No Arabic abstract
Most nervous systems encode information about stimuli in the responding activity of large neuronal networks. This activity often manifests itself as dynamically coordinated sequences of action potentials. Since multiple electrode recordings are now a standard tool in neuroscience research, it is important to have a measure of such network-wide behavioral coordination and information sharing, applicable to multiple neural spike train data. We propose a new statistic, informational coherence, which measures how much better one unit can be predicted by knowing the dynamical state of another. We argue informational coherence is a measure of association and shared information which is superior to traditional pairwise measures of synchronization and correlation. To find the dynamical states, we use a recently-introduced algorithm which reconstructs effective state spaces from stochastic time series. We then extend the pairwise measure to a multivariate analysis of the network by estimating the network multi-information. We illustrate our method by testing it on a detailed model of the transition from gamma to beta rhythms.
In this paper, we clarify the mechanisms underlying a general phenomenon present in pulse-coupled heterogeneous inhibitory networks: inhibition can induce not only suppression of the neural activity, as expected, but it can also promote neural reactivation. In particular, for globally coupled systems, the number of firing neurons monotonically reduces upon increasing the strength of inhibition (neurons death). However, the random pruning of the connections is able to reverse the action of inhibition, i.e. in a sparse network a sufficiently strong synaptic strength can surprisingly promote, rather than depress, the activity of the neurons (neurons rebirth). Thus the number of firing neurons reveals a minimum at some intermediate synaptic strength. We show that this minimum signals a transition from a regime dominated by the neurons with higher firing activity to a phase where all neurons are effectively sub-threshold and their irregular firing is driven by current fluctuations. We explain the origin of the transition by deriving an analytic mean field formulation of the problem able to provide the fraction of active neurons as well as the first two moments of their firing statistics. The introduction of a synaptic time scale does not modify the main aspects of the reported phenomenon. However, for sufficiently slow synapses the transition becomes dramatic, the system passes from a perfectly regular evolution to an irregular bursting dynamics. In this latter regime the model provides predictions consistent with experimental findings for a specific class of neurons, namely the medium spiny neurons in the striatum.
Noise is an inherent part of neuronal dynamics, and thus of the brain. It can be observed in neuronal activity at different spatiotemporal scales, including in neuronal membrane potentials, local field potentials, electroencephalography, and magnetoencephalography. A central research topic in contemporary neuroscience is to elucidate the functional role of noise in neuronal information processing. Experimental studies have shown that a suitable level of noise may enhance the detection of weak neuronal signals by means of stochastic resonance. In response, theoretical research, based on the theory of stochastic processes, nonlinear dynamics, and statistical physics, has made great strides in elucidating the mechanism and the many benefits of stochastic resonance in neuronal systems. In this perspective, we review recent research dedicated to neuronal stochastic resonance in biophysical mathematical models. We also explore the regulation of neuronal stochastic resonance, and we outline important open questions and directions for future research. A deeper understanding of neuronal stochastic resonance may afford us new insights into the highly impressive information processing in the brain.
Neuronal networks are controlled by a combination of the dynamics of individual neurons and the connectivity of the network that links them together. We study a minimal model of the preBotzinger complex, a small neuronal network that controls the breathing rhythm of mammals through periodic firing bursts. We show that the properties of a such a randomly connected network of identical excitatory neurons are fundamentally different from those of uniformly connected neuronal networks as described by mean-field theory. We show that (i) the connectivity properties of the networks determines the location of emergent pacemakers that trigger the firing bursts and (ii) that the collective desensitization that terminates the firing bursts is determined again by the network connectivity, through k-core clusters of neurons.
The brain can be understood as a collection of interacting neuronal oscillators, but the extent to which its sustained activity is due to coupling among brain areas is still unclear. Here we study the joint dynamics of two cortical columns described by Jansen-Rit neural mass models, and show that coupling between the columns gives rise to stochastic initiations of sustained collective activity, which can be interpreted as epileptic events. For large enough coupling strengths, termination of these events results mainly from the emergence of synchronization between the columns, and thus is controlled by coupling instead of noise. Stochastic triggering and noise-independent durations are characteristic of excitable dynamics, and thus we interpret our results in terms of collective excitability.
Networks of excitatory and inhibitory neurons display asynchronous irregular (AI) states, where the activities of the two populations are balanced. At the single cell level, it was shown that neurons subject to balanced and noisy synaptic inputs can display enhanced responsiveness. We show here that this enhanced responsiveness is also present at the network level, but only when single neurons are in a conductance state and fluctuation regime consistent with experimental measurements. In such states, the entire population of neurons is globally influenced by the external input. We suggest that this network-level enhanced responsiveness constitute a low-level form of sensory awareness.