take the form of avalanches with universal scaling of size and duration, embedded in ceaseless timeseries of activity. Our analyses, confirmed by numerical simulation, suggest that inhibition may play a counterintuitive role in excitable networks.
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We study a pulse-coupled dynamics of excitable elements in uncorrelated scale-free networks. Regimes of self-sustained activity are found for homogeneous and inhomogeneous couplings, in which the system displays a wide variety of behaviors, including periodic and irregular global spiking signals, as well as coherent oscillations, an unexpected form of synchronization. Our numerical results also show that the properties of the population firing rate depend on the size of the system, particularly its structure and average value over time. However, a few straightforward dynamical and topological strategies can be introduced to enhance or hinder these global behaviors, rendering a scenario where signal control is attainable, which incorporates a basic mechanism to turn off the dynamics permanently. As our main result, here we present a framework to estimate, in the stationary state, the mean firing rate over a long time window and to decompose the global dynamics into average values of the inter-spike-interval of each connectivity group. Our approach provides accurate predictions of these average quantities when the network exhibits high heterogeneity, a remarkable finding that is not restricted exclusively to the scale-free topology.
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An essential requirement for the representation of functional patterns in complex neural networks, such as the mammalian cerebral cortex, is the existence of stable network activations within a limited critical range. In this range, the activity of neural populations in the network persists between the extremes of quickly dying out, or activating the whole network. The nerve fiber network of the mammalian cerebral cortex possesses a modular organization extending across several levels of organization. Using a basic spreading model without inhibition, we investigated how functional activations of nodes propagate through such a hierarchically clustered network. The simulations demonstrated that persistent and scalable activation could be produced in clustered networks, but not in random networks of the same size. Moreover, the parameter range yielding critical activations was substantially larger in hierarchical cluster networks than in small-world networks of the same size. These findings indicate that a hierarchical cluster architecture may provide the structural basis for the stable and diverse functional patterns observed in cortical networks.
The $1/f$-like decay observed in the power spectrum of electro-physiological signals, along with scale-free statistics of the so-called neuronal avalanches, constitute evidences of criticality in neuronal systems. Recent in vitro studies have shown that avalanche dynamics at criticality corresponds to some specific balance of excitation and inhibition, thus suggesting that this is a basic feature of the critical state of neuronal networks. In particular, a lack of inhibition significantly alters the temporal structure of the spontaneous avalanche activity and leads to an anomalous abundance of large avalanches. Here we study the relationship between network inhibition and the scaling exponent $beta$ of the power spectral density (PSD) of avalanche activity in a neuronal network model inspired in Self-Organized Criticality (SOC). We find that this scaling exponent depends on the percentage of inhibitory synapses and tends to the value $beta = 1$ for a percentage of about 30%. More specifically, $beta$ is close to $2$, namely brownian noise, for purely excitatory networks and decreases towards values in the interval $[1,1.4]$ as the percentage of inhibitory synapses ranges between 20 and 30%, in agreement with experimental findings. These results indicate that the level of inhibition affects the frequency spectrum of resting brain activity and suggest the analysis of the PSD scaling behavior as a possible tool to study pathological conditions.
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