We investigate the regularity of spontaneous spiking activity on Newman-Watts small-world networks consisting of biophysically realistic Hodgkin-Huxley neurons with a tunable intensity of intrinsic noise and fraction of blocked voltage-gated sodium and potassium ion channels embedded in neuronal membranes. We show that there exists an optimal fraction of shortcut links between physically distant neurons, as well as an optimal intensity of intrinsic noise, which warrant an optimally ordered spontaneous spiking activity. This doubly coherence resonance-like phenomenon depends significantly, and can be controlled via the fraction of closed sodium and potassium ion channels, whereby the impacts can be understood via the analysis of the firing rate function as well as the deterministic system dynamics. Potential biological implications of our findings for information propagation across neural networks are also discussed.
We investigate inverse stochastic resonance (ISR), a recently reported phenomenon in which the spiking activity of a Hodgkin-Huxley model neuron subject to external noise exhibits a pronounced minimum as the noise intensity increases. We clarify the mechanism that underlies ISR and show that its most surprising features are a consequence of the dynamical structure of the model. Furthermore, we show that the ISR effect depends strongly on the procedures used to measure it. Our results are important for the experimentalist who seeks to observe the ISR phenomenon.
Inverse Stochastic Resonance (ISR) is a phenomenon in which the average spiking rate of a neuron exhibits a minimum with respect to noise. ISR has been studied in individual neurons, but here, we investigate ISR in scale-free networks, where the average spiking rate is calculated over the neuronal population. We use Hodgkin-Huxley model neurons with channel noise (i.e., stochastic gating variable dynamics), and the network connectivity is implemented via electrical or chemical connections (i.e., gap junctions or excitatory/inhibitory synapses). We find that the emergence of ISR depends on the interplay between each neuron’s intrinsic dynamical structure, channel noise, and network inputs, where the latter in turn depend on network structure parameters. We observe that with weak gap junction or excitatory synaptic coupling, network heterogeneity and sparseness tend to favor the emergence of ISR. With inhibitory coupling, ISR is quite robust. We also identify dynamical mechanisms that underlie various features of this ISR behavior. Our results suggest possible ways of experimentally observing ISR in actual neuronal systems.
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