2,356 research outputs found

    How single neuron properties shape chaotic dynamics and signal transmission in random neural networks

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    While most models of randomly connected networks assume nodes with simple dynamics, nodes in realistic highly connected networks, such as neurons in the brain, exhibit intrinsic dynamics over multiple timescales. We analyze how the dynamical properties of nodes (such as single neurons) and recurrent connections interact to shape the effective dynamics in large randomly connected networks. A novel dynamical mean-field theory for strongly connected networks of multi-dimensional rate units shows that the power spectrum of the network activity in the chaotic phase emerges from a nonlinear sharpening of the frequency response function of single units. For the case of two-dimensional rate units with strong adaptation, we find that the network exhibits a state of "resonant chaos", characterized by robust, narrow-band stochastic oscillations. The coherence of stochastic oscillations is maximal at the onset of chaos and their correlation time scales with the adaptation timescale of single units. Surprisingly, the resonance frequency can be predicted from the properties of isolated units, even in the presence of heterogeneity in the adaptation parameters. In the presence of these internally-generated chaotic fluctuations, the transmission of weak, low-frequency signals is strongly enhanced by adaptation, whereas signal transmission is not influenced by adaptation in the non-chaotic regime. Our theoretical framework can be applied to other mechanisms at the level of single nodes, such as synaptic filtering, refractoriness or spike synchronization. These results advance our understanding of the interaction between the dynamics of single units and recurrent connectivity, which is a fundamental step toward the description of biologically realistic network models in the brain, or, more generally, networks of other physical or man-made complex dynamical units

    Mechanisms of Zero-Lag Synchronization in Cortical Motifs

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    Zero-lag synchronization between distant cortical areas has been observed in a diversity of experimental data sets and between many different regions of the brain. Several computational mechanisms have been proposed to account for such isochronous synchronization in the presence of long conduction delays: Of these, the phenomenon of "dynamical relaying" - a mechanism that relies on a specific network motif - has proven to be the most robust with respect to parameter mismatch and system noise. Surprisingly, despite a contrary belief in the community, the common driving motif is an unreliable means of establishing zero-lag synchrony. Although dynamical relaying has been validated in empirical and computational studies, the deeper dynamical mechanisms and comparison to dynamics on other motifs is lacking. By systematically comparing synchronization on a variety of small motifs, we establish that the presence of a single reciprocally connected pair - a "resonance pair" - plays a crucial role in disambiguating those motifs that foster zero-lag synchrony in the presence of conduction delays (such as dynamical relaying) from those that do not (such as the common driving triad). Remarkably, minor structural changes to the common driving motif that incorporate a reciprocal pair recover robust zero-lag synchrony. The findings are observed in computational models of spiking neurons, populations of spiking neurons and neural mass models, and arise whether the oscillatory systems are periodic, chaotic, noise-free or driven by stochastic inputs. The influence of the resonance pair is also robust to parameter mismatch and asymmetrical time delays amongst the elements of the motif. We call this manner of facilitating zero-lag synchrony resonance-induced synchronization, outline the conditions for its occurrence, and propose that it may be a general mechanism to promote zero-lag synchrony in the brain.Comment: 41 pages, 12 figures, and 11 supplementary figure

    Spontaneous and stimulus-induced coherent states of critically balanced neuronal networks

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    How the information microscopically processed by individual neurons is integrated and used in organizing the behavior of an animal is a central question in neuroscience. The coherence of neuronal dynamics over different scales has been suggested as a clue to the mechanisms underlying this integration. Balanced excitation and inhibition may amplify microscopic fluctuations to a macroscopic level, thus providing a mechanism for generating coherent multiscale dynamics. Previous theories of brain dynamics, however, were restricted to cases in which inhibition dominated excitation and suppressed fluctuations in the macroscopic population activity. In the present study, we investigate the dynamics of neuronal networks at a critical point between excitation-dominant and inhibition-dominant states. In these networks, the microscopic fluctuations are amplified by the strong excitation and inhibition to drive the macroscopic dynamics, while the macroscopic dynamics determine the statistics of the microscopic fluctuations. Developing a novel type of mean-field theory applicable to this class of interscale interactions, we show that the amplification mechanism generates spontaneous, irregular macroscopic rhythms similar to those observed in the brain. Through the same mechanism, microscopic inputs to a small number of neurons effectively entrain the dynamics of the whole network. These network dynamics undergo a probabilistic transition to a coherent state, as the magnitude of either the balanced excitation and inhibition or the external inputs is increased. Our mean-field theory successfully predicts the behavior of this model. Furthermore, we numerically demonstrate that the coherent dynamics can be used for state-dependent read-out of information from the network. These results show a novel form of neuronal information processing that connects neuronal dynamics on different scales.Comment: 20 pages 12 figures (main text) + 23 pages 6 figures (Appendix); Some of the results have been removed in the revision in order to reduce the volume. See the previous version for more result

    Evolutionary robotics and neuroscience

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